Ultrastructural changes in the glomerular filtration barrier and occurrence of proteinuria in Chinese patients with type 2 diabetic nephropathy

被引:31
作者
Zhu, Wei-wei [1 ]
Chen, Hui-ping [1 ]
Ge, Yong-chun [1 ]
Xie, Hong-lang [1 ]
Zeng, Cai-hong [1 ]
Li, Lei-shi [1 ]
Liu, Zhi-hong [1 ]
机构
[1] Nanjing Univ, Sch Med, Res Inst Nephrol, Jingling Hosp, Nanjing 210002, Peoples R China
关键词
T2DN; Endothelial cell; GBM; Podocyte; Proteinuria; STRUCTURAL-FUNCTIONAL RELATIONSHIPS; ALPHA-3(IV) COLLAGEN PRODUCTION; ENDOTHELIAL GROWTH-FACTOR; MOUSE PODOCYTES; BASEMENT-MEMBRANE; MECHANICAL STRAIN; KIDNEY-DISEASE; RENAL-DISEASE; INJURY; EXPRESSION;
D O I
10.1016/j.diabres.2009.09.009
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Aim: Diabetic nephropathy (DN) is one of the most important causes of end stage renal disease in the world. Its hallmark is proteinuria. Therefore, we set out to clarify the structural changes that occur in the glomerular filtration barrier in Chinese patients with true type 2 diabetic nephropathy, and to examine the relationship between these structural changes and proteinuria. Methods: 42 Chinese patients with true T2DN were divided into three groups according to urinary protein excretion. Glomerular volume, endothelial cell density, endothelial cell number, glomerular basement membrane (GBM) width, podocyte density, podocyte number and foot process width were evaluated using light and electron microscopic morphometry. Result: Glomerular volume and endothelial cell number were increased in diabetic patients, but there was no difference between patients with respect to the degree of proteinuria. As proteinuria progressed, endothelial cell density remained unchanged, while the glomerular basement membrane (GBM) and podocyte foot process width increased, podocyte density and number decreased. Conclusions: Podocyte and GBM change more obviously during the development of proteinuria. Besides, proteinuria was inversely related to podocyte density, and directly related to GBM and glomerular volume. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:199 / 207
页数:9
相关论文
共 37 条
[1]
CLINICAL-IDENTIFICATION OF NONDIABETIC RENAL-DISEASE IN DIABETIC-PATIENTS WITH TYPE-I AND TYPE-II DISEASE PRESENTING WITH RENAL DYSFUNCTION [J].
AMOAH, E ;
GLICKMAN, JL ;
MALCHOFF, CD ;
STURGILL, BC ;
KAISER, DL ;
BOLTON, WK .
AMERICAN JOURNAL OF NEPHROLOGY, 1988, 8 (03) :204-211
[2]
EARLY GLOMERULOPATHY IS PRESENT IN YOUNG, TYPE-1 (INSULIN-DEPENDENT) DIABETIC-PATIENTS WITH MICROALBUMINURIA [J].
BANGSTAD, HJ ;
OSTERBY, R ;
DAHLJORGENSEN, K ;
BERG, KJ ;
HARTMANN, A ;
NYBERG, G ;
BJORN, SF ;
HANSSEN, KF .
DIABETOLOGIA, 1993, 36 (06) :523-529
[3]
BJORN SF, 1995, DIABETOLOGIA, V38, P1197, DOI 10.1007/s001250050412
[4]
Blum S, 2007, ISR MED ASSOC J, V9, P107
[5]
Cellular basis of diabetic nephropathy 1. Study design and renal structural-functional relationships in patients with long-standing type 1 diabetes [J].
Caramori, ML ;
Kim, Y ;
Huang, CM ;
Fish, AJ ;
Rich, SS ;
Miller, ME ;
Russell, G ;
Mauer, M .
DIABETES, 2002, 51 (02) :506-513
[6]
Altering expression of α3β1 integrin on podocytes of human and rats with diabetes [J].
Chen, HC ;
Chen, CA ;
Guh, JY ;
Chang, JM ;
Shin, SJ ;
Lai, YH .
LIFE SCIENCES, 2000, 67 (19) :2345-2353
[7]
Podocyte-derived vascular endothelial growth factor mediates the stimulation of α3(IV) collagen production by transforming growth factor-β 1 in mouse podocytes [J].
Chen, S ;
Kasama, Y ;
Lee, JS ;
Jim, B ;
Marin, M ;
Ziyadeh, FN .
DIABETES, 2004, 53 (11) :2939-2949
[8]
Angiotensin II stimulates α3(IV) collagen production in mouse podocytes via TGF-β and VEGF signalling:: implications for diabetic glomerulopathy [J].
Chen, SD ;
Lee, JS ;
Iglesias de la Cruz, MC ;
Wang, A ;
Izquierdo-Lahuerta, A ;
Gandhi, NK ;
Danesh, FR ;
Wolf, G ;
Ziyadeh, FN .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2005, 20 (07) :1320-1328
[9]
Is podocyte injury relevant in diabetic nephropathy? Studies in patients with type 2 diabetes [J].
Dalla Vestra, M ;
Masiero, A ;
Roiter, AM ;
Saller, A ;
Crepaldi, G ;
Fioretto, P .
DIABETES, 2003, 52 (04) :1031-1035
[10]
DIKOW R, 2005, OXFORD TXB CLIN NEPH, V2, P659