Diabetic nephropathy, clinically defined by overt albuminuria, hypertension and declining GFR, affects 25-35% of IDDM patients. The risk of nephropathy peaks during the second decade of IDDM and declines thereafter, suggesting that only a subset of IDDM patients is at risk for nephropathy. A role for hypertension in the progression of established renal damage in IDDM is now accepted; however the role of hypertension in the genesis of diabetic nephropathy is not yet clear. Mesangial expansion is a characteristic lesion of diabetic nephropathology and correlates with renal function. Functional studies are not indicative of underlying renal pathology except relatively late, when glomerular injury is advanced. Microalbuminuria in the 'predictive' range (>30 μg/min) and associated with hypertension and/or declining GFR is a marker of established diabetic glomerulopathy. Only carefully designed longitudinal studies of renal morphology and function with accurate blood pressure monitoring beginning early in the course of IDDM will clarify the relationships between blood pressure and renal damage in IDDM. In NIDDM the frequent presence of non-diabetic renal lesions, of hypertension at or before the onset of diabetes, and the relative paucity of clinical-pathological correlations currently make it difficult to understand the role of hypertension in the genesis and progression of nephropathy. Again, longitudinal studies of blood pressure and renal structure and function are required in NIDDM patients. Finally, animal models of hypertension and diabetes may aid progress in these areas.
|Original language||English (US)|
|Number of pages||6|
|Journal||Clinical and Investigative Medicine|
|State||Published - Dec 1 1991|
- hypertension mesangium proteinuria