Effect of supportive extracorporeal treatment in liver transplantation recipients and advanced liver failure patients.

Recently, continuous venovenous hemodiafiltration (CVVHDF) and plasmapheresis (PF) were suggested as supportive therapy options in combination with standard treatment in advanced liver failure. The aim of this study was to analyze the effects of supportive extracorporeal treatment (SET) in a group of patients with advanced hepatic failure. A total of 25 patients (7 women, 18 men; mean age, 39.3+/-15.4 years; 13 were transplant recipients [6 women, 7 men; mean age, 37.7+/-16.9 years]) were included. All patients were in hepatic coma and receiving standard coma and liver failure management when they received SET. Number of SET sessions; levels of serum blood urea nitrogen, creatinine, albumin, calcium, phosphorus, ammonia, alanine and aspartate aminotransferase, and total/conjugated bilirubin; and prothrombin times (PTT) before and after SET were recorded retrospectively. 7.7+/-7.9 SET sessions were performed. Thirteen liver transplant recipients required SET for an average of 9.7+/-8.3 days after transplantation. Serum ammonia and bilirubin levels were lower after termination of supportive therapy when compared with initial levels (p<0.0001 and p<0.005 respectively). During follow-up, hepatic encephalopathy and liver failure resolved in 11 patients, while 14 patients (7 transplant recipients) died. There was no significant difference between patients in either group except that PTT was shorter in patients who survived (p<0.01). Further analyses revealed that in surviving patients, ammonia clearance was higher (p<0.01). In patients with advanced liver failure, or liver transplants, CVVHDF and/or PF could be supportive options combined with standard treatment.

Acute interstitial nephritis due to cefoperazone.

OBJECTIVE: To describe a case of cefoperazone-induced acute interstitial nephritis (AIN) in which the diagnosis was supported by renal biopsy. CASE SUMMARY: A 35-year-old woman presented to our hospital with decreased urine output and no past history of renal problems. Fifteen days prior to presentation, she had started treatment with intramuscular cefoperazone 1 g/day for a scalp infection. On day 12 of therapy, the patient noted decreased urine output, anorexia, and weakness, but she continued taking cefoperazone for 3 more days. Hemodialysis and oral prednisolone 1 mg/kg (30 mg twice daily) were started. Renal function returned to normal after 2 months of prednisolone treatment. DISCUSSION: Although AIN has been linked with other cephalosporins, as of June 18, 2004, to our knowledge, this is the first report of a cefoperazone-induced case. We based our diagnosis on the features of acute-onset renal failure, abnormal urinalysis findings, eosinophilia, inflammatory infiltrate in the interstitium, and recovery from renal failure after initiation of corticosteroid treatment. Application of the Naranjo probability scale indicated a probable relationship between the acute renal failure secondary to the possible AIN and cefoperazone therapy in this patient. CONCLUSIONS: This case indicates that cefoperazone, like other cephalosporins, can cause AIN. We recommend close monitoring of renal function in patients who are prescribed this drug.