Diabetic nephropathy is responsible for the largest increase in new patients accepted for renal replacement therapy in industrialized countries (1). In Europe, the proportion of new dialysis patients who are diabetic has increased from less than 0.5% in 1972 to 7.3% in 1981 (2). In the U.S., about 3,200 diabetics reach end-stage renal disease (ESRD) each year, representing 20-25% of all new ESRD patients (3).Despite progress in dialysis the diabetic patient remains a formidable challange. ESRD develops pari passu with other complications that ultimately limit the quality of life. As our foremost goal should be to prevent all the complications of diabetes, the recent advances in diabetic nephropathy, retinopathy and neuropathy deserve our attention.
PROGRESSION OF NEPHROPATHYThe role of arterial hypertension. Mogensen has thoroughly reviewed the relationship between diabetic nephropathy and arterial hypertension and called attention to its complexity and need for systematic evaluation (4,5). Complicating the analysis of this relationship is the frequent occurrence of both hypertension and diabetes in the general population and differences between Type I and Type II diabetics (body weight, age, incidence of hypertension, presence or absence of autonomic neuropathy and control of glycemia). The different stage of diabetic nephropathy and their characteristic renal hemodynamics must also be considered (5).A wealth of clinical data is being accumulated showing amelioration in the rate of decline of glomerular filtration rate GFR or protein excretion when blood pressure is lowed (6-13). A recent prospective, longitudinal and cross-sectional study showed a strong correlation between arterial blood pressure, urinary albumin excretion, and renal hemodynamics. The changes suggested a continuum of abnormalities, with distinct stages in the development of diabetic nephropathy (14).Parring et al have studied the effects of long-term, ag-The International Journal Of Artificial Organs I Vol. 9 no. 4, 1986 I p.p. 207-212 gressive antihypertensive therapy on GFR and albiminuria in young Type I patients (13). Their results suggest that prolonged reduction of blood pressure to near normal reduces the rate of decline of GFR and albuminuria. The role of glycemic control. The experimental diabetic rat model and experience with human renal transplantation have provided data suggesting that diabetic nephropathy is the result of hyperglycemia (15). Strict metabolic control with insulin prevents the thickening of the glomerular basement membrane (GBM), the increase in mesangial volume, the increases in GFR, and the onset of albuminuria (16,17). More impressive has been the reversal of renal diabetic changes in rats after pancreatic islet transplantation (18-22). The mesangial changes were reversed, glomerular volume diminished and albumin excretion returned to normal. The GBM, however, remained abnormally thickened.When the human non-diabetic kidney is transplanted into a diabetic host, the characteristic mesangial and GBM changes occ...