Diabetic nephropathy is the leading cause of chronic renal failure in the United States and other Western societies. Diabetic nephropathy may be diffuse or nodular (Kimmelstiel-Wilson lesion). The early stages cause an elevated glomerular filtration rate with enlarged kidneys, but the principal feature of diabetic nephropathy is proteinuria.
The severity of diabetic glomerulopathy is estimated by the thickness of the peripheral basement membrane and mesangium and matrix expressed as a fraction of appropriate spaces (eg, volume fraction of mesangium/glomerulus, matrix/mesangium, or matrix/glomerulus).
Three major histologic changes occur in the glomeruli of persons with diabetic nephropathy. First, mesangial expansion is directly induced by hyperglycemia, perhaps via increased matrix production or glycosylation of matrix proteins. Second, GBM thickening occurs. Third, glomerular sclerosis is caused by intraglomerular hypertension (induced by renal vasodilatation or from ischemic injury induced by hyaline narrowing of the vessels supplying the glomeruli). These different histologic patterns appear to have similar prognostic significance.
Kidney damage in type 1 diabetes is the largest cause of chronic kidney disease in the working age group.
Kidney disease in people with type 2 diabetes is increasing because of the increasing prevalence of people with diabetes, improved cardiovascular survival and the trend to younger onset of type 2 diabetes.
The prevalence of microalbuminuria in patients with type 1 diabetes at 30 years' disease duration is approximately 40%.
The prevalence of microalbuminuria in patients with type 2 diabetes at 10 years' disease duration is approximately 20-25%.
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