Pelikánová T, Pinsker P, Smrcková I, Stríbrná L, Dryáková M
Institut klinické a experimentální medicíny, Praha.
Cas Lek Cesk. 1997 Sep 10;136(17):533-8.
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.
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.
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.
肾血流动力学的改变被认为是糖尿病肾病发生发展的病理生理机制之一。本研究旨在评估胰岛素依赖型糖尿病（IDDM）患者在血糖钳夹诱导的正常血糖和高血糖状态（5和12 mmol/L）下的肾血流动力学及其调节，并在速尿刺激后检测激素血管活性系统。
对21例无微量白蛋白尿的短期IDDM患者（DM）和18例体重、年龄和性别匹配的健康对照者（K）进行了正常血糖-高血糖钳夹和速尿试验，期间使用菊粉和对氨基马尿酸清除率评估肾血流动力学。IDDM组和对照组的肾小球滤过率和有效肾血浆流量相当，且不受高血糖影响。与对照组相比，糖尿病患者的钠分数排泄降低（1.41±0.68 vs 2.23±0.67%；p<0.01），在高血糖期间无变化，速尿刺激后的利钠作用降低（1242±339 vs 1606±340 μmol/min；p<0.01）。高血糖导致两组钾分数排泄下降程度相当（p<0.001）。与对照组相比，糖尿病患者基础尿激肽释放酶（5.77±3.22 vs 10.9±3.7 mEU/min；p<0.05）和速尿刺激后的尿激肽释放酶（12.0±1.6 vs 21.3±2.0 mEU/min；p<0.01）均降低。在钳夹诱导的正常血糖期间，糖尿病患者和对照组的激肽释放酶排泄相当（10.89±5.98 vs 10.38±3.73 mEU/min），糖尿病患者在静脉输注葡萄糖诱导的高血糖期间激肽释放酶排泄显著下降（p<0.01），而对照组无变化。IDDM组和对照组的血浆肾素活性、血浆和尿醛固酮及皮质醇无差异且无变化。
无肾血流动力学改变的短期IDDM患者存在钠潴留倾向，基础和速尿刺激后的激肽释放酶排泄减少，这与血糖水平直接相关。急性诱导的高血糖降低钾分数排泄，这无法用所评估的激素系统变化来解释。
