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Title: Urinary neutrophil gelatinase-associated lipocalin levels reflect damage to glomeruli, proximal tubules, and distal nephrons.
Authors: Kuwabara, Takashige
Mori, Kiyoshi
Mukoyama, Masashi
Kasahara, Masato
Yokoi, Hideki  kyouindb  KAKEN_id
Saito, Yoko
Yoshioka, Tetsuro
Ogawa, Yoshihisa
Imamaki, Hirotaka
Kusakabe, Toru  KAKEN_id
Ebihara, Ken
Omata, Mitsugu
Satoh, Noriko
Sugawara, Akira
Barasch, Jonathan
Nakao, Kazuwa
Author's alias: 森, 潔
Keywords: diabetic nephropathy
nephrotic syndrome
obstructive nephropathy
acute renal failure
albuminuria
Issue Date: Feb-2009
Publisher: Nature Publishing Group
Journal title: Kidney international
Volume: 75
Issue: 3
Start page: 285
End page: 294
Abstract: Urinary neutrophil gelatinase-associated lipocalin (Ngal or lipocalin 2) is a very early and sensitive biomarker of kidney injury. Here we determined the origin and time course of Ngal appearance in several experimental and clinically relevant renal diseases. Urinary Ngal levels were found to be markedly increased in lipoatrophic- and streptozotocin-induced mouse models of diabetic nephropathy. In the latter mice, the angiotensin receptor blocker candesartan dramatically decreased urinary Ngal excretion. The reabsorption of Ngal by the proximal tubule was severely reduced in streptozotocin-induced diabetic mice, but upregulation of its mRNA and protein in the kidney was negligible, compared to those of control mice, suggesting that increased urinary Ngal was mainly due to impaired renal reabsorption. In the mouse model of unilateral ureteral obstruction, Ngal protein synthesis was dramatically increased in the dilated thick ascending limb of Henle and N was found in the urine present in the swollen pelvis of the ligated kidney. Five patients with nephrotic syndrome or interstitial nephritis had markedly elevated urinary Ngal levels at presentation, but these decreased in response to treatment. Our study shows that the urinary Ngal level may be useful for monitoring the status and treatment of diverse renal diseases reflecting defects in glomerular filtration barrier, proximal tubule reabsorption, and distal nephrons.
Description: Published online 1 October 2008
Rights: This is the accepted manuscript of an article is available at http://dx.doi.org/10.1038/ki.2008.499
The full-text file will be made open to the public on 10 April 2009 in accordance with publisher's 'Terms and Conditions for Self-Archiving'.
この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。This is not the published version. Please cite only the published version.
URI: http://hdl.handle.net/2433/202582
DOI(Published Version): 10.1038/ki.2008.499
PubMed ID: 19148153
Appears in Collections:Journal Articles

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