Renal function and structure in subacute hepatic failure

Background and Aims: Subacute hepatic failure (SHF) is a fatal complicaton of acute viral. hepatitis. Renal failure has been implicated as the main ca use of death in this disease. However, renal functional and structural eval uation in such patients have not been performed. The present prospective st udy evaluated the renal functional and structural abnormalities in patients with subacute hepatic failure. Methods: Fourteen consecutive patients with SHF, 11 with acute liver failur e (ALF) and 15 with cirrhosis of the liver (Child's B or C) were included i n the present study. All 40 patients had liver disease caused by hepatitis viruses. The glomerular filtration rate (GFR) and effective renal plasma fl ow (ERPF) estimations were measured in all patients by the use of technetiu m-99m diethylenetriaminepentaacetic acid and [I-131] labeled ortho-iodohipp uric acid, respectively. Ante-mortem or post-mortem liver biopsies were per formed in all patients. In three patients with SHF, post-mortem kidney biop sies were also performed. Results: Thirty six percent (5/14) of patients with SHF, 18% (2/11) of pati ents with ALF and 20% (3/15) of patients with cirrhosis had renal failure. Seven patients with SHF, seven with ALF and nine with cirrhosis died. All t he, patients with renal failure in each of the three groups were among the deceased patients. Glomerular function was markedly affected among patients with SHF,,which was shown by significantly higher (P < 0.05) proteinuria l evels (0.367 +/- 0.38 g/24 h) compared to levels in patients with ALF (0.17 8 +/- 0.11 g/24 h) and cirrhosis (0.212 +/- 0.133 g/24 h). The GFR in SHF ( 56 +/- 27 mL/min per 1.73 m(2)) and cirrhotic patients (58 +/- 36 mL/min pe r 1.73 m(2)) was significantly lower compared to those in ALF patients (102 +/- 51 mL/min per 1.73 m(2); P < 0.05). A significantly higher proportion (P < 0.05) of patients with SHF and cirrhosis (64 and 73%, respectively) ha d a GFR below 80 mL/min per 1.73 m(2) compared to patients with ALF (18%). The GFR Value among the deceased SHF patients (46 +/- 26 mL/min per 1.73 m( 2)) was significantly lower (P < 0.05) than those SHF patients who survived (65 +/- 25 mL/min per 1.73 m(2)). However, similar features could not be d ocumented among patients with ALF or cirrhosis. Subtle structural changes i n the glomerulus were also noted in patients with SHF. These included mesan gial. proliferation and thickening, basal membrane thickening and increased cellularity with interstitial edema. The ERPF was markedly reduced (P = 0. 058) among patients:with SKF (347 +/- 131 mL/min per 1.73 m(2)) and cirrhos is (395 +/- 137 mL/min per 1.73 m(2)) in comparison to ERPF documented amon g patients with ALF (436 +/- 217 mL/min per 1.73 m(2)). Such a reduction in renal tubular blood flow, along with histologic documentation of hyaline p resence, bile and grannular cast in the tubule, indicated a possible tubula r dysfunction in patients with SHF. Conclusion: It is concluded that glomerular and tubular dysfunction with su btle structural abnormalities does occur in patients with SHF. These are si milar to renal changes in cirrhosis and may have similar pathogenetic mecha nisms that require further evaluation. (C) 2000 Blackwell Science Asia Pty Ltd.