RENAL KALLIKREIN EXCRETION IN ALCOHOLIC CIRRHOSIS - RELATIONSHIP TO OTHER VASOACTIVE SYSTEMS

Abstract

Severe liver disease is often associated with renal hemodynamic changes and these changes may involve vasoactive hormones. The vasodilatory renal kallikrein-kinin system has received little previous study in these patients. Urinary kallikrein was measured in 9 patients with alcoholic cirrhosis under rigid metabolic conditions. Renin, aldosterone and urinary prostaglandins were simultaneously evaluated. Plasma renin and aldosterone were generally increased as expected, but urinary kallikrein was surprisingly diminished despite adequate creatinine clearance. Administration of prostaglandin inhibitors reduced urinary prostaglandin E by 72% and creatinine clearance by 56%, but did not alter urinary kallikrein. Mineralocorticoid inhibition by spironolactone induced a natriuresis in 4 patients with ascites, but also failed to alter kallikrein. Kallikrein excretion is paradoxically reduced and seemingly unresponsive to alterations in the prostaglandin and renin-aldosterone systems. If urinary kallikrein quantitatively reflects intrarenal kallikrein-kinin activity, the impairment in this vasodilatory system may mediate the altered renal hemodynamics of severe liver disease.