BioMedLib Search Engine [ goto HOMEPAGE ]

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Kidney amino acid transport.

Near complete reabsorption of filtered amino acids is a main specialized transport function of the kidney proximal tubule.

A number of other amino acid transporters expressed in the basolateral membrane of proximal kidney tubule cells subserve either specialized metabolic functions, such as the production of ammonium, or are part of the cellular housekeeping equipment.

Some mutations of B(0)AT1 differentially interact with these accessory subunits, providing an explanation for differential intestinal phenotypes among Hartnup patients.

The basolateral efflux of numerous amino acids from kidney tubular cells is mediated by heteromeric amino acid transporters that function as obligatory exchangers.

[MeSH-major] Amino Acid Transport Systems / metabolism. Amino Acids / metabolism. Kidney / metabolism

[MeSH-minor] Amino Acid Transport Systems, Neutral / metabolism. Amino Acid Transport Systems, Neutral / physiology. Animals. Anion Transport Proteins / physiology. Antiporters / physiology. Biological Transport. Humans. Kidney Tubules, Proximal / physiology

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nat Genet. 1999 Mar;21(3):293-6 [10080182.001]

[Cites] Nature. 1996 Oct 17;383(6601):634-7 [8857541.001]

[Cites] J Pharmacol Exp Ther. 2004 Aug;310(2):695-702 [15051798.001]

[Cites] Pflugers Arch. 2005 Nov;451(2):338-48 [16133263.001]

[Cites] Curr Opin Clin Nutr Metab Care. 2000 Jan;3(1):51-7 [10642084.001]

[Cites] Gene. 2002 Jun 12;292(1-2):81-90 [12119102.001]

[Cites] J Biol Chem. 1999 Dec 3;274(49):34948-54 [10574970.001]

[Cites] Am J Clin Nutr. 2004 Feb;79(2):185-97 [14749222.001]

[Cites] Pflugers Arch. 2003 Feb;445(5):529-33 [12634921.001]

[Cites] Nat Genet. 2004 Sep;36(9):999-1002 [15286787.001]

[Cites] J Am Soc Nephrol. 2003 Apr;14(4):837-47 [12660317.001]

[Cites] Physiol Rev. 1998 Oct;78(4):969-1054 [9790568.001]

[Cites] J Biol Chem. 2002 Jun 7;277(23):21017-26 [11907033.001]

[Cites] Physiol Rev. 2008 Jan;88(1):249-86 [18195088.001]

[Cites] J Clin Invest. 2008 Dec;118(12):3881-92 [19033659.001]

[Cites] Nature. 2006 Dec 21;444(7122):1088-91 [17167413.001]

[Cites] EMBO J. 1999 Jan 4;18(1):49-57 [9878049.001]

[Cites] Biochem J. 2005 Aug 1;389(Pt 3):745-51 [15804236.001]

[Cites] Nature. 2004 Oct 14;431(7010):811-8 [15483603.001]

[Cites] Pflugers Arch. 2004 Feb;447(5):465-8 [14624363.001]

[Cites] J Biol Chem. 1996 Jun 21;271(25):14883-90 [8662767.001]

[Cites] Tohoku J Exp Med. 2006 Jan;208(1):25-31 [16340170.001]

[Cites] Biochem Biophys Res Commun. 2003 May 16;304(4):747-54 [12727219.001]

[Cites] Nature. 1992 Dec 3;360(6403):467-71 [1280334.001]

[Cites] Gastroenterology. 2004 Nov;127(5):1410-22 [15521011.001]

[Cites] Am J Physiol Renal Physiol. 2007 Feb;292(2):F555-66 [17003226.001]

[Cites] Am J Physiol Renal Physiol. 2006 Feb;290(2):F376-83 [16174864.001]

[Cites] J Biol Chem. 1998 Dec 4;273(49):32437-45 [9829974.001]

[Cites] Pflugers Arch. 2004 Feb;447(5):610-8 [12905028.001]

[Cites] J Biol Chem. 2004 Jun 4;279(23):24467-76 [15044460.001]

[Cites] J Inherit Metab Dis. 2007 Oct;30(5):716-21 [17588131.001]

[Cites] Am J Physiol. 1997 Dec;273(6 Pt 2):F1023-9 [9435692.001]

[Cites] Am J Physiol Renal Physiol. 2007 Feb;292(2):F533-44 [16985211.001]

[Cites] Annu Rev Nutr. 1995;15:133-59 [8527215.001]

[Cites] FASEB J. 2008 Aug;22(8):2880-7 [18424768.001]

[Cites] Pflugers Arch. 2004 Feb;447(5):776-9 [12748860.001]

[Cites] Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E428-34 [11788376.001]

[Cites] Mol Cell Biol. 2004 May;24(10 ):4166-73 [15121838.001]

[Cites] Biochem J. 2005 Mar 15;386(Pt 3):417-22 [15689184.001]

[Cites] Nature. 2005 Sep 8;437(7056):215-23 [16041361.001]

[Cites] J Membr Biol. 2001 Apr 1;180(3):213-20 [11337893.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7206-11 [11390972.001]

[Cites] J Membr Biol. 1999 Dec 1;172(3):181-92 [10568788.001]

[Cites] Am J Physiol Cell Physiol. 2001 Sep;281(3):C963-71 [11502573.001]

[Cites] Am J Physiol Renal Physiol. 2001 Jan;280(1):F10-8 [11133510.001]

[Cites] J Membr Biol. 1982;66(3):213-25 [6808139.001]

[Cites] J Biol Chem. 2005 Mar 11;280(10):8974-84 [15632147.001]

[Cites] Gastroenterology. 2009 Mar;136(3):872-82 [19185582.001]

[Cites] Pflugers Arch. 2007 Jun;454(3):507-16 [17273864.001]

[Cites] Curr Probl Clin Biochem. 1976;6:173-89 [11964.001]

[Cites] Physiology (Bethesda). 2006 Apr;21:93-102 [16565475.001]

[Cites] J Cell Physiol. 2006 Mar;206(3):771-9 [16245314.001]

[Cites] Annu Rev Physiol. 2005;67:557-72 [15709970.001]

[Cites] Physiol Rev. 1990 Jan;70(1):43-77 [2404290.001]

[Cites] J Biol Chem. 2003 Jan 10;278(2):1316-22 [12417581.001]

[Cites] Nat Genet. 1999 Mar;21(3):297-301 [10080183.001]

[Cites] J Am Soc Nephrol. 2005 Apr;16(4):869-77 [15716335.001]

[Cites] Am J Physiol Renal Physiol. 2003 May;284(5):F885-92 [12676733.001]

[Cites] J Biol Chem. 2006 Sep 8;281(36):26552-61 [16825196.001]

[Cites] Nat Genet. 2004 Sep;36(9):1003-7 [15286788.001]

(PMID = 19184091.001).

[ISSN] 1432-2013

[Journal-full-title] Pflugers Archiv : European journal of physiology

[ISO-abbreviation] Pflugers Arch.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Germany

[Chemical-registry-number] 0 / Amino Acid Transport Systems; 0 / Amino Acid Transport Systems, Neutral; 0 / Amino Acids; 0 / Anion Transport Proteins; 0 / Antiporters; 0 / SLC26A8 protein, human; 0 / SLC6A19 protein, human

[Number-of-references] 60

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Comparison of kidney injury molecule-1 and other nephrotoxicity biomarkers in urine and kidney following acute exposure to gentamicin, mercury, and chromium.

Sensitive biomarkers are needed to detect kidney injury at the earliest stages.

The objective of this study was to determine whether the appearance of kidney injury molecule-1 (Kim-1) protein ectodomain in urine and kidney injury molecule-1/hepatitis A viral cellular receptor-1 (Kim-1/Havcr1) gene expression in kidney tissue may be more predictive of renal injury after exposure to nephrotoxicants when compared to traditionally used biomarkers.

The results showed that increases in urinary Kim-1 and kidney Kim-1/Havcr1 gene expression paralleled the degree of severity of renal histopathology and were detected at lower doses of nephrotoxicants when compared to blood urea nitrogen (BUN), serum creatinine, and urinary N-acetyl-beta-D-glucosaminidase (NAG).

Urinary Kim-1 and kidney Kim-1/Havcr1 expression appear to be sensitive and tissue-specific biomarkers that will improve detection of early acute kidney injury following exposure to nephrotoxic chemicals and drugs.

MedlinePlus Health Information. consumer health - Kidney Diseases.

MedlinePlus Health Information. consumer health - Mercury.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. MERCURY, ELEMENTAL .

Hazardous Substances Data Bank. CHROMIUM, ELEMENTAL .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Acta Vitaminol Enzymol. 1984;6(2):103-7 [6496253.001]

[Cites] Am J Physiol Renal Physiol. 2007 Jan;292(1):F313-20 [16896183.001]

[Cites] Environ Health Perspect. 1991 May;92:71-4 [1935854.001]

[Cites] Pharmacol Toxicol. 1991 May;68(5):317-21 [1946176.001]

[Cites] Gen Pharmacol. 1995 Nov;26(7):1477-87 [8690234.001]

[Cites] EMBO J. 1996 Aug 15;15(16):4282-96 [8861957.001]

[Cites] Drug Saf. 1997 Mar;16(3):205-31 [9098657.001]

[Cites] J Biol Chem. 1998 Feb 13;273(7):4135-42 [9461608.001]

[Cites] Toxicol Pathol. 1998 Jan-Feb;26(1):92-103 [9502391.001]

[Cites] J Virol. 1998 Aug;72(8):6621-8 [9658108.001]

[Cites] J Am Soc Nephrol. 2005 Apr;16(4):1126-34 [15744000.001]

[Cites] BMC Nephrol. 2005;6:4 [15854231.001]

[Cites] J Am Soc Nephrol. 2005 Nov;16(11):3365-70 [16177006.001]

[Cites] Am J Physiol Renal Physiol. 2006 Feb;290(2):F517-29 [16174863.001]

[Cites] J Am Soc Nephrol. 2007 Mar;18(3):904-12 [17267747.001]

[Cites] Am J Surg Pathol. 2007 Mar;31(3):371-81 [17325478.001]

[Cites] Ren Fail. 2002 Nov;24(6):687-90 [12472192.001]

[Cites] Free Radic Biol Med. 2003 Jun 1;34(11):1390-8 [12757849.001]

[Cites] Toxicol Sci. 2003 Sep;75(1):208-22 [12832660.001]

[Cites] Am J Physiol Renal Physiol. 2004 Mar;286(3):F552-63 [14600030.001]

[Cites] Am J Med. 1968 May;44(5):664-705 [5646427.001]

[Cites] Toxicol Appl Pharmacol. 1980 Jul;54(3):443-53 [6446781.001]

[Cites] J Toxicol Environ Health. 1982 Jan;9(1):119-26 [6460873.001]

[Cites] Biochem Pharmacol. 1982 Oct 1;31(19):3093-100 [6216890.001]

[Cites] Pharmacol Rev. 2000 Mar;52(1):113-43 [10699157.001]

[Cites] Therapie. 2000 Jan-Feb;55(1):91-6 [10860006.001]

[Cites] J Environ Sci Health B. 2001 Sep;36(5):687-97 [11599730.001]

[Cites] Kidney Int. 2002 Jul;62(1):237-44 [12081583.001]

[Cites] Cleve Clin J Med. 2002 Jul;69(7):569-74 [12109642.001]

[Cites] J Biol Chem. 2002 Oct 18;277(42):39739-48 [12138159.001]

[Cites] Kidney Int. 1991 Apr;39(4):639-46 [1711136.001]

[Cites] Am J Physiol Renal Physiol. 2006 Aug;291(2):F456-64 [16467126.001]

[Cites] Am J Physiol Renal Physiol. 2007 Jan;292(1):F131-9 [16835406.001]

[Cites] Am J Physiol Renal Physiol. 2002 Dec;283(6):F1326-36 [12388382.001]

(PMID = 17934191.001).

[ISSN] 1096-6080

[Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology

[ISO-abbreviation] Toxicol. Sci.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK 072831; United States / NIEHS NIH HHS / ES / ES016723-02; United States / NIDDK NIH HHS / DK / R37 DK039773; United States / NIDDK NIH HHS / DK / DK 074099; United States / NIDDK NIH HHS / DK / R01 DK072381-04; United States / NIDDK NIH HHS / DK / R01 DK072381; United States / NIDDK NIH HHS / DK / R33 DK074099; United States / NIEHS NIH HHS / ES / R00 ES016723-02; United States / NIDDK NIH HHS / DK / DK 039773; United States / NIDDK NIH HHS / DK / R21 DK074099; United States / NIEHS NIH HHS / ES / R00 ES016723; United States / NIDDK NIH HHS / DK / R01 DK039773; None / None / / R01 DK072381-04

[Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; 0 / Cell Adhesion Molecules; 0 / Gentamicins; 0 / Havcr1protein, rat; 0 / Membrane Proteins; 0 / Protein Synthesis Inhibitors; 0R0008Q3JB / Chromium; 63231-63-0 / RNA; 7535-00-4 / Galactosamine; FXS1BY2PGL / Mercury; V956696549 / Acetylglucosamine

[Other-IDs] NLM/ NIHMS110357; NLM/ PMC2744478

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Influence of dialysis duration and modality on kidney transplant outcomes.

BACKGROUND: The influence of pretransplantation dialysis on kidney transplant outcomes has been the subject of longstanding interest.

Although increased time on dialysis prior to kidney transplantation is associated with decreased graft and patient survivals, analyses of the impact of dialysis modality on kidney allograft outcome have produced conflicting results.

OBJECTIVE: The objective of this study was to evaluate the influence of dialysis duration and modality on the function and survival of renal allografts.

PATIENTS: We retrospectively reviewed the clinical data of 421 adults who received first kidney transplantations from cadaveric heart-beating donors performed in our unit from May 1989 to May 2007.

Three hundred seventy-four patients (88.8%) were on hemodialysis (HD) prior to kidney transplantation, including 247 patients (58.7%) on treatment for at least 24 months.

Renal function at 3, 12, 60, and 96 months was similar between the 2 groups.

No differences were observed in renal function or graft and patient survivals comparing HD or peritoneal dialysis (PD).

