Sellars L, Shore A C, Mott V, Wilkinson R
Q J Med. 1985 Aug;56(220):485-96.
Plasma renin activity (PRA), plasma renin concentration (PRC), plasma angiotensin II concentration (AII), plasma and urinary aldosterone (PA, UA) and urinary sodium excretion (UNaV) were measured in 51 normal controls, 16 patients with decompensated cirrhosis (i.e. ascites and/or oedema present) in sodium equilibrium (Group 1) and 13 patients with decompensated cirrhosis in a phase of active sodium retention (Group 2). In Group 1 the mean supine and erect values, although lower, were not significantly different from controls. In Group 2 the mean values were significantly elevated, but several individual values were within the normal range; there were significant direct relationships between plasma renin activity and plasma renin concentration (r = 0.85, p less than 0.001 erect), plasma renin concentration and plasma angiotensin II concentration (r = 0.86, p less than 0.001 erect), and plasma angiotensin II concentration and plasma aldosterone (r = 0.70, p less than 0.01 erect). In Group 2 there was an inverse correlation between urinary sodium excretion and both urinary aldosterone (r = -0.50) and erect plasma aldosterone (r = -0.36) but, perhaps because of the narrow range of sodium excretion rates, significance was not reached. The normal values in Group 1 indicate that hyperaldosteronism is not essential for the maintenance of established ascites, but do not exclude a role for aldosterone in the control of sodium excretion if it is accepted that renal tubular sensitivity to aldosterone is increased in these patients. In Group 2, the raised mean plasma and urinary aldosterone levels and the trend towards an inverse relationship with urinary sodium excretion suggests a role for aldosterone in the active retention of sodium. It appears that stimulation of the renin-angiotensin system is the major factor in the elevation of plasma aldosterone; there was no relationship between plasma aldosterone and either plasma sodium or potassium levels. The mechanism of renin hypersecretion is unclear but this may represent part of a sympathetically mediated response in order to maintain blood pressure. The close relationship between plasma renin activity and plasma renin concentration indicates that the former is a valid measure of circulating renin levels in cirrhosis, despite low renin-substrate levels.
对51名正常对照者、16名处于钠平衡状态的失代偿期肝硬化患者（即有腹水和/或水肿，第1组）以及13名处于钠潴留活跃期的失代偿期肝硬化患者（第2组），测定了血浆肾素活性（PRA）、血浆肾素浓度（PRC）、血浆血管紧张素II浓度（AII）、血浆和尿醛固酮（PA、UA）以及尿钠排泄量（UNaV）。在第1组中，仰卧位和直立位的平均值虽较低，但与对照组相比无显著差异。在第2组中，平均值显著升高，但有几个个体值在正常范围内；血浆肾素活性与血浆肾素浓度之间存在显著的直接关系（直立位时r = 0.85，p < 0.001），血浆肾素浓度与血浆血管紧张素II浓度之间存在显著的直接关系（直立位时r = 0.86，p < 0.001），血浆血管紧张素II浓度与血浆醛固酮之间存在显著的直接关系（直立位时r = 0.70，p < 0.01）。在第2组中，尿钠排泄量与尿醛固酮（r = -0.50）和直立位血浆醛固酮（r = -0.36）均呈负相关，但可能由于钠排泄率范围较窄，未达到显著水平。第1组的正常数值表明，高醛固酮血症并非维持已形成腹水所必需，但如果认为这些患者肾小管对醛固酮的敏感性增加，并不排除醛固酮在控制钠排泄方面的作用。在第2组中，血浆和尿醛固酮水平升高以及与尿钠排泄呈负相关的趋势表明醛固酮在钠的主动潴留中起作用。似乎肾素-血管紧张素系统的刺激是血浆醛固酮升高的主要因素；血浆醛固酮与血浆钠或钾水平之间均无关联。肾素分泌过多的机制尚不清楚，但这可能是交感神经介导的维持血压反应的一部分。血浆肾素活性与血浆肾素浓度之间的密切关系表明，尽管肾素底物水平较低，但前者仍是肝硬化患者循环肾素水平的有效指标。
