Proteinuria in diabetic kidney disease: A mechanistic viewpoint

被引：355

作者：

Jefferson, J. A. ^{[1
]}

Shankland, S. J. ^{[1
]}

Pichler, R. H. ^{[1
]}

机构：

[1] Univ Washington, Dept Med, Div Nephrol, Sch Med, Seattle, WA 98195 USA

来源：

KIDNEY INTERNATIONAL | 2008年 / 74卷 / 01期

关键词：

podocyte; mesangial cell; glomerular endothelial cell; diabetic nephropathy; albuminuria; proteinuria;

D O I：

10.1038/ki.2008.128

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Proteinuria is the hallmark of diabetic kidney disease (DKD) and is an independent risk factor for both renal disease progression, and cardiovascular disease. Although the characteristic pathological changes in DKD include thickening of the glomerular basement membrane and mesangial expansion, these changes per se do not readily explain how patients develop proteinuria. Recent advances in podocyte and glomerular endothelial cell biology have shifted our focus to also include these cells of the glomerular filtration barrier in the development of proteinuria in DKD. This review describes the pathophysiological mechanisms at a cellular level which explain why patients with DKD develop proteinuria.

引用

页码：22 / 36

页数：15

共 175 条

[1] How does proteinuria cause progressive renal damage? [J].

Abbate, Mauro ;

Zoja, Carla ;

Remuzzi, Giuseppe .

JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2006, 17 (11) :2974-2984

[2] Microvascular alterations in diabetic mice correlate with level of hyperglycemia [J].

Algenstaedt, P ;

Schaefer, C ;

Biermann, T ;

Hamann, A ;

Schwarzloh, B ;

Greten, H ;

Rüther, W ;

Hansen-Algenstaedt, N .

DIABETES, 2003, 52 (02) :542-549

[3] THERAPEUTIC ADVANTAGE OF CONVERTING ENZYME-INHIBITORS IN ARRESTING PROGRESSIVE RENAL-DISEASE ASSOCIATED WITH SYSTEMIC HYPERTENSION IN THE RAT [J].

ANDERSON, S ;

RENNKE, HG ;

BRENNER, BM .

JOURNAL OF CLINICAL INVESTIGATION, 1986, 77 (06) :1993-2000

[4] CONTROL OF GLOMERULAR HYPERTENSION LIMITS GLOMERULAR INJURY IN RATS WITH REDUCED RENAL MASS [J].

ANDERSON, S ;

MEYER, TW ;

RENNKE, HG ;

BRENNER, BM .

JOURNAL OF CLINICAL INVESTIGATION, 1985, 76 (02) :612-619

[5] USE OF EXOGENOUS MYOGLOBIN AS AN ULTRASTRUCTURAL TRACER - REABSORPTION AND TRANSLOCATION OF PROTEIN BY RENAL TUBULE [J].

ANDERSON, WA .

JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1972, 20 (09) :672-&

[6] Increased glomerular permeability to negatively charged Ficoll relative to neutral Ficoll in rats [J].

Asgeirsson, Daniel ;

Venturoli, Daniele ;

Rippe, Bengt ;

Rippe, Catarina .

AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2006, 291 (05) :F1083-F1089

[7] THE ANIONIC MATRIX AT THE RAT GLOMERULAR ENDOTHELIAL SURFACE [J].

AVASTHI, PS ;

KOSHY, V .

ANATOMICAL RECORD, 1988, 220 (03) :258-266

[8]

AVASTHI PS, 1979, J LAB CLIN MED, V93, P266

[9] Reduction of VEGF-A and CTGF expression in diabetic nephropathy is associated with podocyte loss [J].

Baelde, H. J. ;

Eikmans, M. ;

Lappin, D. W. P. ;

Doran, P. P. ;

Hohenadel, D. ;

Brinkkoetter, P-T ;

van der Woude, F. J. ;

Waldherr, R. ;

Rabelink, T. J. ;

de Heer, E. ;

Bruijin, J. A. .

KIDNEY INTERNATIONAL, 2007, 71 (07) :637-645

[10] High ambient glucose levels modulates the production of MMP-9 and α5(IV) collagen by cultured podocytes [J].

Bai, YL ;

Wang, LZ ;

Li, YQ ;

Liu, SY ;

Li, JZ ;

Wang, HY ;

Huang, HC .

CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, 2006, 17 (1-2) :57-68

← 1 2 3 4 5 6 7 8 9 10 →