[MeSH-major] Kidney Failure, Chronic / surgery. Kidney Transplantation / physiology. Renal Dialysis

[MeSH-minor] Adult. Age Factors. Female. Graft Survival. Humans. Kidney Function Tests. Living Donors. Male. Middle Aged. Postoperative Complications / epidemiology. Retrospective Studies. Sex Characteristics. Survival Analysis. Survivors. Time Factors. Tissue Donors / supply & distribution. Treatment Outcome. Young Adult

MedlinePlus Health Information. consumer health - Dialysis.

MedlinePlus Health Information. consumer health - Kidney Failure.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19376365.001).

[ISSN] 0041-1345

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

Advertisement

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The effect of successful kidney transplantation on ventricular dysfunction and pulmonary hypertension.

BACKGROUND: Heart disease is a frequent complication of chronic kidney disease and the major cause of death in patients on renal replacement therapy.

The purpose of this study was to evaluate the impact of successful kidney transplantation on systolic and diastolic ventricular dysfunction and pulmonary arterial hypertension in patients with chronic kidney disease (CKD).

METHODS: The study included 35 patients >18 years of age with CKD who had successful kidney transplantations.

The LVEF of the entire group increased from 52% to 64% (P < .001) by 12 months after kidney transplant.

CONCLUSIONS: Because kidney transplantation led to considerable improvement in left ventricular systolic and diastolic function as well as pulmonary arterial pressure of patients with CKD, optimal treatment for dysfunction and transplant as soon as possible is recommended.

[MeSH-major] Hypertension, Pulmonary / etiology. Kidney Failure, Chronic / surgery. Kidney Transplantation. Ventricular Dysfunction, Left / etiology

Genetic Alliance. consumer health - Pulmonary Hypertension.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Kidney Failure.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

MedlinePlus Health Information. consumer health - Pulmonary Hypertension.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright © 2010 Elsevier Inc. All rights reserved.

(PMID = 21094809.001).

[ISSN] 1873-2623

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Transplant tourism: Outcomes of United States residents who undergo kidney transplantation overseas.

BACKGROUND: Although international commerce in kidney transplantation is a reality, little is known about U.S. residents who travel abroad for kidney transplantation.

METHODS: We retrospectively reviewed the clinical outcomes of patients who were evaluated at the University of Minnesota Medical Center or Hennepin County Medical Center, but then surreptitiously underwent kidney transplantation overseas.

RESULTS: We identified 10 patients who underwent kidney transplantation outside the United States between September 16, 2002 and June 30, 2006 and then returned for care in our programs.

CONCLUSIONS: Kidney function and graft survival were generally good after surreptitious overseas kidney transplantation.

[MeSH-major] Graft Survival. Kidney Transplantation. Travel

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

MedlinePlus Health Information. consumer health - Traveler's Health.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17198255.001).

[ISSN] 0041-1337

[Journal-full-title] Transplantation

[ISO-abbreviation] Transplantation

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Native kidney function after renal transplantation combined with other solid organs in preemptive patients.

Kidney transplantations combined with other solid organs are progressively increasing in number.

There are no guidelines regarding the nephrologic indications for combined transplantations, namely liver-kidney (LKT), or heart-kidney (HKT), in preemptive patients with chronic kidney failure who are not on regular dialysis therapy.

The objective of this study was to assess the functional contribution of the native kidneys after preemptive kidney transplantation combined with other solid organs.

From 2004, 9 patients (aged 50.3 +/- 8.5 years) with chronic kidney failure (creatinine 2.5 +/- 1.0 mg/dL) caused by polycystic kidney disease (n = 4), vascular nephropathy (n = 2), interstitial nephropathy (n = 1), glomerulonephritis (n = 1), or end-stage kidney disease (n = 1), underwent combined transplantations (8 LKT, 1 HKT).

A scintigraphic functional study (Tc-99DMSA or Tc-99mMAG3), was performed at 4 +/- 3 months after transplantation to evaluate the functional contribution of both the native kidneys and the graft.

At the time of scintigraphy, renal function in all patients was 1.3 +/- 0.3 mg/dL.

The functional contribution of the transplanted kidneys was on average 77 +/- 18%.

At follow-up after 36 months, patient and kidney survivals were 100%.

The study confirmed a high risk of loss of native kidney function in the presence of organic nephropathy.

[MeSH-major] Kidney Transplantation / physiology. Organ Transplantation / physiology

[MeSH-minor] Adult. Creatinine / blood. Female. Glomerular Filtration Rate. Heart Transplantation / physiology. Humans. Kidney Diseases / classification. Kidney Diseases / surgery. Kidney Failure, Chronic / surgery. Kidney Function Tests. Liver Transplantation / physiology. Male. Middle Aged. Polycystic Kidney Diseases / surgery

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

MedlinePlus Health Information. consumer health - Organ Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright (c) 2010. Published by Elsevier Inc.

(PMID = 20534213.001).

[ISSN] 1873-2623

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] AYI8EX34EU / Creatinine

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Establishment of a rat model of cervical syndrome with kidney deficiency].

OBJECTIVE: To establish a rat model of cervical syndrome (CS) with kidney deficiency.

METHODS: A group of 30 three-month-old female Sprague-Dawley rats were randomly divided into normal control group, CS group and CS with kidney deficiency group (combined group), with 10 rats in each group.

Rats in the normal control group received no treatment, rats in the CS group underwent only resection of cervical muscles and ligaments as unbalanced dynamic and static animal model, and rats in combined group underwent resection of both cervical muscles and ovaries as kidney deficiency model.

Kidney deficiency was determined by observing the morphologic changes of uterus and appendages, detecting the weight of uterus and appendages and the content of serum estradiol (E(2)).

CONCLUSION: The rat model of CS with kidney deficiency is established.

Kidney deficiency can aggravate cervical intervertebral disc degeneration.

[MeSH-minor] Animals. Female. Kidney Diseases. Ovariectomy. Random Allocation. Rats. Rats, Sprague-Dawley

MedlinePlus Health Information. consumer health - Neck Injuries and Disorders.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18847538.001).

[ISSN] 1672-1977

[Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine

[ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Long-term follow-up of living kidney donors: a longitudinal study.

OBJECTIVE: To analyse retrospectively the general health status and renal and cardiovascular consequences of living-related kidney donation, as the long-term effects of unilateral nephrectomy for kidney donation are of particular interest with the currently increasing practice of living-donor transplantation.

PATIENTS AND METHODS: Living-related kidney donors (1400) who had donated their kidneys between 1976 and 2002 were asked to attend a dedicated donor follow-up clinic starting in 2004.

We attempted to contact all donors to determine the long-term outcome of their remaining kidney.

All kidney donors who responded had a detailed assessment, and were questioned about rehabilitation and their feelings on donating a kidney.

[MeSH-major] Health Status. Kidney. Living Donors. Nephrectomy / adverse effects. Tissue and Organ Harvesting / adverse effects

MedlinePlus Health Information. consumer health - Organ Donation.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17941927.001).

[ISSN] 1464-410X

[Journal-full-title] BJU international

[ISO-abbreviation] BJU Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Tumor size does not predict risk of metastatic disease or prognosis of small renal cell carcinomas.

PURPOSE: We characterized the clinicopathological features and the prognosis of small solid renal tumors defined as tumors 4 cm or smaller.

MATERIALS AND METHODS: We identified 1,208 patients who were treated with nephrectomy at 5 international academic centers for small solid renal tumors.

RESULTS: Of the tumors 88% were renal cell carcinoma and 12% were benign.

Of those with renal cell carcinoma 995 (93%) were localized (N0M0) and 72 (7%) presented with metastatic disease.

Tumor size did not predict synchronous metastatic disease.

The incidence of metastatic disease in the tumor size ranges 0.1 to 1.0, 1.1 to 2.0, 2.1 to 3.0 and 3.1 to 4.0 cm was 7%, 6%, 5% and 8%, respectively (p = 0.322).

The majority of patients who died of renal cell carcinoma (54%) presented with synchronous metastatic disease, but 3% of patients with localized disease also died of renal cell carcinoma.

Progression-free survival (28 months) was better than for patients with metastatic disease having a primary tumor greater than 4 cm (8 months).

Tumor size was not retained as an independent prognostic factor of survival in multivariate analyses.

The University of California Integrated Staging System and the Karakiewicz nomogram were the best predictors of cancer specific survival for all renal cell carcinoma stages (c-index 0.87).

CONCLUSIONS: More than 85% of small solid renal tumors are renal cell carcinoma.

The majority of localized small renal tumors can be cured with existing surgical approaches.

Tumor size alone is not sufficient to distinguish renal cell carcinoma with benign behavior from aggressive small renal cell carcinoma.

Survival of patients with small metastatic renal cell carcinoma is better then expected.

The biology of these unique tumors should be further studied.

[MeSH-major] Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology

[MeSH-minor] Female. Humans. Male. Middle Aged. Neoplasm Recurrence, Local. Nephrectomy. Prognosis. Survival Rate

MedlinePlus Health Information. consumer health - Kidney Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentIn] Eur Urol. 2009 Mar;55(3):751-2 [19650211.001]

[CommentIn] J Urol. 2008 May;179(5):1657 [18343448.001]

(PMID = 18343437.001).

[ISSN] 1527-3792

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Differences in kidney function and incident hypertension: the multi-ethnic study of atherosclerosis.

BACKGROUND: Kidney disease and hypertension commonly coexist, yet the direction of their association is still debated.

OBJECTIVE: To evaluate whether early kidney dysfunction, measured by serum cystatin C levels and urinary albumin excretion, predates hypertension in adults without clinically recognized kidney or cardiovascular disease.

PARTICIPANTS: 2767 MESA participants without prevalent hypertension, cardiovascular disease, or clinically recognized kidney disease (an estimated glomerular filtration rate <60 mL/min per 1.73 m2 or microalbuminuria).

LIMITATIONS: Unmeasured characteristics may have confounded observed associations of kidney markers with hypertension.

CONCLUSION: Differences in kidney function, indicated by cystatin C levels, are associated with incident hypertension among individuals without clinical kidney or cardiovascular disease.

These population-based findings complement experimental work implicating early kidney damage in the pathogenesis of essential hypertension.

MedlinePlus Health Information. consumer health - High Blood Pressure.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Am J Kidney Dis. 1996 Dec;28(6):811-21 [8957032.001]

[Cites] J Hum Hypertens. 1996 Oct;10(10):691-4 [9004096.001]

[Cites] Diabetes Care. 1998 Jul;21(7):1076-9 [9653598.001]

[Cites] Ann Intern Med. 1999 Mar 16;130(6):461-70 [10075613.001]

[Cites] Scand J Clin Lab Invest. 1999 Feb;59(1):1-8 [10206092.001]

[Cites] Lancet. 1963 Mar 30;1(7283):677-82 [14014100.001]

[Cites] Circulation. 2005 Mar 22;111(11):1370-6 [15738353.001]

[Cites] Am J Transplant. 2001 Sep;1(3):222-7 [12102255.001]

[Cites] Lancet. 2002 Aug 31;360(9334):659-65 [12241871.001]

[Cites] Arch Intern Med. 2005 Apr 25;165(8):923-8 [15851645.001]

[Cites] Kidney Int. 2005 Jun;67(6):2089-100 [15882252.001]

[Cites] N Engl J Med. 2005 May 19;352(20):2049-60 [15901858.001]

[Cites] Kidney Int Suppl. 2005 Aug;(97):S68-77 [16014104.001]

[Cites] Mayo Clin Proc. 2005 Oct;80(10):1270-7 [16212138.001]

[Cites] J Am Soc Nephrol. 2006 Feb;17(2):331-5 [16434504.001]

[Cites] Ann Intern Med. 2006 Aug 15;145(4):247-54 [16908915.001]

[Cites] Am J Kidney Dis. 2000 Jul;36(1):29-34 [10873868.001]

[Cites] N Engl J Med. 2002 Mar 21;346(12):913-23 [11907292.001]

[Cites] J Am Soc Nephrol. 2002 Apr;13(4):1034-9 [11912263.001]

[Cites] Am J Epidemiol. 2002 Nov 1;156(9):871-81 [12397006.001]

[Cites] Am J Kidney Dis. 2003 Jan;41(1):1-12 [12500213.001]

[Cites] N Engl J Med. 2003 Jan 9;348(2):101-8 [12519920.001]

[Cites] Diabetes Care. 2003 Nov;26(11):3160-7 [14578255.001]

[Cites] Hypertension. 2003 Dec;42(6):1206-52 [14656957.001]

[Cites] Kidney Int. 2004 Apr;65(4):1416-21 [15086483.001]

[Cites] Am J Med. 1972 May;52(5):584-94 [4337474.001]

[Cites] Circ Res. 1975 Jun;36(6):692-6 [1093748.001]

[Cites] J Clin Invest. 1986 Jun;77(6):1993-2000 [3011863.001]

[Cites] Arch Intern Med. 1987 May;147(5):943-4 [3555378.001]

[Cites] J Clin Epidemiol. 1992 Jun;45(6):683-92 [1607909.001]

[Cites] N Engl J Med. 1992 Jul 16;327(3):151-6 [1608406.001]

[Cites] Lancet. 1992 Dec 12;340(8833):1435-6 [1360561.001]

[Cites] BMJ. 1993 Jan 2;306(6869):24-7 [8435572.001]

[Cites] Hypertension. 1994 Sep;24(3):301-8 [8082936.001]

[Cites] Kidney Int. 1995 Jan;47(1):312-8 [7731163.001]

[Cites] Clin Exp Hypertens. 1996 Apr-May;18(3-4):305-21 [8743023.001]

[Cites] Circulation. 1996 Sep 15;94(6):1310-5 [8822985.001]

[CommentIn] Ann Intern Med. 2008 Aug 19;149(4):284; author reply 284 [18711167.001]

(PMID = 18378946.001).

[ISSN] 1539-3704

[Journal-full-title] Annals of internal medicine

[ISO-abbreviation] Ann. Intern. Med.

