Diabetic nephropathy. The basis for dietary and converting enzyme inhibitor therapy.
Once initiated, renal disease progresses in most patients to end-stage over a matter of months or years. This progressive consumption of renal mass seems to result from maladaptations to the initial insult by the remaining kidney. This review stresses the hemodynamic underpinnings of this progression of renal disease. The evidence is reviewed that indicates that loss of renal mass from surgical reduction in kidney tissue or from diabetes mellitus results in increased blood flow, filtration, and glomerular pressure in the remaining nephrons. Prevention of this glomerular hypertension by reduction in dietary protein or by the addition of converting enzyme inhibitors affords protection. The clinical implications of these observations are reviewed.
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000150:complications / Q000178:diet therapy* / Q000188:drug therapy; D004044:Dietary Proteins / Q000009:adverse effects; D006439:Hemodynamics; D006801:Humans; D006977:Hypertension, Renal / Q000150:complications / Q000503:physiopathology; D007674:Kidney Diseases / Q000150:complications / Q000503:physiopathology
D000806:Angiotensin-Converting Enzyme Inhibitors; D004044:Dietary Proteins