Co-administration of diltiazem and cyclosporine for kidney transplant recipients: a four year follow-up study.

BACKGROUND: Diltiazem and cyclosporin A (CsA) share a similar metabolism and degradation via the hepatic cytochrome p 450 subfamily 3A4. Co-administration of diltiazem with CsA may lead to CsA dosage reduction, blood pressure control and renal protection. OBJECTIVES: To study the four year outcome of kidney transplant recipients who received diltiazem administration with CsA. This was compared to the outcomes of patients who received CsA without diltiazem and were matched for blood pressure control and other baseline characteristics. MATERIAL AND METHOD: Forty eight patients were included in the diltiazem group and seventy patients in the non-diltiazem group. CsA monitoring was done by using trough level (monoclonal fluorescent polarization immunoassay). RESULTS: The results showed that both groups has similar 4-year graft survival (92 and 95 %) with a similar mean final serum creatinine (1.3 mg/dl). Mean dose of CsA during the first month was 30 % lower in the diltiazem than non-diltiazem group. At one year CsA dose was 11% lower in the diltiazem than non-diltiazem group. However the diltiazem group was associated with significantly higher probability to have chronic allograft nephropathy than the non-diltiazem group (31% VS 19%) (RR 2.93; p = 0.03; Multivariate Cox regression). CONCLUSION: Co administration of diltiazem with trough level adjusted CsA is associated with benefits in terms of CsA dose reduction and good graft survival and function. However there appeared to be no protective effect of diltiazem on the progression to chronic allograft nephropathy.

Failure of hepatitis B surface antibody to protect acute fulminating hepatitis in a renal transplant recipient.

A 58-year-old man who had a living-related kidney transplantation (KT) 13 years ago and had received a double-dosage course of hepatitis B virus (HBV) vaccination prior to KT developed acute liver failure. An exhaustive work-up for the cause of acute liver failure revealed that HBsAg was negative but anti-HBs and anti-HBcAbs were positive. HBV DNA was 535,000 copies/ml. The strongly positive staining of HBsAg and HBcAg of liver biopsy was shown by immunohistochemistry examination. HBV harboring surface mutant of hepatitis B surface gene was thought to be the cause of acute fulminant hepatitis despite the presence of protective immunity to wild-type HBV. The patient expired from acute liver failure even though an antiviral drug was started promptly. This is the first case report of liver biopsy suggestive of acute fulminating HBV that developed in a long-term kidney recipient despite the presence of high anti-HBsAb titer.