DECREASED URINARY DOPAMINE EXCRETION AND DISTURBED DOPAMINE SODIUM RELATIONSHIP IN TYPE-1 DIABETES-MELLITUS

In Type 1 diabetes an increased total body sodium and an impaired abil ity to excrete a sodium load have been described. A possible involveme nt of the renal dopaminergic system in this abnormal sodium handling w as evaluated through measurements of the urinary output of dopamine, s odium, the dopamine/sodium correlation, and through examining the effe ct of a dopamine infusion on urinary sodium excretion. Twenty-four hou r urinary dopamine excretion was significantly lower in Type 1 diabeti c patients as compared to normal controls. A significant correlation b etween urinary dopamine and sodium excretion was present in normoalbum inuric Type 1 diabetic patients and in normal controls. However, no su ch correlation could be found in microalbuminuric patients. The increa se in fractional excretion of sodium during a 1 h low-dose dopamine (3 mu g kg(-1)min(-1)) infusion in Type 1 diabetic patients was negative ly correlated with diabetes duration. Patients with short duration of diabetes (less than 15 years) had a comparable dopamine-induced increa se in fractional excretion of sodium as normal controls. However, pati ents with longer duration of diabetes (more than 15 years) and microal buminuric patients displayed no significant changes in sodium output d uring dopamine infusion. These findings suggest that in Type 1 diabete s mellitus a deficiency of renal dopamine production could be responsi ble for the impaired sodium handling. Longer duration of the disease a nd microalbuminuria seem to be associated with an uncoupling of the ur inary dopamine/sodium relationship.