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HC / N01-HC-95162; United States / NHLBI NIH HHS / HC / N01-HC-95163; United States / NHLBI NIH HHS / HL / N01HC95169; United States / NHLBI NIH HHS / HC / N01-HC-95159; United States / NCRR NIH HHS / RR / KL2 RR025015-01; United States / NHLBI NIH HHS / HC / N01-HC-95165; United States / NCATS NIH HHS / TR / TL1 TR000422; United States / NHLBI NIH HHS / HC / N01-HC-95169; United States / NHLBI NIH HHS / HC / N01-HC-95164; United States / NHLBI NIH HHS / HL / N01HC95165; United States / NHLBI NIH HHS / HL / N01HC95159; United States / NHLBI NIH HHS / HC / N01-HC-95160; United States / NIDDK NIH HHS / DK / K23 DK63274-01; United States / NCRR NIH HHS / RR / KL2 RR025015; United States / NHLBI NIH HHS / HC / N01-HC-95161; United States / NCATS NIH HHS / TR / UL1 TR000423; United States / NIDDK NIH HHS / DK / K23 DK063274

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / CST3 protein, human; 0 / Cystatin C; 0 / Cystatins; AYI8EX34EU / Creatinine

[Other-IDs] NLM/ NIHMS267500; NLM/ PMC3044648

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pilot study of probiotic dietary supplementation for promoting healthy kidney function in patients with chronic kidney disease.

INTRODUCTION: Uremic syndrome consists of nitrogenous waste retention, deficiency in kidney-derived hormones, and reduced acid excretion, and, if untreated, may progress to coma and eventual death.

Previous experience suggests that oral administration of a probiotic formulation of selected microbial strains may extend renoprotection via intraintestinal extraction of toxic waste solutes in patients with chronic kidney disease (CKD)stages 3 and 4.

[MeSH-major] Probiotics. Renal Insufficiency, Chronic / therapy. Uremia / prevention & control

[MeSH-minor] Adult. Aged. Argentina. Canada. Creatinine / analysis. Dietary Supplements / standards. Disease Progression. Double-Blind Method. Female. Humans. Kidney Function Tests. Male. Middle Aged. Nigeria. Pilot Projects. Protective Agents / pharmacokinetics. Quality of Life. Self Report. Treatment Outcome. United States. Uric Acid / analysis. Young Adult

Genetic Alliance. consumer health - Kidney Disease.

MedlinePlus Health Information. consumer health - Chronic Kidney Disease.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20721651.001).

[ISSN] 1865-8652

[Journal-full-title] Advances in therapy

[ISO-abbreviation] Adv Ther

[Language] eng

[Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial

[Publication-country] United States

[Chemical-registry-number] 0 / Protective Agents; 268B43MJ25 / Uric Acid; AYI8EX34EU / Creatinine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Sirolimus-based immunosuppression in kidney transplantation for type 2 diabetic nephropathy.

INTRODUCTION: Kidney transplantation is the best replacement therapy of type 2 diabetic patients and recently similar graft and patient survival between diabetic and nondiabetic recipients has been reported.

We present our experience with sirolimus-based immunosuppression in a population of 24 type 2 diabetic patients who underwent a kidney transplantation.

PATIENTS AND METHODS: From January 2001 to December 2006, 396 kidney transplantations were performed.

Twenty-four patients had type 2 diabetes mellitus as a cause of end-stage renal disease.

A slightly better kidney functionality was observed in group B patients.

CONCLUSIONS: Sirolimus-based immunosuppression is safe and efficacious in type 2 diabetic patients who underwent a kidney transplantation, allowing a better glucose metabolism control.

[MeSH-major] Diabetes Mellitus, Type 2 / complications. Diabetic Nephropathies / etiology. Diabetic Nephropathies / surgery. Immunosuppression. Immunosuppressive Agents / therapeutic use. Kidney Transplantation. Sirolimus / therapeutic use

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Diabetes Type 2.

MedlinePlus Health Information. consumer health - Diabetic Kidney Problems.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

Hazardous Substances Data Bank. SIROLIMUS .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2010 S. Karger AG, Basel.

(PMID = 20389159.001).

[ISSN] 1423-0399

[Journal-full-title] Urologia internationalis

[ISO-abbreviation] Urol. Int.

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Immunosuppressive Agents; W36ZG6FT64 / Sirolimus

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Study strategies for neurobiology mechanism of "kidney storing will and responding to fear"].

The theory of traditional Chinese medicine (TCM) deems that kidney essence is the material basis of formation, development and function of the brain and it maintains human being's psychomotility and behavior.

Moreover, kidney essence is the material basis of emotional activity.

The emotion theory in TCM deems that kidney stores will and responds to fear.

Combining the TCM theory with the modern psychological theory on stress, and from the points of views of the emotion regulation, the formation, consolidation, extraction and extinction of fear memory, and the plasticity of amygdala-hippocampus-prefrontal cortex nervous pathway, as well as the results of pharmacological studies of prescriptions and herbs for invigorating the kidney, the authors explained in this article the pathological mechanisms of kidney deficiency due to attack of fear, and revealed the material basis, the action modes, and the neurobiological mechanisms of the kidney in controlling and regulating emotional activity.

[MeSH-major] Fear / physiology. Kidney / physiology. Medicine, Chinese Traditional. Stress, Psychological

MedlinePlus Health Information. consumer health - Stress.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20141730.001).

[ISSN] 1672-1977

[Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine

[ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Pulse wave velocity and vascular calcification at different stages of chronic kidney disease.

BACKGROUND: Increased arterial stiffness and vascular calcification have been recognized as important predictors of cardiovascular mortality in patients with chronic kidney disease.

METHOD: In order to examine the precise temporal link between aortic stiffness and cardiovascular risk at the earliest stages of chronic kidney disease, we studied a cohort of 150 patients with chronic kidney disease (52 stage 2/3 patients, 51 stage 4/5 patients and 47 stage 5D patients).

RESULTS: Regardless of the disease stage, patients with chronic kidney disease had higher adjusted pulse wave velocity than controls with preserved renal function (14.6 +/- 3.8 vs. 10.7 +/- 1.7 m/s, respectively; P < 0.0001).

Regarding aortic calcification, there was a gradual but significant rise in later chronic kidney disease stages.

CONCLUSION: We found that both vascular stiffness and vascular calcification appear early in patients with chronic kidney disease, but only vascular calcification worsens as the disease progresses.

The increase of vascular stiffness in adult patients with chronic kidney disease seems to be more related to age, systolic blood pressure, diabetes and vascular calcification than to uremic toxicity.

[MeSH-major] Aorta, Abdominal / pathology. Aorta, Thoracic / pathology. Blood Circulation / physiology. Blood Pressure / physiology. Calcinosis / pathology. Kidney Failure, Chronic / pathology

Genetic Alliance. consumer health - Kidney Disease.

MedlinePlus Health Information. consumer health - Kidney Failure.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19927012.001).

[ISSN] 1473-5598

[Journal-full-title] Journal of hypertension

[ISO-abbreviation] J. Hypertens.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Preclinical evaluation of erythropoietin administration in a model of radiation-induced kidney dysfunction.

PURPOSE: To test whether the clinically available growth factor erythropoietin (EPO) influences radiation-induced normal-tissue damage in a model of kidney dysfunction.

METHODS: Animal experiments were conducted to test the role of EPO administration in a C3H mouse model of unilateral kidney irradiation with 6, 8, and 10 Gy and to assess the effects of 2 different dose levels of EPO.

The kidney function was assessed before radiotherapy, as well as 19, 25, 31, and 37 weeks thereafter by means of (99m)Tc-dimercaptosuccinat scans (static scintigraphy).

RESULTS: Concomitant EPO administration significantly increased the degree of radiation-induced kidney dysfunction.

CONCLUSION: Administration of growth factors concomitant to radiotherapy might modify the development of kidney dysfunction.

Although insulin-like growth factor-1 has previously been shown to protect the kidney, such an effect could not be demonstrated for EPO.

[MeSH-major] Erythropoietin / adverse effects. Kidney / radiation effects. Radiation Injuries, Experimental / prevention & control. Radiation Tolerance / drug effects

Hazardous Substances Data Bank. EPOETIN ALFA .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[ErratumIn] Int J Radiat Oncol Biol Phys. 2006 Jul 1;65(3):960. Schnaitera, Andrea [corrected to Schnaiter, Andrea]; Caia, Lu [corrected to Cai, Lu]

(PMID = 16580501.001).

[ISSN] 0360-3016

[Journal-full-title] International journal of radiation oncology, biology, physics

[ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Radiopharmaceuticals; 0 / Recombinant Proteins; 11096-26-7 / Erythropoietin; 494JNQ8L28 / Technetium Tc 99m Dimercaptosuccinic Acid; 64FS3BFH5W / Epoetin Alfa

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Distant-organ changes after acute kidney injury.

Acute kidney injury (AKI) contributes significantly to morbidity and mortality in both adults and children.

Leukocyte trafficking, cytokine expression, cell adhesion-molecule expression and membrane ion and water-channel expression in distant organs are deranged after kidney injury.

The responses to oxidative stress after AKI are also altered, suggesting complex mechanisms of crosstalk between the injured kidney and distant organs.

[MeSH-major] Acute Kidney Injury / complications. Acute Kidney Injury / immunology. Cytokines / immunology. Models, Immunological. Multiple Organ Failure / complications. Multiple Organ Failure / immunology. Neutrophil Activation / immunology

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Copyright 2008 S. Karger AG, Basel.

(PMID = 18802379.001).

[ISSN] 1660-2137

[Journal-full-title] Nephron. Physiology

[ISO-abbreviation] Nephron Physiol

[Language] eng

[Grant] United States / NHLBI NIH HHS / HV / N01 HV028180

[Publication-type] Journal Article; Review

[Publication-country] Switzerland

[Chemical-registry-number] 0 / Cytokines

[Number-of-references] 26

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Microinjection and electroporation of embryonic kidney explants: an improved method.

Embryonic kidney explants are routinely used to study the molecular regulation of kidney development.

In this study, we show that a high voltage with a short pulse time is preferable for mouse kidney explants.

We suggest that our described conditions will make microinjection and electroporation a more effective method to study gene function in the developing mouse kidney.

[MeSH-major] Electroporation / methods. Kidney / embryology. Microinjections / methods

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17495853.001).

[ISSN] 0085-2538

[Journal-full-title] Kidney international

[ISO-abbreviation] Kidney Int.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins; EC 3.2.1.23 / beta-Galactosidase

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Familial multilocular cystic nephroma: a variant of a unique renal neoplasm.

Multilocular cystic nephroma (MCN) is a benign renal lesion believed to be unilateral and nonfamilial.

[MeSH-major] Kidney Neoplasms / genetics

[MeSH-minor] Child, Preschool. Humans. Infant. Kidney Diseases, Cystic / pathology. Male

MedlinePlus Health Information. consumer health - Kidney Cancer.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17656243.001).

[ISSN] 1527-9995

[Journal-full-title] Urology

[ISO-abbreviation] Urology

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Urgency priority in kidney transplantation in Rio Grande do Sul.

In 2002, it was established a system of urgency priority for kidney transplantations in cases with no vascular or peritoneal access for dialysis.

We reviewed cases of urgency priority request for kidney transplantation addressed to the CNCDO from May 2002 to August 2005.

Within this period the CNCDO received 35 urgency priority requests for kidney transplantation (mean, 1 every 1.2 months).

Among the 31 accepted, 26 (83%) had the transplantation performed in an average time of 19.6 days (range, 1-90), representing only 3.2% of all cadaveric kidney transplantations during that period.

[MeSH-major] Kidney Transplantation / statistics & numerical data. Tissue and Organ Procurement / statistics & numerical data. Waiting Lists

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17362736.001).

[ISSN] 0041-1345

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Kidney transplantation in older adults: does age affect graft survival?

INTRODUCTION: There is a paucity of data on long-term patient and graft survival in the older kidney recipients.

Our aim was to evaluate the long-term outcomes of kidney transplantation in patients aged 50 years and older and compare them with outcomes in younger recipients.

Patients who had received a cadaveric kidney allograft were excluded from the study.

CONCLUSION: Kidney transplantation should be considered in patients older than 50 years, since the graft survival rate is acceptable in this population, and early mortality and complications in this group are not different than those of younger recipients.

Although older patients have a shorter life expectancy, they benefit from renal transplantation in ways similar to younger kidney transplant recipients.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17629878.001).

[ISSN] 1735-1308

[Journal-full-title] Urology journal

[ISO-abbreviation] Urol J

[Language] eng

[Publication-type] Journal Article

[Publication-country] Iran

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Acute renal failure and severe hypertension from a page kidney post-transplant biopsy.

Page kidney refers to a clinical picture characterized by acute onset of hypertension due to external compression of the kidneys from hematoma, tumor, lymphocele, or urinoma.

Hypertension is believed to result from renin-angiotensin-aldosterone activation triggered by renal hypoperfusion and microvascular ischemia.

Renal failure, in addition to hypertension, may occur in the setting of a single functional kidney or a diseased contralateral kidney.

We report a case of a patient who had a transplant kidney biopsy complicated by a subcapsular perinephric hematoma.

The patient presented with an acute increase in blood pressure and a rapid rise in serum creatinine following a transplant kidney routine biopsy.

Early recognition and rapid intervention are needed in order to correct hypertension and reverse acute renal failure in Page kidney occurring in renal transplant recipients.

[MeSH-major] Acute Kidney Injury / physiopathology. Hematoma / physiopathology. Hypertension / physiopathology. Kidney Transplantation / adverse effects

MedlinePlus Health Information. consumer health - High Blood Pressure.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 20694451.001).

[ISSN] 1537-744X

[Journal-full-title] TheScientificWorldJournal

[ISO-abbreviation] ScientificWorldJournal

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] England

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Regulatory T cells suppress innate immunity in kidney ischemia-reperfusion injury.

Both innate and adaptive mechanisms participate in the pathogenesis of kidney ischemia-reperfusion injury (IRI), but the role of regulatory immune mechanisms is unknown.

We hypothesized that the anti-inflammatory effects of CD4(+)CD25(+)FoxP3(+) regulatory T cells (Tregs) protect against renal IRI.

Partial depletion of Tregs with an anti-CD25 mAb potentiated kidney damage induced by IRI.

Reducing the number of Tregs resulted in more neutrophils, macrophages, and innate cytokine transcription in the kidney after IRI but did not affect CD4(+) T cells or B cells.

FoxP3(+) Treg-deficient mice accumulated a greater number of inflammatory leukocytes after renal IRI than mice containing Tregs.

