Insulin action and insulin therapy in uremic insulin-dependent diabetic patients.

Because, to our present knowledge, improved metabolic control1-4 and vigorous antihypertensive therapy 5.6 only postpone but do not prevent end-stage renal failure (ESRF) in diabetic patients and because diabetic patients in many parts of the world are no longer excluded from ESRF programs, it is not surprising that a substantial and ever increasing number of candidates for dialysis therapy and kidney transplantation have diabetes mellitus. In the United States and Western Europe approximately 20% of the population admitted to ESRF programs are diagnosed as diabetic. Perfect glycemic control is still the goal of therapy in this group to reduce further morbidity in patients already heavily burdened by severe complications. However, optimization of glycemic control in uremic diabetic patients is even more difficult than in diabetic patients with normal kidney function because of uremic insulin resistance, altered insulin metabolism, and modalities of therapy (hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), kidney transplantation) often interfering with glucose metabolism. Consequently, profound insight into the pathophysiology of glucose homeostasis and insulin kinetics in this complicated clinical condition is necessary to ensure optimal therapy in nondialyzed, dialyzed and recently kidney transplanted insulin-dependent diabetic patients.