[Renal hemodynamics and its regulation in recently diagnosed type 1 diabetes mellitus (insulin-dependent diabetes mellitus). The effect of hyperglycemia]

Abstract

Background: The changes in renal haemodynamics are considered to be one of the pathophysiological mechanisms of the development of diabetic nephropathy. The aim of the study was to evaluate the renal haemodynamics and its regulation in insulin-dependent diabetes mellitus (IDDM) during glycemic clamp-induced eu- and hyperglycaemia (5 and 12 mmol/l), and to test the hormonal vasoactive systems after stimulation with furosemide.

Methods and results: Renal haemodynamics using the clearances of inulin and paraaminophippuric acid during eu-hyperglycaemic clamp and furosemide test were performed in 21 short-term IDDM patients without microalbuminuria (DM) and in 18 weight-, age- and sex-matched healthy controls (K). The glomerular filtration rate and effective renal plasma flow were comparable in IDDM and C and were not affected by hyperglycaemia. Compared to C diabetics had lowered fractional excretion of sodium (1.41 +/- 0.68 vs 2.23 +/- 0.67%; p < 0.01), which did not change during hyperglycaemia, and lowered furosemide stimulated natriuresis (1242 +/- 339 vs 1606 +/- 340 mumol/min; p < 0.01). Hyperglycaemia resulted in comparable fall in fractional excretion of potassium in both groups (p < 0.001). Decreased basal (5.77 +/- 3.22 vs 10.9 +/- 3.7 mEU/min; p < 0.05) and furosemide-stimulated (12.0 +/- 1.6 vs 21.3 +/- 2.0 mEU/min; p < 0.01) urinary kallikrein has been found in diabetic compared to control subjects. During clamp-induced euglycaemia, kallikrein excretion was comparable in diabetic and control subjects (10.89 +/- 5.98 vs 10.38 +/- 3.73 mEU/min) and significantly declined during intravenous dextrose-induced hyperglycaemia in diabetics (p < 0.01), while it did not change in controls. There were no differences and no changes in plasma renin activity, plasma and urine aldosterone and cortisol in IDDM and C.

Conclusions: The short-term IDDM without renal haemodynamic alterations is associated with the tendency to sodium retention and decreased basal and furosemide-stimulated kallikrein excretion, which is directly related to the blood glucose level. Acutely-induced hyperglycaemia decreases fractional excretion of potassium, which cannot be explained by the changes of evaluated hormonal systems.