To confirm that a lack of Tregs potentiated renal injury, we co-transferred isolated Tregs and Scurfy lymph node cells; Treg repletion significantly attenuated IRI-induced renal injury and leukocyte accumulation.

Furthermore, although adoptive transfer of wild-type Tregs into RAG-1 knockout mice was sufficient to prevent kidney IRI, transfer of IL-10-deficient Tregs was not.

Taken together, these results demonstrate that Tregs modulate injury after kidney IRI through IL-10-mediated suppression of the innate immune system.

MedlinePlus Health Information. consumer health - Kidney Diseases.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Immunol. 2005 Aug 1;175(3):1965-73 [16034141.001]

[Cites] Hum Immunol. 2005 Mar;66(3):222-30 [15784460.001]

[Cites] J Am Soc Nephrol. 2005 Nov;16(11):3315-25 [16192425.001]

[Cites] Trends Immunol. 2005 Dec;26(12):632-6 [16243583.001]

[Cites] J Immunol. 2006 Mar 1;176(5):3108-14 [16493070.001]

[Cites] Kidney Int. 2006 May;69(9):1601-8 [16572108.001]

[Cites] Am J Physiol Renal Physiol. 2006 Jun;290(6):F1516-24 [16403835.001]

[Cites] Nature. 2006 May 11;441(7090):235-8 [16648838.001]

[Cites] J Immunol. 2006 Sep 1;177(5):3380-7 [16920979.001]

[Cites] J Am Soc Nephrol. 2006 Oct;17(10):2731-41 [16988067.001]

[Cites] J Immunol. 2006 Nov 15;177(10):6780-6 [17082591.001]

[Cites] J Immunol. 2006 Nov 15;177(10):7155-63 [17082633.001]

[Cites] J Leukoc Biol. 2007 Jan;81(1):144-53 [16959895.001]

[Cites] Cancer Sci. 2007 Mar;98(3):416-23 [17270031.001]

[Cites] J Autoimmun. 2006 Dec;27(4):289-96 [17207605.001]

[Cites] J Immunol. 2007 Apr 1;178(7):4136-46 [17371969.001]

[Cites] J Immunol. 2007 May 1;178(9):5899-911 [17442974.001]

[Cites] J Autoimmun. 2007 Aug;29(1):10-9 [17521882.001]

[Cites] Blood. 2007 Aug 15;110(4):1225-32 [17449799.001]

[Cites] Nat Med. 2007 Oct;13(10):1248-52 [17891146.001]

[Cites] J Immunol. 2008 Apr 1;180(7):4366-70 [18354156.001]

[Cites] Eur J Immunol. 2008 Jun;38(6):1643-53 [18493984.001]

[Cites] J Immunol. 2008 Sep 1;181(5):3524-34 [18714025.001]

[Cites] J Immunol. 2008 Nov 15;181(10):6934-41 [18981113.001]

[Cites] Infect Immun. 2008 Dec;76(12):5834-42 [18824539.001]

[Cites] Kidney Int. 2008 Dec;74(12):1526-37 [18843253.001]

[Cites] J Immunol. 2009 Jan 1;182(1):259-73 [19109157.001]

[Cites] Kidney Int. 2009 Jan;75(2):167-75 [18971925.001]

[Cites] Nat Med. 2009 Feb;15(2):192-9 [19169263.001]

[Cites] J Leukoc Biol. 2008 Dec;84(6):1400-9 [18765477.001]

[Cites] Annu Rev Immunol. 2001;19:683-765 [11244051.001]

[Cites] J Clin Invest. 2001 Nov;108(9):1283-90 [11696572.001]

[Cites] Kidney Int. 2001 Dec;60(6):2118-28 [11737586.001]

[Cites] J Exp Med. 2002 Sep 16;196(6):851-7 [12235217.001]

[Cites] J Immunol. 2002 Nov 1;169(9):4850-60 [12391195.001]

[Cites] J Exp Med. 2003 Jan 6;197(1):111-9 [12515818.001]

[Cites] Nat Immunol. 2003 Apr;4(4):330-6 [12612578.001]

[Cites] Blood. 2003 Jul 1;102(1):328-35 [12623845.001]

[Cites] Eur J Immunol. 2003 Aug;33(8):2090-7 [12884282.001]

[Cites] J Immunol. 2003 Sep 15;171(6):3210-5 [12960350.001]

[Cites] Arthritis Res Ther. 2004;6(5):215-22 [15380036.001]

[Cites] J Clin Invest. 1996 Feb 15;97(4):1056-63 [8613529.001]

[Cites] Am J Physiol. 1996 Mar;270(3 Pt 2):F500-9 [8780254.001]

[Cites] J Immunol. 2005 Mar 1;174(5):2957-63 [15728508.001]

[Cites] Am J Physiol Renal Physiol. 2005 Apr;288(4):F722-31 [15561971.001]

[Cites] Nat Immunol. 2005 Nov;6(11):1142-51 [16227984.001]

(PMID = 19497969.001).

[ISSN] 1533-3450

[Journal-full-title] Journal of the American Society of Nephrology : JASN

[ISO-abbreviation] J. Am. Soc. Nephrol.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK62324; United States / NIAMS NIH HHS / AR / AR-051203; United States / NIDDK NIH HHS / DK / DK56223; United States / NIAMS NIH HHS / AR / R01 AR051203; United States / NIDCR NIH HHS / DE / DE-017579; United States / NIDDK NIH HHS / DK / R01 DK062324; United States / NIDDK NIH HHS / DK / R01 DK056223; United States / NIDDK NIH HHS / DK / T32 DK072922; United States / NIDDK NIH HHS / DK / DK58413; United States / NIDDK NIH HHS / DK / R44 DK058413; United States / NHLBI NIH HHS / HL / P01 HL073361; United States / NIDDK NIH HHS / DK / R41 DK058413

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Interleukin-2 Receptor alpha Subunit; 130068-27-8 / Interleukin-10

[Other-IDs] NLM/ PMC2723989

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Wnt9b signaling regulates planar cell polarity and kidney tubule morphogenesis.

Although many vertebrate organs, such as kidneys, lungs and liver, are composed of epithelial tubules, little is known of the mechanisms that establish the length or diameter of these tubules.

In the kidney, defects in the establishment or maintenance of tubule diameter are associated with one of the most common inherited human disorders, polycystic kidney disease.

Here we show that attenuation of Wnt9b signaling during kidney morphogenesis affects the planar cell polarity of the epithelium and leads to tubules with significantly increased diameter.

Although previous studies showed that polarized cell divisions maintain the diameter of postnatal kidney tubules, we find that cell divisions are randomly oriented during embryonic development.

COS Scholar Universe. author profiles.

Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).

Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

The Lens. Cited by Patents in .

Xenbase. Xenbase .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Lancet. 2007 Apr 14;369(9569):1287-301 [17434405.001]

[Cites] J Am Soc Nephrol. 2007 May;18(5):1389-98 [17429050.001]

[Cites] Development. 2007 Jul;134(13):2533-9 [17537789.001]

[Cites] Dev Cell. 2007 Aug;13(2):214-25 [17681133.001]

[Cites] Development. 2007 Sep;134(17):3049-54 [17652351.001]

[Cites] Nat Rev Genet. 2007 Oct;8(10):791-802 [17878895.001]

[Cites] Pediatr Nephrol. 2007 Nov;22(11):1825-38 [17554566.001]

[Cites] Cell. 1998 Jul 10;94(1):109-18 [9674432.001]

[Cites] Am J Physiol. 1999 Jul;277(1 Pt 2):F146-56 [10409308.001]

[Cites] J Biol Chem. 2004 Dec 10;279(50):52703-13 [15456783.001]

[Cites] Curr Biol. 2005 Apr 26;15(8):787-93 [15854914.001]

[Cites] Nat Genet. 2005 May;37(5):537-43 [15852005.001]

[Cites] Dev Cell. 2005 Aug;9(2):283-92 [16054034.001]

[Cites] Nat Genet. 2005 Sep;37(9):980-5 [16116426.001]

[Cites] EMBO J. 1999 Nov 1;18(21):5931-42 [10545105.001]

[Cites] Development. 2000 May;127(10):2227-38 [10769246.001]

[Cites] Nature. 2000 May 4;405(6782):76-81 [10811221.001]

[Cites] Nature. 2000 May 4;405(6782):81-5 [10811222.001]

[Cites] Development. 2000 Jul;127(14):3091-100 [10862746.001]

[Cites] Nature. 2000 Sep 28;407(6803):527-30 [11029006.001]

[Cites] Int J Dev Biol. 2001;45(1):225-7 [11291850.001]

[Cites] Oncogene. 2001 Sep 20;20(42):5972-81 [11593404.001]

[Cites] Am J Physiol Renal Physiol. 2002 Mar;282(3):F541-52 [11832437.001]

[Cites] J Clin Invest. 2002 Feb;109(4):533-40 [11854326.001]

[Cites] Dev Biol. 2002 Apr 15;244(2):305-18 [11944939.001]

[Cites] Curr Biol. 2002 Jun 4;12(11):876-84 [12062050.001]

[Cites] Curr Biol. 2002 Jun 4;12(11):R378-80 [12062067.001]

[Cites] Dev Biol. 2002 Jul 1;247(1):165-81 [12074560.001]

[Cites] J Am Soc Nephrol. 2002 Jul;13(7):1837-46 [12089379.001]

[Cites] J Am Soc Nephrol. 2002 Oct;13(10):2508-16 [12239239.001]

[Cites] Development. 2003 Jan;130(2):249-58 [12466193.001]

[Cites] Nat Genet. 2007 Nov;39(11):1350-60 [17906624.001]

[Cites] Development. 2007 Dec;134(23):4273-82 [17978004.001]

[Cites] Nat Cell Biol. 2008 Jan;10(1):70-6 [18084282.001]

[Cites] Dev Biol. 2008 Feb 1;314(1):112-26 [18177851.001]

[Cites] PLoS One. 2008;3(4):e1964 [18398480.001]

[Cites] Dev Biol. 2008 May 1;317(1):225-33 [18384766.001]

[Cites] Hum Mol Genet. 2008 Jun 1;17(11):1578-90 [18263895.001]

[Cites] Nat Genet. 2008 Aug;40(8):1010-5 [18604206.001]

[Cites] J Cell Biol. 2008 Nov 3;183(3):377-84 [18981227.001]

[Cites] Development. 2009 Jan;136(1):161-71 [19060336.001]

[Cites] Nat Genet. 2003 Feb;33(2):129-37 [12514735.001]

[Cites] Development. 2003 May;130(9):1725-34 [12642479.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5286-91 [12672950.001]

[Cites] Nat Genet. 2003 Aug;34(4):413-20 [12872123.001]

[Cites] J Biol Chem. 2003 Sep 5;278(36):34211-8 [12821668.001]

[Cites] Hum Mol Genet. 2003 Oct 15;12(20):2703-10 [12925574.001]

[Cites] Development. 2004 Aug;131(16):4085-93 [15269167.001]

[Cites] Nature. 2004 Aug 5;430(7000):689-93 [15254551.001]

[Cites] Curr Opin Cell Biol. 2004 Oct;16(5):493-9 [15363798.001]

[Cites] Kidney Int. 2004 Oct;66(4):1345-55 [15458427.001]

[Cites] Nature. 1989 Mar 16;338(6212):263-4 [2493583.001]

[Cites] Development. 1992 Dec;116(4):901-14 [1295743.001]

[Cites] Genes Dev. 1994 Jan;8(1):118-30 [8288125.001]

[Cites] Nature. 1997 May 15;387(6630):292-5 [9153394.001]

[Cites] Nat Genet. 1997 Oct;17(2):179-81 [9326937.001]

[Cites] Development. 1998 Mar;125(6):983-94 [9463345.001]

[Cites] Cell. 2003 Jan 10;112(1):19-28 [12526790.001]

[Cites] Genes Dev. 2003 Jan 15;17(2):295-309 [12533515.001]

[Cites] Kidney Int. 2005 Nov;68(5):2010-8 [16221201.001]

[Cites] Dev Biol. 2005 Dec 1;288(1):179-93 [16277981.001]

[Cites] Nat Genet. 2006 Jan;38(1):21-3 [16341222.001]

[Cites] Curr Biol. 2006 Jan 24;16(2):180-5 [16431370.001]

[Cites] Curr Biol. 2006 Jan 24;16(2):186-94 [16431371.001]

[Cites] Dev Cell. 2006 Mar;10(3):391-6 [16516841.001]

[Cites] Curr Biol. 2006 Jun 20;16(12):1224-31 [16782014.001]

[Cites] Semin Cell Dev Biol. 2006 Apr;17(2):194-203 [16839790.001]

[Cites] Development. 2007 Jan;134(1):147-55 [17164420.001]

[Cites] Differentiation. 2006 Dec;74(9-10):638-47 [17177859.001]

[Cites] Blood. 2007 Feb 15;109(4):1345-52 [17068148.001]

[Cites] Cell Cycle. 2007 Apr 1;6(7):776-9 [17377490.001]

(PMID = 19543268.001).

[ISSN] 1546-1718

[Journal-full-title] Nature genetics

[ISO-abbreviation] Nat. Genet.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / 5 P30 DK07403802; United States / NIDDK NIH HHS / DK / P30 DK074038; United States / NIDDK NIH HHS / DK / 1 R01 DK080004; United States / NIDDK NIH HHS / DK / R37 DK042921; United States / NIDDK NIH HHS / DK / P30 DK079328; United States / NIDDK NIH HHS / DK / DK074038-01; United States / NIDDK NIH HHS / DK / R01 DK080004; United States / NIDDK NIH HHS / DK / P30 DK074038-01

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Wnt Proteins; 0 / Wnt9b protein, mouse

[Other-IDs] NLM/ NIHMS119253; NLM/ PMC2761080

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] When less is more: apoptosis during acute kidney injury.

The paper by Ma and Devarajan suggests that the subtle apoptotic events that occur in the distal nephron after acute kidney injury might have a greater than expected impact on the adjacent proximal tubules and kidney function.

Understanding these events might facilitate development of therapeutic means to ameliorate acute kidney injury.

