Diabetic nephropathy. Pathogenesis and prevention.
Already at the time of diagnosis of juvenile onset diabetes mellitus, there are morphological and functional changes in the kidney. The kidneys and the individual glomeruli are considerably enlarged, and the glomerular filtration increased. In experimental diabetes mellitus the metabolism of the glomerular basement membrane is increased. These abnormalities are reversible by meticulous metabolic control. Their relationship to the diabetic glomerulosclerosis that causes uremia twenty to thirty years later is not clear. Carefully analyzed extensive clinical experience confirms that good metabolic control delays the onset of symptomatic diabetic renal disease, as expected from experimental studies. Normalization of even a slightly elevated blood pressure may be important to slow the progression of the renal insufficiency. Better methods for the management of the diabetic state and better education of the patients may be important to postpone the heroic endeavours of renal or pancreatic transplantation or dialysis.
D000818:Animals; D001485:Basement Membrane / Q000032:analysis; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control; D005919:Glomerular Filtration Rate; D006801:Humans; D007136:Immunoglobulins / Q000032:analysis; D007676:Kidney Failure, Chronic / Q000209:etiology; D007678:Kidney Glomerulus / Q000503:physiopathology; D008565:Membrane Proteins / Q000032:analysis; D051381:Rats
D007136:Immunoglobulins; D008565:Membrane Proteins