Studies of the renal vasoactive systems in hyporeninemic hypoaldosteronism

J.A. Hahn, R.D. Zipser, A. Barg, R.A. Stone, P.K. Zia, W.A. Hsueh, R. Horton
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引用次数: 5

Abstract

Plasma renin activity, total renin, active renin, and aldosterone were measured as well as urinary prostaglandin E2 and kallikrein in a group of patients with hyperkalemia (6.1–7.7 mEq per liter) and hypo reninemic hypoaldosteronism. Plasma renin activity and aldosterone were low and the response was markedly blunted to upright posture, and furosemide. The rise in cortisol but not aldosterone was normal following ACTH stimulation. Active renin was depressed; however, total renin was normal. Urine PGE was variable including some low values, but the mean of the group was normal (p >0.1). Urine kallikrein excretion was markedly diminished and undetectable in most cases. Fludrocortisone normalized potassium but minimally increased kallikrein in the patients. The possibility exists that kallikrein deficiency in these patients may underlie the inability to generate active renin.

低肾素血症性低醛固酮增多症肾血管活性系统的研究
在一组高钾血症(6.1-7.7 mEq / l)和低肾素性低醛固酮血症患者中,测定血浆肾素活性、总肾素、活性肾素和醛固酮,以及尿前列腺素E2和钾化因子。血浆肾素活性和醛固酮较低,对直立姿势和速尿的反应明显减弱。促肾上腺皮质激素刺激后皮质醇升高而醛固酮未升高是正常的。活性肾素降低;然而,总肾素正常。尿PGE有变化,包括一些低值,但组的平均值是正常的(p >0.1)。尿钾激肽排泄明显减少,在大多数病例中检测不到。氟化可的松使患者的钾正常化,但最小限度地增加了钾激肽。可能存在的是,这些患者的钾激肽缺乏症可能是无法产生活性肾素的基础。
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