Failure of Cirrhotic Sera to Inhibit Renal Tubule Hippurate Transport in Vitro

Abstract

Late in the course of cirrhosis, renal failure is often a complication (1, 2). In many cases, histologic examination of the kidneys fails to reveal specific lesions to explain progressive azotemia and oliguria ( 2 , 3). While renal tubule function seems well preserved, reductions of glomerular filtration rate (GFR) and renal plasma flow (RPF) have been observed (4, 5). Baldus et al. (1) and Shear et d. ( 5 ) noted reduced paraaminohippurate (PAH) extraction ratios (EPAH) in patients with cirrhosis. The latter authors attributed this decreased ( EPAEI) to possible intrarenal shunting of blood as seen in other circulations (5). Recently Schroeder et d.(6) evaluated 22 cirrhotic patients and suggested that decreased EpaH was not a consequence of decreased GFR or RPF and suggested renal cortical vasoconstriction with relative increase in medullary flow as a possible explanation of changes in renal function in cirrhotic patients. An alternative explanation for the reduced EpaH suggested by Schroeder et al. was the possible impairment of renal tubule transport of PAH either by an altered transport mechanism or a circulating substance that inhibited transport. Preuss et al. ( 7 ) have shown recently that a substance or substances present in azotemic sera inhibits PAH transport in an in vitro preparation of renal tubules. Whether such substances, which could alter hippurate transport, were also present in the sera of cirrhotics has not been reported. The purpose of this study was to determine if a substance or substances exist in cirrhotic sera that alter renal hippurate transport and thus could