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Pathophysiologic abnormalities in diabetic nephropathy usually begin with long-standing poorly controlled blood glucose levels. This is followed by multiple changes in the filtration units of the kidneys, the [[nephron]]s. (There are normally about 750,000–1.5 million nephrons in each adult kidney). Initially, there is constriction of the [[efferent arterioles]] and dilation of [[afferent arterioles]], with resulting glomerular capillary hypertension and hyperfiltration particularly as nephrons become obsolescent and the adaption of hyperfiltration paradoxically causes further [[shear stress]] related damage to the delicate glomerular capillaries, further proteinuria, rising blood pressure and a vicious circle of additional nephron damage and decline in overall renal function. Concurrently, there are changes within the glomerulus itself: these include a thickening of the [[basement membrane]], a widening of the slit membranes of the [[podocytes]], an increase in the number of [[mesangial cell]]s, and an increase in mesangial matrix. This matrix invades the glomerular capillaries and produces deposits called Kimmelstiel-Wilson nodules. The mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration.

Translations:Diabetic nephropathy/3/en - Revision history

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