[MeSH-major] Acute Kidney Injury / pathology. Apoptosis / physiology. Reperfusion Injury / pathology

[MeSH-minor] Animals. Humans. Kidney / physiopathology. Kidney Tubules, Proximal / physiopathology. Nephrons / physiopathology

[Email] Email this result item

Email the results to the following email address:   [X] Close

[CommentOn] Kidney Int. 2008 Aug;74(3):310-8 [18480747.001]

(PMID = 18626494.001).

[ISSN] 1523-1755

[Journal-full-title] Kidney international

[ISO-abbreviation] Kidney Int.

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] United States

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Alemtuzumab (Campath-1H) in kidney transplantation.

Kidney transplantation has become the treatment of choice for both the quality of life and survival in patients with end-stage renal disease (ESRD).

However, the immunosuppressive regimen which allows optimal kidney transplant outcome remains elusive.

One of the more promising induction agents, Alemtuzumab, was introduced to kidney transplantation by Calne in the late 1990s with low dose cyclosporine A monotherapy, with the hope of establishing 'prope' or near tolerance.

[MeSH-major] Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Graft Rejection / prevention & control. Immunosuppressive Agents / therapeutic use. Kidney Transplantation

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 18093269.001).

[ISSN] 1600-6143

[Journal-full-title] American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

[ISO-abbreviation] Am. J. Transplant.

[Language] eng

[Publication-type] Comparative Study; Journal Article; Review

[Publication-country] Denmark

[Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Immunosuppressive Agents; 3A189DH42V / alemtuzumab

[Number-of-references] 41

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Erythrocytosis related with hydronephrosis in a horseshoe kidney].

We report a case of a man with erythrocytosis secondary to hydronephrosis in a right horseshoe kidney.

Following nephrectomy of the right kidney erythrocyte count returned to normal values.

Secondary polyglobulia may be due to increased erythropoietine values and has been related in some patients with renal diseases such as hydronephrosis, but very rarely in association with hydronephrotic horseshoe kidney.

[MeSH-major] Hydronephrosis / complications. Kidney / abnormalities. Polycythemia / etiology

Genetic Alliance. consumer health - Horseshoe kidney.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15981431.001).

[ISSN] 0210-4806

[Journal-full-title] Actas urologicas espanolas

[ISO-abbreviation] Actas Urol Esp

[Language] spa

[Publication-type] Case Reports; Journal Article

[Publication-country] Spain

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] The alphabet soup of kidney transplantation: SCD, DCD, ECD--fundamentals for the practicing nephrologist.

There is significant variability in the quality of deceased-donor kidneys that are used for transplantation.

The quality of the donor kidney has a direct effect on important clinical outcomes such as acute rejection, delayed graft function, and patient and allograft survival.

Expanded-criteria donors (ECDs) refer to older kidney donors (> or =60 yr) or donors who are aged 50 to 59 yr and have two of the following three features: Hypertension, terminal serum creatinine >1.5 mg/dl, or death from cerebrovascular accident.

By definition, ECD kidneys have a 70% greater likelihood of failure compared with one from a 35-yr-old male donor who died from a motor vehicle accident.

An ECD kidney transplant recipient has a projected average added-life-years of 5.1 yr compared with 10 yr for a kidney recipient from a standard-criteria donor.

Kidney transplantation from DCD seems to have similar allograft and patient survival compared with kidney from donation after brain death; however DCD transplantation has a 42 to 51% risk for delayed graft function (need for at least one dialysis treatment during the first week after transplantation) compared with 24% in an standard-criteria donor kidney transplant.

Familiarity with the comprehensive allocation rules governing different categories of deceased-donor kidneys by the nephrologists and dialysis team providers is essential to maximizing patient autonomy and to improve the outcomes of kidney transplantation.

[MeSH-major] Kidney Transplantation. Nephrology. Tissue Donors. Tissue and Organ Procurement

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

MedlinePlus Health Information. consumer health - Organ Donation.

COS Scholar Universe. author profiles.

ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 19808229.001).

[ISSN] 1555-905X

[Journal-full-title] Clinical journal of the American Society of Nephrology : CJASN

[ISO-abbreviation] Clin J Am Soc Nephrol

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / K24 DK062234

[Publication-type] Journal Article; Review

[Publication-country] United States

[Number-of-references] 24

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Polycystic liver and kidney diseases.

There have been remarkable advances in research on polycystic liver and kidney diseases recently, covering cloning of new genes, refining disease classifications, and advances in understanding more about the molecular pathology of these diseases.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary disease affecting kidneys.

It affects 1/400 to 1/1000 live births and accounts for 5% of the end stage renal disease in the United States and Europe, and is caused by gene defects in the PKD1 or PKD2 genes.

Autosomal recessive polycystic kidney disease (ARPKD) belongs to a group of congenital hepatorenal fibrocystic syndromes.

[MeSH-major] Cysts / genetics. Liver Diseases / genetics. Polycystic Kidney Diseases / genetics

[MeSH-minor] Diagnosis, Differential. Genetic Markers. Humans. Membrane Proteins / genetics. Proteins / genetics. TRPP Cation Channels

Genetics Home Reference. consumer health - polycystic kidney disease.

MedlinePlus Health Information. consumer health - Liver Diseases.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16338757.001).

[ISSN] 0785-3890

[Journal-full-title] Annals of medicine

[ISO-abbreviation] Ann. Med.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] Sweden

[Chemical-registry-number] 0 / Genetic Markers; 0 / Membrane Proteins; 0 / Proteins; 0 / SEC63 protein, human; 0 / TRPP Cation Channels; 0 / polycystic kidney disease 1 protein; 0 / polycystic kidney disease 2 protein

[Number-of-references] 95

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Chronic kidney disease after hematopoietic stem cell transplantation.

Acute and chronic kidney diseases occur after hematopoietic stem cell transplantation.

Recent estimates show that near 15% of subjects undergoing hematopoietic stem cell transplantation will develop chronic kidney disease, which is a complication rate that can affect outcome and reduce survival.

Investigation of the causes of chronic kidney disease is needed, as are ways to prevent, mitigate, and treat it.

Genetic Alliance. consumer health - Kidney Disease.

Genetic Alliance. consumer health - Transplantation.

MedlinePlus Health Information. consumer health - Chronic Kidney Disease.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Copyright] Published by Elsevier Inc.

[Cites] J Pathol. 2000 Mar;190(4):484-8 [10699999.001]

[Cites] Curr Drug Targets. 2010 Nov;11(11):1423-9 [20583975.001]

[Cites] Radiat Res. 2002 Apr;157(4):393-401 [11893241.001]

[Cites] J Lab Clin Med. 2002 Apr;139(4):251-7 [12024113.001]

[Cites] Am J Transplant. 2003 Mar;3(3):301-5 [12614285.001]

[Cites] Blood. 2003 Oct 1;102(7):2695; author reply 2695-6 [14504068.001]

[Cites] Pediatr Transplant. 2004 Oct;8(5):507-12 [15367289.001]

[Cites] N Engl J Med. 1975 Apr 17;292(16):832-43 [234595.001]

[Cites] Int J Radiat Oncol Biol Phys. 1989 Jun;16(6):1501-9 [2656600.001]

[Cites] Nephron. 1989;51(4):555-6 [2662038.001]

[Cites] Kidney Int. 1989 Jun;35(6):1336-44 [2671466.001]

[Cites] N Engl J Med. 1990 Feb 22;322(8):485-94 [2300120.001]

[Cites] Ann Intern Med. 1991 Jan 15;114(2):113-8 [1984385.001]

[Cites] Ann Intern Med. 1991 Dec 15;115(12):925-30 [1952488.001]

[Cites] Nephron. 1993;64(4):626-35 [8366991.001]

[Cites] N Engl J Med. 1994 Mar 24;330(12):827-38 [8114836.001]

[Cites] Lab Invest. 1996 Sep;75(3):349-60 [8804358.001]

[Cites] Lancet. 1998 Jan 17;351(9097):178-81 [9449873.001]

[Cites] Bone Marrow Transplant. 1997 Dec;20(12):1069-74 [9466280.001]

[Cites] Nephron. 1998 Aug;79(4):408-12 [9689155.001]

[Cites] Int J Radiat Biol. 1999 Apr;75(4):473-9 [10331853.001]

[Cites] Clin Transplant. 1999 Aug;13(4):330-5 [10485375.001]

[Cites] Kidney Int Suppl. 2005 Aug;(97):S68-77 [16014104.001]

[Cites] Br J Haematol. 2005 Oct;131(1):74-9 [16173966.001]

[Cites] Am J Transplant. 2006 Jan;6(1):89-94 [16433761.001]

[Cites] Bone Marrow Transplant. 2006 Sep;38(5):351-7 [16862167.001]

[Cites] Semin Radiat Oncol. 2007 Apr;17(2):141-8 [17395044.001]

[Cites] Bone Marrow Transplant. 2007 May;39(9):571-2 [17351643.001]

[Cites] Nephrol Dial Transplant. 2007 May;22(5):1369-76 [17255123.001]

[Cites] Bone Marrow Transplant. 2007 Jun;39(11):717-23 [17401393.001]

[Cites] Medicine (Baltimore). 2007 Jul;86(4):215-24 [17632263.001]

[Cites] Clin J Am Soc Nephrol. 2007 Sep;2(5):1014-23 [17702721.001]

[Cites] Biol Blood Marrow Transplant. 2008 Apr;14(4):403-8 [18342782.001]

[Cites] Int J Radiat Oncol Biol Phys. 2008 Apr 1;70(5):1546-51 [18029109.001]

[Cites] Nephrology (Carlton). 2008 Jun;13(4):322-30 [18221254.001]

[Cites] Biol Blood Marrow Transplant. 2008 Jun;14(6):658-63 [18489991.001]

[Cites] Nephrol Dial Transplant. 2008 Aug;23(8):2700-1; author reply 2701 [18385388.001]

[Cites] Cancer. 2008 Oct 1;113(7):1580-7 [18704986.001]

[Cites] Am J Transplant. 2008 Nov;8(11):2378-90 [18925905.001]

[Cites] Radiat Res. 2009 Feb;171(2):164-72 [19267541.001]

[Cites] Radiat Res. 2009 Aug;172(2):260-4 [19630531.001]

[Cites] Biol Blood Marrow Transplant. 2009 Oct;15(10):1251-7 [19747632.001]

[Cites] Transplant Proc. 2009 Sep;41(7):2895-7 [19765466.001]

[Cites] Nephrol Dial Transplant. 2010 Jan;25(1):278-82 [19762604.001]

[Cites] Kidney Int. 2010 Feb;77(3):219-24 [19940841.001]

[Cites] Bone Marrow Transplant. 2010 Feb;45(2):219-34 [19584824.001]

[Cites] Exp Hematol. 2010 Apr;38(4):270-81 [20116413.001]

[Cites] Clin J Am Soc Nephrol. 2010 Jun;5(6):1107-13 [20299374.001]

[Cites] Clin Transplant. 2010 Jul-Aug;24(4):E94-102 [19919608.001]

[Cites] Radiat Res. 2001 Mar;155(3):474-80 [11182799.001]

(PMID = 21146127.001).

[ISSN] 1558-4488

[Journal-full-title] Seminars in nephrology

[ISO-abbreviation] Semin. Nephrol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / U19 AI067734; United States / NIAID NIH HHS / AI / 1U19AI067734

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review

[Publication-country] United States

[Other-IDs] NLM/ NIHMS249843; NLM/ PMC3005300

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Improvement of kidney failure with fetal kidney precursor cell transplantation.

BACKGROUND: Current therapies for end-stage renal disease have severe limitations.

Dialysis is only a temporary treatment and does not restore kidney function.

Here, we show that the transplantation of fetal kidney precursor cells reconstitutes kidney tissues, reduces uremic symptoms, and provides life-saving metabolic support in kidney failure animal models.

METHODS: Kidney failure was surgically induced by resecting kidneys, leaving approximately 1/6 of the total kidney mass (5/6 nephrectomy).

Fetal kidney precursor cells were isolated from metanephroi of E17.5 rat fetuses using collagenase/dispase digestion.

Five weeks after the nephrectomy procedure, isolated fetal kidney precursor cells were transplanted under the kidney capsule of rats using fibrin gel matrix.

The cell transplantation into the kidneys of kidney failure-induced rats resulted in kidney tissue reconstitution and the transplanted cells were observed in the reconstitution region of the kidneys as evidenced by the presence of fluorescently labeled cells.

In addition, biochemical parameters from serum and urine samples showed improved kidney functions compared with non-treated group without severe immune response after ten weeks.

CONCLUSION: Transplanting fetal kidney precursor cells showed the potential for the partial augmentation of kidney structure and function in the treatment of kidney failure.

[MeSH-major] Embryonic Stem Cells / transplantation. Renal Insufficiency / physiopathology. Renal Insufficiency / surgery

[MeSH-minor] Animals. Cell Membrane. Disease Models, Animal. Disease Progression. Disease Susceptibility. Glomerulosclerosis, Focal Segmental / pathology. Glomerulosclerosis, Focal Segmental / physiopathology. Graft Rejection / etiology. Hypertrophy. Kidney / pathology. Kidney / physiopathology. Kidney Glomerulus / pathology. Kidney Glomerulus / physiopathology. Nephrectomy. Phenotype. Rats. Rats, Sprague-Dawley. Regeneration. Survival Analysis. Uremia / physiopathology

The Lens. Cited by Patents in .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17496543.001).

[ISSN] 0041-1337

[Journal-full-title] Transplantation

[ISO-abbreviation] Transplantation

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Prognostic associations between lipid markers and outcomes in kidney transplant recipients.

BACKGROUND: Hyperlipidemia is highly prevalent in kidney transplant recipients, but the prognostic significance for mortality and allograft survival in these patients has not been established sufficiently.

METHODS: We prospectively enrolled 733 kidney transplant recipients between 1996 and 1998.

Using multivariate proportional hazard regression, independent relations of fasting plasma triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol levels to risk for death from any cause and risk for kidney allograft loss were examined.

RESULTS: During a median follow-up of 6.1 years, 154 patients died and 260 kidney allografts were lost.

Further analysis of associations between high-density lipoprotein cholesterol or low-density lipoprotein cholesterol categories and patient mortality or kidney allograft loss did not show associations.

CONCLUSION: Elevated levels of TC or its subfractions and elevated TG levels are not associated with increased risk for patient mortality or allograft loss in these kidney transplant recipients.

