Brown E A, Markandu N D, Sagnella G A, Squires M, Jones B E, MacGregor G A
Lancet. 1982 Dec 4;2(8310):1237-40. doi: 10.1016/s0140-6736(82)90102-7.
8 of 16 patients with nephrotic syndrome had normal or low plasma renin activity while spontaneously retaining sodium. The other 8 patients had a high plasma renin activity which may have caused the sodium retention. Oral captopril and albumin infusion given separately both suppressed the renin system in these patients. Despite this, urinary sodium excretion remained less than sodium intake and patients continued to retain sodium and gain weight. These results suggest that, even in patients with nephrotic syndrome who do have stimulation of the renin angiotensin system, some other overriding mechanism is responsible for sodium retention. Therefore it seems unlikely that angiotensin-converting enzyme inhibitors will be useful in the treatment of sodium retention in nephrotic syndrome.
16例肾病综合征患者中有8例在自发性潴钠时血浆肾素活性正常或降低。另外8例患者血浆肾素活性较高，这可能导致了钠潴留。分别给予口服卡托普利和输注白蛋白均抑制了这些患者的肾素系统。尽管如此，尿钠排泄仍低于钠摄入，患者继续潴钠并体重增加。这些结果表明，即使在确实有肾素-血管紧张素系统激活的肾病综合征患者中，一些其他主导机制也导致了钠潴留。因此，血管紧张素转换酶抑制剂似乎不太可能用于治疗肾病综合征中的钠潴留。
