Pathological and prognostic value of urinary neutrophil gelatinase-associated lipocalin in macroproteinuric patients with worsening renal function

被引:64
作者
Bolignano, Davide [1 ]
Coppolino, Giuseppe [1 ]
Lacquaniti, Antonio [1 ]
Nicocia, Giacomo [2 ]
Buemi, Michele [1 ]
机构
[1] Univ Messina, Dept Internal Med, Chair Nephrol, Messina, Italy
[2] Univ Messina, Dept Pathol & Expt Microbiol, Messina, Italy
关键词
neutrophil gelatinase-associated lipocalin; proteinuria; chronic renal failure; membranous glomerulonephritis; renal function; prognostic factor;
D O I
10.1159/000151665
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Background/Aims: Persistent proteinuria is a sign of renal damage caused by several factors, but it is itself a cause of tubular injury leading to chronic renal failure. Neutrophil gelatinase-associated lipocalin (NGAL) is a stress protein released by tubular cells which urinary excretion (uNGAL) increases in response to various stimuli. Methods: In the present study we analyzed uNGAL levels in 23 macroproteinuric patients with membranous glomerulonephritis. Results: In these subjects, uNGAL concentrations were significantly higher than in controls, directly correlated with proteinuria and inversely related to residual renal function. Patients were further categorized into two groups, according to a cut-off baseline uNGAL value of 350 ng/ml and evaluated during a 1-year follow-up period. After 12 months, subjects with higher uNGAL levels showed a significant worsening in baseline renal function and a 3.36 risk ratio of developing a severe decrease in GFR (>= 50% of baseline values) compared with others. Conclusions: These findings suggest that NGAL may play a key role in tubular adaptations to persistent macroproteinuria. Furthermore, a new, interesting application of NGAL measurement could be proposed in clinical nephrology as a predictor of worsening renal function in patients affected by chronic kidney disease. Copyright (C) 2008 S. Karger AG, Basel.
引用
收藏
页码:274 / 279
页数:6
相关论文
共 13 条
[11]   Proteinuria induces tubular cell turnover: A potential mechanism for tubular atrophy [J].
Thomas, ME ;
Brunskill, NJ ;
Harris, KPG ;
Bailey, E ;
Pringle, JH ;
Furness, PN ;
Walls, J .
KIDNEY INTERNATIONAL, 1999, 55 (03) :890-898
[12]   Tubular kidney injury molecule-1 in protein-overload nephropathy [J].
van Timmeren, Mirjan M. ;
Bakker, Stephan J. L. ;
Vaidya, Vishal S. ;
Bailly, Veronique ;
Schuurs, Theo A. ;
Damman, Jeffrey ;
Stegeman, Coen A. ;
Bonventre, Joseph V. ;
van Goor, Harry .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2006, 291 (02) :F456-F464
[13]   Iron, lipocalin, and kidney epithelia [J].
Yang, J ;
Mori, K ;
Li, JY ;
Barasch, J .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2003, 285 (01) :F9-F18