Kaufman J S, Peck M, Hamburger R J, Flamenbaum W
Nephron. 1986;43(3):203-10. doi: 10.1159/000183830.
To further define the pathophysiology of the syndrome of acquired isolated hypoaldosteronism, we determined plasma concentrations of active and inactive renin and urinary kallikrein and prostaglandin E2 excretion rates in 11 patients with the syndrome, 12 patients with similar serum creatinine levels, but without hyperkalemia, and in 12 normotensive patients with normal renal function and low plasma renin activities (PRA). Ten of 11 patients with the syndrome had low baseline PRA, and, unlike the control groups, six of 11 failed to double their PRA after furosemide stimulation. There were also consistent abnormalities in the percentage of inactive renin, no patient having a value less than and no control subjects having a value greater than 65%. Seven of 11 patients had prostaglandin E2 excretion rates lower than either control groups. Urinary kallikrein excretion rates in the patients with isolated hypoaldosteronism were significantly lower than in the control groups, but increased in response to therapy with fludrocortisone.
为了进一步明确获得性孤立性醛固酮缺乏综合征的病理生理学机制，我们测定了11例该综合征患者、12例血清肌酐水平相似但无高钾血症的患者以及12例肾功能正常且血浆肾素活性（PRA）较低的血压正常患者的活性和非活性肾素的血浆浓度、尿激肽释放酶以及前列腺素E2排泄率。11例综合征患者中有10例基线PRA较低，与对照组不同的是，11例中有6例在速尿刺激后PRA未能翻倍。非活性肾素的百分比也存在一致的异常，没有患者的值低于65%，也没有对照组的值高于65%。11例患者中有7例前列腺素E2排泄率低于任何一个对照组。孤立性醛固酮缺乏症患者的尿激肽释放酶排泄率显著低于对照组，但在接受氟氢可的松治疗后升高。
