Venkat Raman G, Albano J D, Millar J G, Lee H A
Department of Renal Medicine, University of Southhampton, UK.
J Intern Med. 1990 Nov;228(5):525-31. doi: 10.1111/j.1365-2796.1990.tb00273.x.
We here report a case of Bartter's syndrome occurring in association with diabetes mellitus. The patient, an insulin-dependent diabetic, presented with hypokalaemia, inappropriate kaliuresis and metabolic alkalosis. He had high plasma renin activity, relatively low plasma aldosterone, and resistance to infused angiotensin II. A high potassium diet raised total body potassium and serum potassium, did not affect plasma renin activity, but raised plasma aldosterone significantly and did not alter the resistance to angiotensin II. Indomethacin administered acutely reduced urinary potassium and kallikrein excretion and, on chronic administration, lowered plasma renin activity, urinary chloride excretion, and raised serum potassium. Salt restriction resulted in a prompt and significant reduction in urinary sodium and chloride excretion. Urinary kallikrein excretion was very high throughout, increased with sodium restriction, and decreased with sodium loading. Oral potassium supplementation partially corrected the hypokalaemia, but did not affect blood sugar control. In this patient the primary defect appears to have been primary urinary potassium wasting, rather than sodium or chloride wasting. The striking effects of indomethacin suggest that prostaglandins may play a fundamental role in the genesis of the syndrome.
我们在此报告一例与糖尿病相关的巴特综合征病例。该患者为胰岛素依赖型糖尿病患者，表现为低钾血症、不适当的尿钾排泄增多和代谢性碱中毒。他的血浆肾素活性高，血浆醛固酮相对较低，对输注的血管紧张素II有抵抗。高钾饮食使全身钾和血清钾升高，不影响血浆肾素活性，但显著升高血浆醛固酮，且不改变对血管紧张素II的抵抗。急性给予吲哚美辛可减少尿钾和激肽释放酶排泄，长期给药可降低血浆肾素活性、尿氯排泄，并升高血清钾。限制盐摄入导致尿钠和氯排泄迅速且显著减少。尿激肽释放酶排泄始终很高，随钠限制而增加，随钠负荷而减少。口服补钾部分纠正了低钾血症，但不影响血糖控制。在该患者中，主要缺陷似乎是原发性尿钾丢失，而非钠或氯丢失。吲哚美辛显著的作用表明前列腺素可能在该综合征的发生中起重要作用。
