To study whether renal susceptibility to nephrotoxic stimuli is increased in obstructive jaundice, the effect of gentamicin on the renal function in bile duct-ligated rats was investigated. Gentamicin (50 mg/kg/day, subcutaneously) or saline was given to bile duct-ligated rats or sham-operated rats for six days. Mortality in the bile duct-ligated group that received gentamicin was 64% whereas that in the other groups was 0%. In the bile duct-ligated group, although serum creatinine and blood urea nitrogen were minimally affected, focal granulo-vacuolar degeneration in the proximal tubule was observed, which was accompanied by an increase in renal malondialdehyde. Gentamicin significantly increased serum creatinine and blood urea nitrogen levels and caused marked degeneration in the proximal tubule in the bile duct-ligated group, which was accompanied by a further increase in renal malondialdehyde, while these changes were not observed in the sham group. The kidney in obstructive jaundice appears to be susceptible to gentamicin. Enhanced production of oxygen radicals may be responsible for this effect.
Nonalcoholic steatohepatitis is an increasingly recognized clinicopathologic condition. We report two cases of nonalcoholic steatohepatitis in middle-aged Japanese women whose clinical and laboratory data mimicked autoimmune hepatitis. Histologic findings of both cases were definite steatohepatitis with portal and pericellular fibrosis. Both patients' HLA-DR haplotypes were DR4 and DR2, which are frequently observed in Japanese patients with autoimmune hepatitis. Our cases suggest a diversity in the pathogenesis of nonalcoholic steatohepatitis.
A rare case of choledochal cyst complicated by papillary adenocarcinoma in the cystically dilated intrahepatic bile duct is reported. The tumor was located in the neck of the cystic lesion, and imaging modalities failed to show communication between the cystic lesion and the bile ducts.
To investigate the role of nitric oxide in renal function and hemodynamics in cirrhotic patients with ascites, L-arginine (30 g in 300 mL of distilled water), a substrate for nitric oxide synthase, was infused into six cirrhotic patients with ascites, and the effects were compared with those of saline infusion. Healthy controls (n = 5) were also studied under the same conditions. In the patients, L-arginine infusion significantly decreased systolic and diastolic blood pressures while markedly increasing urinary flow and urinary sodium excretion; no significant changes were seen with saline infusion. In controls, only diastolic blood pressure was decreased by L-arginine infusion, whereas urinary flow and urinary sodium excretion were increased by both L-arginine and saline infusion. In both groups, a similar increase of plasma atrial natriuretic factor (ANF) was seen with L-arginine and saline infusions; endothelin and catecholamines were not affected by either infusion. In both groups, plasma levels of vasopressin were increased by L-arginine infusion. In the cirrhotic patients, urinary excretions of cyclic guanosine monophosphate (cGMP) and nitrates/nitrites (NOx) were significantly increased by L-arginine infusion, whereas no significant changes were seen with saline infusion. In controls, only the excretion of cGMP was increased by L-arginine infusion. In summary, L-arginine infusion induces diuresis and natriuresis accompanied by increased excretions of cGMP and NOx in cirrhotic patients with ascites. This differs from the response in controls, where the increase in urinary sodium excretion is not accompanied by an increase in markers of increased nitric oxide synthesis.
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