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Abstract
Diabetic nephropathy is the most common cause of end-stage renal disease and accounts for significant morbidity and mortality among individuals with diabetes mellitus. Therefore, the clarification of the pathogenesis of diabetic nephropathy is an urgent issue. Podocytes cover the outer layer of the glomerulus and maintain its integrity so that fluid and toxins exit in urine, but cells and important proteins are kept in the blood stream. Diabetes mellitus alters this structure, it becomes scarred and then the ability of the kidney to clear toxins is lost. Recent evidence shows that early in diabetes the podocyte number is reduced, areas of the glomerular basement membrane are denuded, and podocyte number predicts long-term urinary albumin excretion in the patients with diabetes and microalbuminuria. These results suggest that podocytes play a critical role in the early stage of diabetic nephropathy. It is the purpose of this article to review the pathogenetic role of podocytes in diabetic nephropathy.
Figures and Tables
Fig. 1
The glomerular urinary filtration barrier in normal non-diabetic rat. Representative photograph of electron microscopy shows three layers of urinary filtration barrier, the fenestrated glomerular endothelium (E), the glomerular basement membrane (BM), and the slit diaphragm of the podocyte. Magnification, × 40,000 [Permission from Lee et al. (reference 4)].
Fig. 2
Podocyte injury in diabetic rats. Representative electron photomicrographs show examples of effaced podocytes (P) and decreased number of slit pores (arrows) in the diabetic rats. Magnification, × 40,000 [Permission from Lee et al. (reference 4)].
References
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