[MeSH-major] Cholesterol / blood. Graft Survival. Kidney Transplantation

MedlinePlus Health Information. consumer health - Cholesterol.

MedlinePlus Health Information. consumer health - Kidney Transplantation.

COS Scholar Universe. author profiles.

Hazardous Substances Data Bank. CHOLESTEROL .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16490631.001).

[ISSN] 1523-6838

[Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation

[ISO-abbreviation] Am. J. Kidney Dis.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; 0 / Triglycerides; 97C5T2UQ7J / Cholesterol

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Kidney dimensions at sonography are correlated with glomerular filtration rate in renal transplant recipients and in kidney donors.

The gold standard to assess renal function is the measurement of glomerular filtration rate (GFR).

For practical reasons, renal function is often evaluated from serum creatinine (S Cr) or cystatin C (S Cys), and GFR is predicted from SCr.

Ultrasound scanning of the kidneys is used only to evaluate renal morphology.

The aim of this study was to evaluate the relationship between sonographic renal dimensions and GFR in renal transplant recipients and in kidney donors.

GFR was also predicted using the Cockcroft and Gault (CG) formula and with the simplified Modification of Diet in Renal Disease (MDRD) formula.

Length, width, and depth of kidneys and renal sinus were measured using renal sonography.

Among sonographic measurements, kidney length showed the best correlation with GFR.

In either case, the correlation of kidney length with GFR was greater than that of S Cr or S Cys, and similar to that of CG or MDRD GFR.

Accuracy of kidney length as an indicator of GFR impairment was not statistically different from laboratory tests.

In conclusion, renal dimensions at sonography closely correlated with GFR.

Thus, renal sonography can give information also on the function of the renal graft and of the remaining kidney of living donors.

[MeSH-major] Glomerular Filtration Rate. Kidney / anatomy & histology. Kidney / physiology. Kidney Transplantation / physiology. Tissue Donors

MedlinePlus Health Information. consumer health - Kidney Transplantation.

MedlinePlus Health Information. consumer health - Organ Donation.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 17692610.001).

[ISSN] 0041-1345

[Journal-full-title] Transplantation proceedings

[ISO-abbreviation] Transplant. Proc.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; 0 / CST3 protein, human; 0 / Cystatin C; 0 / Cystatins; AYI8EX34EU / Creatinine

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Detection of differentially expressed genes in human autosomal dominant polycystic kidney tissue].

OBJECTIVE: To detect the differentially expressed genes in human polycystic kidney by cDNA microarray.

Both mRNAs isolated from polycystic kidney tissue and normal kidney tissue were reversely transcribed to cDNAs with the incorporation of fluorescent dUTP (Cy5-dUTP and Cy3-dUTP) for preparing the hybridization probes.

RESULTS: The result indicated that the expressions of 263 genes were up regulated while the expressions of 94 genes were down regulated in the polycystic kidney tissue among the 8398 target genes.

Three hundred and fifty-seven differentially expressed genes with different functions were revealed in the polycystic kidney tissue, which may play some roles in the progression of polycystic kidney.

[MeSH-major] Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Polycystic Kidney, Autosomal Dominant / genetics

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16331579.001).

[ISSN] 1003-9406

[Journal-full-title] Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics

[ISO-abbreviation] Zhonghua Yi Xue Yi Chuan Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Carbocyanines; 0 / DNA, Complementary; 0 / Fluorescent Dyes; 0 / cyanine dye 3; 0 / cyanine dye 5; 67763-96-6 / Insulin-Like Growth Factor I

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Early biological and immune response to semi-identical liver or kidney allograft in miniature swine.

In inbred miniature swine, semi-identical liver allograft recipients survive up to 3 months without immunosuppression, whereas similarly mismatched kidney allografts are uniformly rejected within 2 weeks.

SLA(d/d) pigs (MGH, Harvard Medical School, Boston, MA, USA) received liver or kidney allograft from heterozygous SLA(c/d) miniature swine.

Kidney allografts were uniformly rejected within 2 weeks, whereas liver allografts survived for up to 87 days.

After both liver and kidney transplantation, the peripheral lymphocyte count decreased during the first week concomitantly to a significant elevation of plasma cortisol level.

Early decrease of peripheral platelet count was observed after liver but not renal transplantation.

Up-regulation of transforming growth factor beta1 (TGF-beta1) and interferon-gamma (IFN-gamma) was observed during the first postoperative week in semi-identical liver allografts and IFN-gamma as well as IL-10 in kidney allografts.

In liver recipients, labelled autologous lymphocytes accumulated in the liver graft and native spleen, whereas after renal allograft, lymphocytes accumulated in the native spleen and liver but never in the kidney allograft.

Specific cellular anti-donor unresponsiveness was observed from the first post-transplant day in both liver and kidney recipients, while the humoral anti-donor response remained intact.

In semi-identical liver allograft, recipient rejection is milder and slower than in similarly matched kidney allograft.

The rapid, nonspecific accumulation of recipient lymphocytes in the liver allograft but not in kidney allograft might also play a role in the different survival time in this model.

[MeSH-major] Kidney Transplantation / physiology. Liver Transplantation / physiology

MedlinePlus Health Information. consumer health - Kidney Transplantation.

MedlinePlus Health Information. consumer health - Liver Transplantation.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 15612988.001).

[ISSN] 0934-0874

[Journal-full-title] Transplant international : official journal of the European Society for Organ Transplantation

[ISO-abbreviation] Transpl. Int.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Cytokines; 0 / DNA Primers; 0 / RNA, Messenger

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Stem cells in kidney regeneration following acute renal injury.

Acute renal failure has 50-80% mortality.

Stem cells offer an exciting potential for kidney regeneration.

This review discusses pathogenesis of acute renal failure resulting from ischemia-reperfusion injury and the role of stem cells in reversing or mitigating this disorder.

Specifically, the issues of differentiation of kidney cells from embryonic stem cells and bone marrow stem cells, and whether adult kidney stem/progenitor cells exist in the postnatal kidney are discussed.

Evidence to support the conclusion that intra-renal cells, including surviving tubular epithelial cells and potential renal stem/progenitor cells, are the main source for renal regeneration is provided.

Future research in selecting the type(s) of stem cells and optimizing the dose, frequency and route of administration of the cells will be fundamental in successful cell replacement therapy in acute renal failure.

Methods for enhancing endogenous renal cell proliferation and differentiation for renal repair continue to be important research directions.

[MeSH-major] Kidney / physiopathology. Regeneration. Stem Cells / cytology

[MeSH-minor] Bone Marrow Cells / cytology. Cell Differentiation. Humans. Renal Insufficiency / physiopathology. Renal Insufficiency / therapy

MedlinePlus Health Information. consumer health - Stem Cells.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16549552.001).

[ISSN] 0031-3998

[Journal-full-title] Pediatric research

[ISO-abbreviation] Pediatr. Res.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / K08 DK062839; United States / NIDDK NIH HHS / DK / R01 DK66535

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Number-of-references] 48

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Potential pharmacological interventions in polycystic kidney disease.

Polycystic kidney diseases (autosomal dominant and autosomal recessive) are progressive renal tubular cystic diseases, which are characterised by cyst expansion and loss of normal kidney structure and function.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common life- threatening, hereditary disease.

Early diagnosis and treatment of hypertension with inhibitors of the renin-angiotensin-aldosterone system (RAAS) and its potential protective effect on left ventricular hypertrophy has been one of the major therapeutic goals to decrease cardiac complications and contribute to improved prognosis of the disease.

Because of activation of the mammalian target of rapamycin (mTOR) pathway, the use of sirolimus (rapamycin) an mTOR inhibitor, markedly reduced cyst formation and decreased polycystic kidney size in several animal models.

Caspase inhibitors have been shown to decrease cytogenesis and renal failure in rats with cystic disease.

Cystic fluid secretion results in cyst enlargement and somatostatin analogues have been shown to decrease renal cyst progression in patients with ADPKD.

[MeSH-major] Polycystic Kidney Diseases / drug therapy

Genetic Alliance. consumer health - Kidney Disease.

Genetic Alliance. consumer health - Polycystic Kidney Disease.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Am Soc Nephrol. 2006 Aug;17(8):2220-7 [16807403.001]

[Cites] Kidney Int. 2002 Apr;61(4):1220-30 [11918728.001]

[Cites] Adv Cancer Res. 2000;77:25-79 [10549355.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7037-44 [11416184.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9260-5 [12082174.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13254-9 [12239346.001]

[Cites] Mamm Genome. 2003 Apr;14(4):242-9 [12682776.001]

[Cites] J Am Soc Nephrol. 1997 Aug;8(8):1292-7 [9259356.001]

[Cites] Science. 1998 Apr 3;280(5360):32-4 [9556450.001]

[Cites] Mol Cell Biol. 2002 Jul;22(14):4984-96 [12077328.001]

[Cites] Kidney Int. 1991 Jan;39(1):57-62 [2002633.001]

[Cites] Cell Signal. 2003 May;15(5):463-9 [12639709.001]

[Cites] Biochem Biophys Res Commun. 2001 Mar 23;282(1):341-50 [11264013.001]

[Cites] Am J Physiol. 1991 Dec;261(6 Pt 2):F951-6 [1661085.001]

[Cites] Cell Signal. 1999 Sep;11(9):651-63 [10530873.001]

[Cites] J Am Soc Nephrol. 2001 Feb;12(2):379-84 [11158230.001]

[Cites] Kidney Int. 1996 Oct;50(4):1327-36 [8887295.001]

[Cites] Am J Kidney Dis. 1994 Oct;24(4):561-8 [7942810.001]

[Cites] Am J Physiol. 1995 Aug;269(2 Pt 1):C487-95 [7653531.001]

[Cites] J Clin Invest. 1997 Mar 15;99(6):1380-9 [9077548.001]

[Cites] J Biol Chem. 2001 Jun 8;276(23):20451-7 [11278652.001]

[Cites] J Pharmacol Exp Ther. 1995 Feb;272(2):546-51 [7853167.001]

[Cites] Biochem Biophys Res Commun. 2004 Oct 1;322(4):1374-83 [15336986.001]

[Cites] Kidney Int. 2004 Sep;66(3):964-73 [15327388.001]

[Cites] Dev Cell. 2003 May;4(5):753-9 [12737809.001]

[Cites] Kidney Int. 1989 Feb;35(2):675-80 [2709672.001]

[Cites] Adv Nephrol Necker Hosp. 1998;28:439-78 [9890004.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Feb 17;95(4):1432-7 [9465032.001]

[Cites] Kidney Int. 2005 Mar;67(3):909-19 [15698430.001]

[Cites] J Am Soc Nephrol. 2002 Sep;13(9):2384-98 [12191984.001]

[Cites] FASEB J. 2001 Nov;15(13):2536-8 [11641256.001]

[Cites] J Cell Biochem. 2002;86(1):21-8 [12112012.001]

[Cites] Curr Biol. 2002 Jun 4;12(11):R378-80 [12062067.001]

[Cites] Crit Rev Oncol Hematol. 2000 Jan;33(1):7-23 [10714959.001]

[Cites] Methods. 2003 Jul;30(3):191-7 [12798133.001]

[Cites] Kidney Int. 1999 Jan;55(1):29-62 [9893113.001]

[Cites] J Urol. 1998 Jan;159(1):291-6 [9400497.001]

[Cites] J Am Soc Nephrol. 2003 Feb;14 (2):367-76 [12538737.001]

[Cites] Am J Physiol Renal Physiol. 2003 Nov;285(5):F998-F1012 [12837680.001]

[Cites] J Am Soc Nephrol. 2000 Jul;11(7):1179-87 [10864573.001]

[Cites] Clin Cancer Res. 1998 Apr;4(4):821-8 [9563874.001]

[Cites] Kidney Int. 2000 Apr;57(4):1460-71 [10760082.001]

[Cites] Pediatrics. 2003 May;111(5 Pt 1):1072-80 [12728091.001]

[Cites] Biochem Biophys Res Commun. 1993 Dec 30;197(3):1083-93 [8280123.001]

[Cites] J Am Soc Nephrol. 1993 Jan;3(7):1378-86 [8094982.001]

[Cites] J Membr Biol. 2001 Nov 1;184(1):71-9 [11687880.001]

[Cites] J Biol Chem. 2004 Jul 9;279(28):29728-39 [15123714.001]

[Cites] Nat Genet. 2005 May;37(5):537-43 [15852005.001]

[Cites] Circulation. 2001 May 15;103(19):2387-94 [11352889.001]

[Cites] Kidney Int. 2005 Jul;68(1):206-16 [15954910.001]

[Cites] Kidney Int. 1988 Nov;34(5):683-90 [2974094.001]

[Cites] Am J Kidney Dis. 1996 Dec;28(6):788-803 [8957030.001]

[Cites] Am J Kidney Dis. 1997 Nov;30(5):703-9 [9370187.001]

[Cites] Pol Arch Med Wewn. 1996 Oct;96(4):329-43 [9082344.001]

[Cites] Physiol Rev. 1998 Oct;78(4):1165-91 [9790573.001]

[Cites] Cell. 2004 Jun 11;117(6):693-7 [15186771.001]

[Cites] J Clin Invest. 2000 Jan;105(1):9-13 [10619855.001]

[Cites] Am J Physiol Renal Physiol. 2004 Oct;287(4):F775-88 [15187005.001]

[Cites] J Pediatr. 1987 May;110(5):729-34 [2883274.001]

[Cites] Kidney Int. 1992 Jan;41(1):206-10 [1317477.001]

[Cites] J Clin Invest. 1998 Mar 1;101(5):935-9 [9486961.001]

[Cites] Kidney Int. 2005 Apr;67(4):1234-47 [15780076.001]

[Cites] J Cell Sci. 2003 Apr 15;116(Pt 8):1519-25 [12640036.001]

[Cites] J Am Soc Nephrol. 2002 Oct;13(10):2508-16 [12239239.001]

[Cites] Kidney Int. 1992 Aug;42(2):364-73 [1405319.001]

[Cites] Proc Natl Acad Sci U S A. 1998 Jan 20;95(2):554-9 [9435230.001]

[Cites] J Clin Invest. 2002 Oct;110(8):1083-91 [12393844.001]

