Renal failure in patients with cirrhosis of the liver: III. Evaluation of intrarenal blood flow by para-aminohippurate extraction and response to angiotensin

Abstract

Renal functional abnormalities associated with advanced liver disease were evaluated in twenty-two patients by determining the effects of angiotensin infusions and of increasing tubular loads of para-aminohippurate (PAH) upon the extraction of PAH. Angiotensin infused intravenously produced variable changes in renal blood flow, glomerular filtration rate and urinary excretion of sodium and water, but did not alter extraction of PAH. This agent did not change the distribution of blood flow within the kidney as estimated from PAH extraction. To the extent that in some patients renal ischemia and hypoxia may have been induced, these changes also had no effect upon the extraction ratio of PAH (E PAH). The E PAH was below normal during control periods in eight of the twenty-two patients. Reduced E PAH was associated with, but was not a consequence of, decreased renal plasma flow and glomerular filtration rate and a poor urine flow response to water administration. Chronic renal disease, tubular necrosis, renal hypoxia, excessive tubular load of PAH or low urine flow rate could not be incriminated as causes of the decreased E PAH. The decreased E PAH and associated renal functional changes noted in some patients with cirrhosis are explained best by a hemodynamic alteration involving renal cortical vasoconstriction with relative increase in medullary blood flow. Ten patients were given a PAH load. Five responded normally. In the other five changes in E PAH were consistent with the presence of a defect in ability to transport PAH.