| Netrin-1 and kidney injury. II. Netrin-1 is an early biomarker of acute kidney injury. | |
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MedLine Citation:
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PMID: 18234954 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Acute kidney injury is an important complication in hospitalized patients often diagnosed late and associated with high mortality and morbidity. Although biomarkers for nephrotoxicity are available, they often lack sensitivity and specificity for detecting tubular injury. Netrin-1 is a laminin-like molecule highly expressed in many organs including kidney. To determine the value of netrin-1 as a biomarker of renal injury, we analyzed its urinary excretion following ischemia-reperfusion-, cisplatin-, folic acid-, and endotoxin-induced renal injury in mice. Urinary netrin-1 levels increased markedly within 3 h of ischemia-reperfusion (40 +/- 14-fold, P < 0.01 vs. baseline), reached a peak level at 6 h, and decreased thereafter, returning to near baseline by 72 h. Serum creatinine significantly increased only after 24 h of reperfusion. Similarly, in cisplatin-, folic acid-, and lipopolysaccharide-treated mice, urine netrin-1 excretion increased as early as 1 h and reached a peak level at 6 h after injection. However, serum creatinine was raised significantly after 6, 24, and 72 h after folic acid, lipopolysaccharide, and cisplatin administration, respectively. NGAL excretion in folic acid- and lipopolysaccharide-treated mice urine samples could only be detected by 24 h after drug administration. Furthermore, urinary netrin-1 excretion increased dramatically in 13 acute renal failure patients, whereas none was detected in 6 healthy volunteer urine samples. Immunohistochemical localization showed that netrin-1 is highly expressed in tubular epithelial cells in transplanted human kidney. We conclude that urinary netrin-1 is a promising early biomarker of renal injury. |
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Authors:
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W Brian Reeves; Osun Kwon; Ganesan Ramesh |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2008-01-30 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 294 ISSN: 1931-857X ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2008 Apr |
Date Detail:
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Created Date: 2008-04-03 Completed Date: 2008-06-13 Revised Date: 2011-04-28 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F731-8 Citation Subset: IM |
Affiliation:
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Division of Nephrology, H040, Pennsylvania State Univ. College of Medicine, 500 Univ. Drive, Hershey, PA 17033, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute Kidney Injury
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chemically induced,
diagnosis* Acute-Phase Proteins Animals Biological Markers / analysis Cisplatin / therapeutic use Creatinine / blood Humans Kidney / injuries* Kidney Diseases / diagnosis* Lipocalins / blood Lipopolysaccharides / toxicity Male Mice Mice, Inbred C57BL Nerve Growth Factors / urine* Proto-Oncogene Proteins / blood Renal Circulation Reperfusion Injury / chemically induced, diagnosis Tumor Suppressor Proteins / urine* |
| Grant Support | |
ID/Acronym/Agency:
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R01-DK-063120/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acute-Phase Proteins; 0/Biological Markers; 0/LCN2 protein, human; 0/Lipocalins; 0/Lipopolysaccharides; 0/Nerve Growth Factors; 0/Proto-Oncogene Proteins; 0/Tumor Suppressor Proteins; 15663-27-1/Cisplatin; 158651-98-0/netrin-1; 60-27-5/Creatinine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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