Chan R, Sealey J E, Michelis M F, Swan A, Pfaffle A E, Devita M V, Zabetakis P M
Department of Medicine, Lenox Hill Hospital, and the Cardiovascular Center, Cornell University Medical College, New York, New York, USA.
J Lab Clin Med. 1998 Sep;132(3):229-35. doi: 10.1016/s0022-2143(98)90172-x.
Thirty-four patients (65.3+/-3.3 years of age, mean+/-SEM) with hyperkalemia (serum potassium >5.0 mEq/L) had measurement of their renin-aldosterone system. Nineteen patients (56%) had plasma renin activity (PRA) >1.5 ng/mL/h, which was not low, while 15 (44%) had PRA <1.5. Twelve of the 15 hyporeninemic hyperkalemic patients were studied to determine whether their renin-aldosterone system responded to 2 weeks of furosemide, 20 mg daily. Four were nonresponders: PRA averaged 0.3+/-0.1 ng/mL/h, and it did not increase with furosemide or respond to captopril before or after furosemide. Eight patients were responders: PRA averaged 0.6+/-0.2 ng/mL/h and increased with furosemide to 5.5+/-3.4 ng/mL/h. Captopril failed to increase PRA before furosemide, but PRA increased to 15.3+/-8.4 ng/mL/h after furosemide. Plasma aldosterone was low in both nonresponders and responders (3.5+/-1.2 ng/dL vs 5.8+/-2.5 ng/dL) and did not increase significantly with furosemide (4.3+/-1.7 ng/dL vs 8.7+/-2.5 ng/dL). Serum potassium did not fall and therefore did not limit the rise in aldosterone. Renin responders had greater body weight, were predominantly female (6/8 vs 2/4) and were more likely to have diabetes mellitus (7/8 vs 0/4). Plasma atrial natriuretic peptide (ANP) fell with furosemide in 8 of 8 responders and in 1 of the 2 nonresponders in whom it was measured. Neither group had suppressed plasma prorenin levels, indicating no suppression of renin gene expression. These results indicate that many hyperkalemic patients do not have suppressed PRA. Further, a majority of patients with suppressed PRA have high levels of ANP and can respond to diuretic therapy with a rise in PRA and a fall in ANP, suggesting physiologic suppression of the renin system by volume expansion. A minority of hyperkalemic patients with suppressed PRA had PRA that did not increase under these study conditions.
34例高钾血症患者（年龄65.3±3.3岁，均值±标准误）检测了其肾素 - 醛固酮系统。19例患者（56%）血浆肾素活性（PRA）>1.5 ng/mL/h，并非降低，而15例（44%）PRA<1.5。对15例低肾素性高钾血症患者中的12例进行研究，以确定其肾素 - 醛固酮系统对每日20 mg速尿治疗2周是否有反应。4例无反应者：PRA平均为0.3±0.1 ng/mL/h，速尿治疗后未升高，且在速尿治疗前后对卡托普利均无反应。8例有反应者：PRA平均为0.6±0.2 ng/mL/h，速尿治疗后升高至5.5±3.4 ng/mL/h。卡托普利在速尿治疗前未能升高PRA，但速尿治疗后PRA升高至15.3±8.4 ng/mL/h。无反应者和有反应者的血浆醛固酮均较低（分别为3.5±1.2 ng/dL和5.8±2.5 ng/dL），速尿治疗后无显著升高（分别为4.3±1.7 ng/dL和8.7±2.5 ng/dL）。血清钾未下降，因此未限制醛固酮的升高。肾素反应者体重更大，女性居多（6/8 vs 2/4），且更易患糖尿病（7/8 vs 0/4）。8例有反应者中的8例以及2例检测了血浆心钠素（ANP）的无反应者中的1例，ANP随速尿下降。两组患者的血浆前肾素水平均未受抑制，表明肾素基因表达未受抑制。这些结果表明，许多高钾血症患者的PRA未受抑制。此外，大多数PRA受抑制的患者ANP水平较高，并可通过速尿治疗使PRA升高、ANP下降，提示容量扩张对肾素系统有生理性抑制作用。少数PRA受抑制的高钾血症患者在这些研究条件下PRA未升高。
