Ziegler T W
Med Hypotheses. 1976 Jan-Feb;2(1):15-21. doi: 10.1016/s0306-9877(76)80017-5.
The functional renal failure accompanying advanced liver disease is characterized by azotemia, a urine of very low sodium concentration and systemic hypotension with decreased renal perfusion and high renal vascular resistance. Patients with this disorder have a markedly reduced ability to excrete free water and develop hyponatremia, ascites and edema. It is postulated that this renal dysfunction is due to hepatic failure to make renin substrate. Renin released from the kidney is thus unable to exert its pressor effect. The resultant hypotension and renal hypoperfusion continue to stimulate excessive synthesis and release of renin. It is postulated that the overdriven renal renin system increases renovascular resistance at the level of the glomerular arterioles. This causes decreased renal blood flow and decreased glomerular filtration rate leading to salt and water retention and azotemia. Since no renin substrate is available for human infusion, this hypothesis could be tested either by infusion of angiotensin II to restore systemic blood pressure and renal perfusion or by beta adrenergic blockade with propranolol to attempt to decrease the intrarenal effects of renin, restore glomerular blood flow and filtration and thus return of renal function.
晚期肝病伴发的功能性肾衰竭的特征为氮质血症、尿钠浓度极低、全身低血压伴肾灌注减少及肾血管阻力增高。患有这种病症的患者排泄自由水的能力显著降低，并会出现低钠血症、腹水和水肿。据推测，这种肾功能障碍是由于肝脏无法产生肾素底物所致。因此，从肾脏释放的肾素无法发挥其升压作用。由此产生的低血压和肾灌注不足持续刺激肾素的过度合成和释放。据推测，过度驱动的肾素系统会增加肾小球小动脉水平的肾血管阻力。这会导致肾血流量减少和肾小球滤过率降低，进而导致盐和水潴留以及氮质血症。由于没有可用于人体输注的肾素底物，这一假说可以通过输注血管紧张素II以恢复全身血压和肾灌注，或者通过使用普萘洛尔进行β肾上腺素能阻滞来尝试降低肾素的肾内效应、恢复肾小球血流和滤过，从而使肾功能恢复来进行验证。