[Cites] Semin Nephrol. 1991 Nov;11(6):653-60 [1767138.001]

[Cites] Nat Genet. 2003 Feb;33(2):129-37 [12514735.001]

[Cites] J Am Soc Nephrol. 1993 Oct;4(4):1064-72 [7904485.001]

[Cites] Kidney Int. 1988 Jun;33(6):1084-90 [3043076.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5286-91 [12672950.001]

[Cites] J Biol Chem. 2001 Mar 9;276(10):7320-6 [11058599.001]

[Cites] Am J Physiol Renal Physiol. 2002 Dec;283(6):F1313-25 [12388409.001]

[Cites] Trends Cell Biol. 2004 Feb;14 (2):78-85 [15102439.001]

[Cites] Oncogene. 1999 Nov 11;18(47):6505-12 [10597253.001]

[Cites] J Am Soc Nephrol. 2005 Jan;16(1):46-51 [15563559.001]

[Cites] Am J Physiol. 1998 Sep;275(3 Pt 2):F387-94 [9729511.001]

[Cites] Hum Mol Genet. 2003 Aug 1;12(15):1875-80 [12874107.001]

[Cites] Nat Genet. 1995 Jun;10(2):151-60 [7663510.001]

[Cites] Nat Med. 2004 Apr;10(4):363-4 [14991049.001]

[Cites] Circ Res. 2005 Apr 29;96(8):873-80 [15790956.001]

[Cites] FASEB J. 2004 May;18(7):884-6 [15001556.001]

[Cites] Curr Biol. 2001 May 1;11(9):R356-60 [11369247.001]

[Cites] Mayo Clin Proc. 1991 Oct;66(10):1010-7 [1921483.001]

[Cites] J Clin Invest. 2004 Mar;113(6):814-25 [15067314.001]

[Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1395-413 [9779987.001]

[Cites] J Anat. 2001 Oct;199(Pt 4):393-405 [11693300.001]

[Cites] J Am Soc Nephrol. 2005 Apr;16(4):846-51 [15728778.001]

[Cites] N Engl J Med. 2004 Jan 8;350(2):151-64 [14711914.001]

[Cites] J Am Soc Nephrol. 2002 Nov;13(11):2723-9 [12397042.001]

[Cites] J Biol Chem. 1997 Jul 18;272(29):17907-11 [9218414.001]

[Cites] J Biol Chem. 2000 Oct 13;275(41):31921-9 [10931830.001]

[Cites] Mol Cell Biol. 1999 May;19(5):3423-34 [10207066.001]

[Cites] Kidney Int. 2003 Nov;64(5):1792-9 [14531813.001]

[Cites] Am J Kidney Dis. 1995 Sep;26(3):501-7 [7645559.001]

[Cites] Proc Natl Acad Sci U S A. 1999 May 25;96(11):6241-8 [10339572.001]

[Cites] Trends Biochem Sci. 2004 Jan;29(1):32-8 [14729330.001]

[Cites] Lab Invest. 1974 Oct;31(4):303-13 [4412080.001]

[Cites] Hum Mol Genet. 2003 Oct 15;12(20):2703-10 [12925574.001]

[Cites] Dev Biol. 1990 Mar;138(1):225-30 [1968405.001]

[Cites] Am J Nephrol. 1985;5(3):176-81 [3893129.001]

[Cites] J Am Soc Nephrol. 1994 Dec;5(6):1349-54 [7894001.001]

[Cites] Nephron. 1979;24(4):198-204 [40149.001]

[Cites] Cancer Res. 1995 Jan 15;55(2):354-9 [7812968.001]

[Cites] J Am Soc Nephrol. 1998 May;9(5):903-16 [9596091.001]

[Cites] Genes Dev. 2002 Jun 15;16(12 ):1472-87 [12080086.001]

[Cites] Am J Kidney Dis. 2000 Mar;35(3):427-32 [10692268.001]

[Cites] Am J Physiol. 1999 Jun;276(6 Pt 2):F837-46 [10362772.001]

[Cites] EMBO J. 2004 Apr 7;23(7):1657-68 [15029248.001]

[Cites] N Engl J Med. 1990 Oct 18;323(16):1091-6 [2215576.001]

[Cites] J Clin Endocrinol Metab. 1987 May;64(5):975-9 [2881944.001]

[Cites] N Engl J Med. 1983 Dec 15;309(24):1495-501 [6139753.001]

[Cites] Exp Toxicol Pathol. 2001 Jun;53(2-3):123-8 [11484829.001]

[Cites] Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):11960-5 [11035810.001]

[Cites] Br Med J (Clin Res Ed). 1986 Jun 28;292(6537):1701-2 [2873863.001]

[Cites] Kidney Int. 1995 Feb;47(2):490-9 [7723235.001]

[Cites] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3700-4 [8170972.001]

[Cites] Mol Cell. 2001 Apr;7(4):823-32 [11336705.001]

[Cites] Nat Genet. 2005 Jan;37(1):19-24 [15624019.001]

[Cites] J Biol Chem. 2003 Jan 31;278(5):2807-18 [12429740.001]

[Cites] Cell. 2000 Jul 7;102(1):1-4 [10929706.001]

[Cites] Nat Med. 1997 Oct;3(10):1089-95 [9334719.001]

[Cites] J Biol Chem. 2004 Jan 23;279(4):2975-83 [14593099.001]

[Cites] J Clin Invest. 2001 May;107(9):1145-52 [11342578.001]

[Cites] Physiol Rev. 1997 Jan;77(1):75-197 [9016301.001]

[Cites] J Am Soc Nephrol. 1998 Jul;9(7):1169-77 [9644626.001]

[Cites] Kidney Int. 2000 Jan;57(1):33-40 [10620185.001]

[Cites] Physiol Res. 2004;53(6):629-34 [15588131.001]

[Cites] Nature. 1995 Dec 21-28;378(6559):785-9 [8524413.001]

[Cites] J Hypertens. 1997 Sep;15(9):925-33 [9321739.001]

[Cites] Cell Calcium. 2005 Jun;37(6):593-601 [15862350.001]

[Cites] Science. 2002 Aug 23;297(5585):1352-4 [12193789.001]

[Cites] Oncogene. 1996 Sep 19;13(6):1153-60 [8808689.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9666-70 [11493700.001]

[Cites] Kidney Int. 1992 May;41(5):1222-36 [1319521.001]

[Cites] Clin Nephrol. 1975;3(3):99-105 [1139805.001]

[Cites] Biochim Biophys Acta. 1999 May 31;1423(3):C19-30 [10382537.001]

[Cites] Contrib Nephrol. 1995;115:118-21 [8585897.001]

[Cites] Kidney Int. 1972 Aug;2(2):107-13 [4671535.001]

[Cites] Transplantation. 2002 Oct 27;74(8):1070-6 [12438948.001]

[Cites] Cell. 2000 Oct 13;103(2):253-62 [11057898.001]

[Cites] Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3934-9 [10097141.001]

[Cites] Proc Natl Acad Sci U S A. 2005 May 10;102(19):6954-9 [15863619.001]

[Cites] Am J Nephrol. 1998;18(5):391-8 [9730562.001]

[Cites] Mol Cell. 2000 Nov;6(5):1267-73 [11106764.001]

[Cites] Biol Cell. 2001 Sep;93(1-2):53-62 [11730323.001]

[Cites] J Am Soc Nephrol. 2000 Aug;11(8):1505-11 [10906164.001]

[Cites] J Urol. 1969 Aug;102(2):156-61 [5796888.001]

[Cites] J Natl Cancer Inst. 1998 Jul 15;90(14):1087-94 [9672257.001]

[Cites] J Am Soc Nephrol. 1995 Jun;5(12):2048-56 [7579053.001]

[Cites] Kidney Int. 2003 Jun;63(6):1983-94 [12753285.001]

[Cites] Pediatr Nephrol. 1988 Jul;2(3):296-302 [3153029.001]

[Cites] Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1182-7 [11252306.001]

[Cites] J Clin Endocrinol Metab. 1993 Nov;77(5):1323-8 [7915721.001]

[Cites] Cell. 2003 Jul 11;114(1):61-73 [12859898.001]

[Cites] J Am Soc Nephrol. 2002 Jul;13(7):1733-9 [12089368.001]

[Cites] Nat Cell Biol. 2002 Mar;4(3):191-7 [11854751.001]

[Cites] Nat Med. 2003 Oct;9(10):1323-6 [14502283.001]

[Cites] Kidney Blood Press Res. 2006;29(3):182-8 [16943682.001]

[Cites] Am J Pathol. 1993 Apr;142(4):1051-60 [8097368.001]

[Cites] Kidney Int. 2003 Nov;64(5):1573-9 [14531789.001]

[Cites] Mol Cell Biol. 1998 Nov;18(11):6666-78 [9774681.001]

[Cites] J Urol. 1995 Mar;153(3 Pt 1):578-83 [7861486.001]

[Cites] Kidney Int. 2004 Nov;66(5):1766-73 [15496147.001]

[Cites] Am J Nephrol. 2001 Mar-Apr;21(2):98-103 [11359016.001]

[Cites] JAMA. 1991 Feb 20;265(7):888-92 [1992187.001]

[Cites] J Biol Chem. 1995 Jan 20;270(3):1149-55 [7836373.001]

[Cites] Nephrol Dial Transplant. 1999 May;14(5):1113-6 [10344347.001]

[Cites] Am J Pathol. 2004 Nov;165(5):1719-30 [15509540.001]

[Cites] Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5466-71 [16567633.001]

[Cites] Acta Med Scand. 1986;219(4):399-405 [3716882.001]

[Cites] Arch Dermatol Res. 2004 Jul;296(2):74-82 [15278365.001]

[Cites] Curr Opin Pharmacol. 2003 Aug;3(4):371-7 [12901945.001]

[Cites] Cancer Res. 2002 Oct 15;62(20):5645-50 [12384518.001]

[Cites] N Engl J Med. 1995 Jul 6;333(1):18-25 [7776989.001]

[Cites] Kidney Int. 1996 Jan;49(1):135-46 [8770959.001]

(PMID = 18034588.001).

[ISSN] 0012-6667

[Journal-full-title] Drugs

[ISO-abbreviation] Drugs

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / U01 DK624

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] New Zealand

[Number-of-references] 190

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] HIV viremia and changes in kidney function.

OBJECTIVE: To evaluate the effect of HIV infection on longitudinal changes in kidney function and to identify independent predictors of kidney function changes in HIV-infected individuals.

CONCLUSION: Compared with controls, HIV-infected persons were more likely both to have clinical decline and clinical improvement in kidney function during 5 years of follow-up.

The extent of viremic control had a strong association with longitudinal changes in kidney function.

Genetic Alliance. consumer health - HIV.

MedlinePlus Health Information. consumer health - HIV/AIDS.

MedlinePlus Health Information. consumer health - HIV/AIDS in Women.

MedlinePlus Health Information. consumer health - Kidney Diseases.

COS Scholar Universe. author profiles.

Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] J Am Soc Nephrol. 2006 Jan;17(1):254-61 [16267155.001]

[Cites] J Am Soc Nephrol. 2005 May;16(5):1404-12 [15788478.001]

[Cites] Antivir Ther. 2006;11(5):641-5 [16964834.001]

[Cites] N Engl J Med. 2006 Nov 30;355(22):2283-96 [17135583.001]

[Cites] AIDS. 2007 May 11;21(8):1003-9 [17457094.001]

[Cites] AIDS. 2007 May 31;21(9):1119-27 [17502722.001]

[Cites] Clin J Am Soc Nephrol. 2006 Jan;1(1):117-29 [17699198.001]

[Cites] Nephrol Dial Transplant. 2007 Nov;22(11):3186-90 [17575315.001]

[Cites] Arch Intern Med. 2007 Nov 12;167(20):2213-9 [17998494.001]

[Cites] Kidney Int. 2007 Dec;72(11):1380-7 [17805235.001]

[Cites] AIDS. 2007 Nov 30;21(18):2435-43 [18025880.001]

[Cites] J Clin Endocrinol Metab. 2008 Jan;93(1):216-24 [17940113.001]

[Cites] Am J Med Sci. 2008 Feb;335(2):89-94 [18277114.001]

[Cites] Am J Kidney Dis. 2008 Mar;51(3):395-406 [18295055.001]

[Cites] AIDS. 2008 Feb 19;22(4):481-7 [18301060.001]

[Cites] Clin Infect Dis. 2008 Apr 15;46(8):1271-81 [18444867.001]

[Cites] Am J Kidney Dis. 2008 Jun;51(6):914-24 [18455851.001]

[Cites] Arch Intern Med. 2008 Nov 10;168(20):2212-8 [19001197.001]

[Cites] AIDS. 2009 Jan 2;23(1):71-82 [19050388.001]

[Cites] Kidney Int. 2009 Feb;75(4):428-34 [19052538.001]

[Cites] Am J Nephrol. 2009;30(3):171-8 [19349699.001]

[Cites] Biometrics. 2000 Sep;56(3):779-88 [10985216.001]

[Cites] Am J Kidney Dis. 2002 Aug;40(2):221-6 [12148093.001]

[Cites] J Am Soc Nephrol. 2002 Dec;13(12):2997-3004 [12444220.001]

[Cites] AIDS. 2004 Feb 20;18(3):541-6 [15090808.001]

[Cites] Kidney Int. 2004 Sep;66(3):1145-52 [15327410.001]

[Cites] J Clin Epidemiol. 1988;41(11):1105-16 [3204420.001]

[Cites] Am J Nephrol. 1995;15(3):217-21 [7618646.001]

[Cites] Kidney Int. 1995 Aug;48(2):311-20 [7564098.001]

[Cites] Scand J Clin Lab Invest. 1999 Feb;59(1):1-8 [10206092.001]

[Cites] Stat Methods Med Res. 1999 Mar;8(1):3-15 [10347857.001]

[Cites] J Am Soc Nephrol. 2004 Dec;15(12):3184-91 [15579522.001]

[Cites] J Am Soc Nephrol. 2005 Feb;16(2):459-66 [15615823.001]

[Cites] Am J Epidemiol. 2006 May 1;163(9):860-9 [16524955.001]

(PMID = 19352136.001).

[ISSN] 1473-5571

[Journal-full-title] AIDS (London, England)

[ISO-abbreviation] AIDS

[Language] ENG

[Grant] United States / NHLBI NIH HHS / HL / R01-HL-74814; United States / NIDDK NIH HHS / DK / R01 DK057508-01S1; United States / NCRR NIH HHS / RR / M01 RR000083-38S30468; United States / NIDDK NIH HHS / DK / R01 DK057508; United States / NCRR NIH HHS / RR / M01-RR00083; United States / NHLBI NIH HHS / HL / R01 HL074814-07; United States / NIDDK NIH HHS / DK / R01 DK057508-01; United States / NCRR NIH HHS / RR / M01 RR000083-380468; United States / NCRR NIH HHS / RR / M01 RR000083-40S10468; United States / NCRR NIH HHS / RR / M01 RR000083-430512; United States / NCRR NIH HHS / RR / M01 RR000865; United States / NCRR NIH HHS / RR / M01 RR000036; United States / NHLBI NIH HHS / HL / R01 HL074814-04; United States / NCRR NIH HHS / RR / M01 RR000083-38S20468; United States / NCRR NIH HHS / RR / M01 RR000083-420512; United States / NHLBI NIH HHS / HL / R01 HL074814-06; United States / NIDDK NIH HHS / DK / R01 DK057508-03S1; United States / NCRR NIH HHS / RR / M01 RR000054; United States / NCRR NIH HHS / RR / M01-RR00052; United States / NIDDK NIH HHS / DK / R01 DK057508-03S2; United States / NCRR NIH HHS / RR / M01 RR000052; United States / NHLBI NIH HHS / HL / R01 HL074814-05; United States / NCRR NIH HHS / RR / M01 RR000051; United States / NCRR NIH HHS / RR / M01-RR00051; United States / NCRR NIH HHS / RR / M01-RR00036; United States / NHLBI NIH HHS / HL / R01 HL074814; United States / NIDDK NIH HHS / DK / R01 DK057508-02; United States / NCRR NIH HHS / RR / M01 RR000083-400468; United States / NHLBI NIH HHS / HL / R01-HL-53359; United States / NCRR NIH HHS / RR / M01-RR00636; United States / NCRR NIH HHS / RR / M01 RR000083-390468; United States / NCRR NIH HHS / RR / M01-RR00054; United States / NCRR NIH HHS / RR / M01 RR000083; United States / NIDDK NIH HHS / DK / R01 DK057508-03; United States / NIDDK NIH HHS / DK / R01-DK-57508

[Publication-type] Journal Article; Multicenter Study; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Cystatin C

[Other-IDs] NLM/ NIHMS492632; NLM/ PMC3725756

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Progression from acute kidney injury to chronic kidney disease: a pediatric perspective.

Although emerging evidence indicates that the incidence of both acute kidney injury (AKI) and chronic kidney disease (CKD) in children is rising and the etiologies are dramatically changing, relatively little is currently known regarding the potential for transition from AKI to CKD.

These include neutrophil gelatinase-associated lipocalin, liver-type fatty acid-binding protein, and kidney injury molecule-1.

Genetic Alliance. consumer health - Kidney Disease.

MedlinePlus Health Information. consumer health - Chronic Kidney Disease.

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Nephrol Dial Transplant. 2008 Jan;23(1):414-6 [17893105.001]

[Cites] Transplantation. 2007 Dec 27;84(12):1625-30 [18165774.001]

[Cites] Kidney Int. 2008 Feb;73(4):465-72 [18094680.001]

[Cites] Curr Opin Nephrol Hypertens. 2008 Mar;17(2):127-32 [18277143.001]

[Cites] Crit Care. 2007;11(6):R127 [18070344.001]

[Cites] Clin J Am Soc Nephrol. 2008 May;3(3):665-73 [18337554.001]

[Cites] Pediatr Crit Care Med. 2008 May;9(3):279-84 [18446113.001]

[Cites] Adv Chronic Kidney Dis. 2008 Jul;15(3):222-34 [18565474.001]

[Cites] Pediatr Nephrol. 2000 Nov;15(1-2):11-3 [11095002.001]

[Cites] Curr Opin Pediatr. 2002 Apr;14(2):183-8 [11981288.001]

[Cites] Kidney Int. 2002 Jul;62(1):237-44 [12081583.001]

[Cites] Crit Care Med. 2002 Sep;30(9):2156-7 [12352064.001]

[Cites] Pediatr Nephrol. 2002 Dec;17(12):1032-7 [12478353.001]

[Cites] Kidney Int. 2003 May;63(5):1714-24 [12675847.001]

[Cites] Pediatr Nephrol. 2003 Aug;18(8):796-804 [12811650.001]

[Cites] J Am Soc Nephrol. 2003 Oct;14(10):2534-43 [14514731.001]

[Cites] Ann Thorac Surg. 2003 Nov;76(5):1443-9 [14602265.001]

[Cites] Pediatr Nephrol. 2004 Jan;19(1):91-5 [14634863.001]

[Cites] Am J Nephrol. 2004 May-Jun;24(3):307-15 [15148457.001]

[Cites] Crit Care. 2004 Aug;8(4):R204-12 [15312219.001]

[Cites] Am J Kidney Dis. 1995 Jan;25(1):113-8 [7810517.001]

[Cites] Am J Kidney Dis. 2005 Jan;45(1):96-101 [15696448.001]

[Cites] Lancet. 2005 Apr 2-8;365(9466):1231-8 [15811456.001]

[Cites] J Am Soc Nephrol. 2005 Nov;16(11):3365-70 [16177006.001]

[Cites] Am J Kidney Dis. 2005 Dec;46(6):1038-48 [16310569.001]

[Cites] J Am Soc Nephrol. 2005 Dec;16(12):3736-41 [16267160.001]

[Cites] Kidney Int. 2006 Jan;69(1):184-9 [16374442.001]

[Cites] Ann Thorac Surg. 2006 Feb;81(2):542-6 [16427848.001]

[Cites] Mol Cell Biochem. 2006 Mar;284(1-2):175-82 [16532260.001]

[Cites] Pediatr Nephrol. 2006 Jun;21(6):856-63 [16528543.001]

[Cites] Pediatr Nephrol. 2006 Jul;21(7):989-94 [16773412.001]

[Cites] Crit Care Med. 2006 Jul;34(7):1913-7 [16715038.001]

[Cites] Am J Transplant. 2006 Jul;6(7):1639-45 [16827865.001]

[Cites] Crit Care. 2006;10(3):R73 [16696865.001]

[Cites] Arthritis Rheum. 2006 Aug;54(8):2577-84 [16868980.001]

[Cites] Pediatrics. 2006 Sep;118(3):e786-91 [16894011.001]

[Cites] Pediatr Nephrol. 2007 Jan;22(1):101-8 [17072653.001]

[Cites] Pediatr Crit Care Med. 2007 Jan;8(1):29-35 [17251879.001]

[Cites] Clin Immunol. 2007 May;123(2):227-34 [17360238.001]

[Cites] Kidney Int. 2007 May;71(10):1028-35 [17396113.001]

[Cites] J Pathol. 2007 Jun;212(2):209-17 [17471468.001]

[Cites] Am J Nephrol. 2007;27(4):373-8 [17570904.001]

[Cites] Kidney Int. 2007 Aug;72(3):348-58 [17495861.001]

[Cites] Am J Kidney Dis. 2007 Aug;50(2):169-80 [17660017.001]

[Cites] Clin J Am Soc Nephrol. 2006 Sep;1(5):1006-15 [17699320.001]

[Cites] J Am Soc Nephrol. 2007 Oct;18(10):2704-14 [17898236.001]

[Cites] J Am Soc Nephrol. 2007 Nov;18(11):2894-902 [17942962.001]

[Cites] Pediatr Nephrol. 2007 Dec;22(12):2089-95 [17874137.001]

[Cites] Semin Nephrol. 2007 Nov;27(6):637-51 [18061846.001]

[Cites] Crit Care. 2007;11(4):R84 [17678545.001]

(PMID = 18565478.001).

[ISSN] 1548-5609

[Journal-full-title] Advances in chronic kidney disease

[ISO-abbreviation] Adv Chronic Kidney Dis

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / R01 DK069749-04; United States / NIDDK NIH HHS / DK / DK069749-04; United States / NIDDK NIH HHS / DK / R21 DK070163-02; United States / NIDDK NIH HHS / DK / R01 DK069749; United States / NIDDK NIH HHS / DK / R21 DK070163

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers

[Number-of-references] 54

[Other-IDs] NLM/ NIHMS57871; NLM/ PMC2481383

   

[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Distinct patterns of kidney and liver cyst growth in pkd2(WS25/-) mice.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is a common genetic disease that results in the development of cystic kidneys and liver.

Providing the foundation for future long-term studies, the present work documents distinct patterns of long-term cyst growth in the kidneys and liver of male and female pkd2(WS25/-) mice.

METHODS: Gravimetric measurements documented the progression of kidney and liver growth in male and female pkd2(WS25/-) mice over 12 months.

A fast imaging with steady-state precision-magnetic resonance imaging (FISP-MRI) technique to measure kidney and liver organ and cyst volumes was optimized and validated.

RESULTS: Male and female pkd2(WS25/-) mice had significant increases in kidney weights after 4 months of age.

The progression of kidney growth was minimal after 4 months of age.

CONCLUSIONS: Pkd2(WS25/-) mice are a genetic mouse model that recapitulates the early phenotypic characteristics of human ADPKD kidney cystogenesis.

MedlinePlus Health Information. consumer health - Liver Diseases.

COS Scholar Universe. author profiles.

NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

[Email] Email this result item

Email the results to the following email address:   [X] Close

[Cites] Hepatology. 1988 Nov-Dec;8(6):1627-34 [3192176.001]

[Cites] Kidney Int. 2004 Apr;65(4):1511-6 [15086495.001]

[Cites] Magn Reson Imaging. 1991;9(3):429-34 [1881263.001]

[Cites] Hepatology. 1997 Nov;26(5):1282-6 [9362373.001]

[Cites] Cell. 1998 Apr 17;93(2):177-88 [9568711.001]

[Cites] N Engl J Med. 2006 May 18;354(20):2122-30 [16707749.001]

[Cites] Nephron Clin Pract. 2006;103(4):c173-80 [16636585.001]

[Cites] J Magn Reson Imaging. 2006 Sep;24(3):646-56 [16878308.001]

[Cites] N Engl J Med. 2007 Apr 12;356(15):1560 [17429087.001]

[Cites] Clin J Am Soc Nephrol. 2006 Jan;1(1):64-9 [17699192.001]

[Cites] Clin Cancer Res. 2007 Nov 1;13(21):6450-8 [17975157.001]

[Cites] Kidney Int. 2008 Mar;73(6):778-81 [18185504.001]

[Cites] Am J Physiol Lung Cell Mol Physiol. 2008 Jul;295(1):L152-61 [18441091.001]

[Cites] AJR Am J Roentgenol. 2008 Aug;191(2):352-8 [18647901.001]

[Cites] N Engl J Med. 2008 Oct 2;359(14):1477-85 [18832246.001]

[Cites] Acad Radiol. 2009 Jan;16(1):88-95 [19064216.001]

[Cites] Kidney Int. 2009 Jan;75(2):235-41 [18971924.001]

[Cites] J Am Soc Nephrol. 2009 Jan;20(1):6-8 [19073819.001]

[Cites] Recent Pat Anticancer Drug Discov. 2009 Jan;4(1):36-53 [19149687.001]

[Cites] Annu Rev Med. 2009;60:321-37 [18947299.001]

[Cites] Nat Genet. 2000 Jan;24(1):75-8 [10615132.001]

[Cites] J Am Soc Nephrol. 2000 Aug;11(8):1505-11 [10906164.001]

[Cites] Kidney Int. 2000 Dec;58(6):2492-501 [11115083.001]

[Cites] Comp Med. 2002 Oct;52(5):433-8 [12405636.001]

[Cites] J Magn Reson Imaging. 2003 Feb;17(2):190-6 [12541226.001]

[Cites] Kidney Int. 2003 Sep;64(3):1035-45 [12911554.001]

[Cites] Hepatology. 1990 Jun;11(6):1033-7 [2365280.001]

(PMID = 20388629.001).

[ISSN] 1460-2385

[Journal-full-title] Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

[ISO-abbreviation] Nephrol. Dial. Transplant.

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK-074835; United States / NCRR NIH HHS / RR / UL1 RR025780; United States / NIDDK NIH HHS / DK / R01 DK074835; United States / NCI NIH HHS / CA / P30 CA046934; United States / NIDDK NIH HHS / DK / DK-056851; United States / NIDDK NIH HHS / DK / R01 DK056851

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / TRPP Cation Channels; 0 / polycystic kidney disease 2 protein

[Other-IDs] NLM/ PMC2980992

   

[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Value of electron microscopy in kidney biopsy diagnosis.

Kidney biopsy reports given during 2003 were collected from the authors' pathology database.

Five tumor samples were not studied with electron microscopy (EM).

EM was not performed in 10/24 transplant biopsies, or in 11/82 cases of suspected primary kidney disease.

(1) EM was essential for diagnosis, (2) EM contributed to the interpretation and cleared uncertainties, and (3) EM had no influence on the diagnostic process.

In transplant biopsies EM influenced the final diagnosis in 86% of cases (category 2).

In biopsies performed for primary kidney disease EM was essential for diagnosis in 18.3% clearly contributed in 53.5%, and had no influence on the final diagnosis in 28.2% of cases.

Because only about 25% of the EM reports did not have any influence on the diagnostic process, it is recommended that kidney biopsy protocols should include EM in all biopsy cases, or at least tissue should be reserved for EM studies of all cases.

[MeSH-major] Kidney / ultrastructure. Kidney Diseases / diagnosis

[MeSH-minor] Adult. Aged. Biopsy. Diagnosis, Differential. Humans. Kidney Transplantation / pathology. Male. Microscopy, Electron, Transmission

MedlinePlus Health Information. consumer health - Kidney Diseases.

COS Scholar Universe. author profiles.

[Email] Email this result item

Email the results to the following email address:   [X] Close

(PMID = 16316946.001).

[ISSN] 0191-3123

[Journal-full-title] Ultrastructural pathology

[ISO-abbreviation] Ultrastruct Pathol

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States