JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Risk factors for consequent kidney impairment and differential impact of liver transplantation on renal function.
Nephrology, Dialysis, Transplantation 2010 August
BACKGROUND: Chronic kidney disease (CKD) develops frequently after liver transplantation (LTx), and it is important to identify and correct risk factors that negatively affect kidney function. Risk factors have not been well evaluated in Asian countries where hepatitis B virus (HBV) infection is a dominant cause.
METHODS: Four hundred thirty-one Korean recipients who underwent LTx between 1997 and 2008 were analysed. CKD was defined as a sustained decrease in estimated glomerular filtration rate (eGFR) of <60 (mL/min/1.73 m(2)) for at least three consecutive months using an abbreviated Modification in Renal Disease (MDRD) formula.
RESULTS: Eighty percent of the patients had HBV-related underlying diseases. The recipients whose pretransplant eGFR had been low (<30 mL/min/1.73 m(2)) improved their renal function after LTx, but significant functional decline occurred in recipients whose pretransplant eGFR was high (>or=60 mL/min/1.73 m(2)). A multivariate Cox regression analysis revealed that the overall risk of CKD development (eGFR < 60 mL/min/1.73 m(2)) was associated with old age of recipients, cyclosporine, posttransplant acute renal failure (ARF), cause [calcineurin inhibitor (CNI) nephrotoxicity] and severity of posttransplant ARF, low pretransplant eGFR, pretransplant hepatorenal syndrome, pretransplant proteinuria, high Child-Pugh score and high Model for End-Stage Renal Disease (MELD) score. Especially in recipients whose pre-operative eGFR was high (>or=60 mL/min/1.73 m(2)), rapid progression of kidney disease was associated with high tacrolimus level, non-HBV disease, posttransplant ARF, cause (CNI nephrotoxicity) and severity of posttransplant ARF and Child-Pugh score. CNI toxicity and focal segmental sclerosis, but not immune-complex disease, were revealed as significant contributors to CKD after LTx in HBV recipients.
CONCLUSION: Judicious use of CNIs should be applied to liver recipients to prevent kidney dysfunction.
METHODS: Four hundred thirty-one Korean recipients who underwent LTx between 1997 and 2008 were analysed. CKD was defined as a sustained decrease in estimated glomerular filtration rate (eGFR) of <60 (mL/min/1.73 m(2)) for at least three consecutive months using an abbreviated Modification in Renal Disease (MDRD) formula.
RESULTS: Eighty percent of the patients had HBV-related underlying diseases. The recipients whose pretransplant eGFR had been low (<30 mL/min/1.73 m(2)) improved their renal function after LTx, but significant functional decline occurred in recipients whose pretransplant eGFR was high (>or=60 mL/min/1.73 m(2)). A multivariate Cox regression analysis revealed that the overall risk of CKD development (eGFR < 60 mL/min/1.73 m(2)) was associated with old age of recipients, cyclosporine, posttransplant acute renal failure (ARF), cause [calcineurin inhibitor (CNI) nephrotoxicity] and severity of posttransplant ARF, low pretransplant eGFR, pretransplant hepatorenal syndrome, pretransplant proteinuria, high Child-Pugh score and high Model for End-Stage Renal Disease (MELD) score. Especially in recipients whose pre-operative eGFR was high (>or=60 mL/min/1.73 m(2)), rapid progression of kidney disease was associated with high tacrolimus level, non-HBV disease, posttransplant ARF, cause (CNI nephrotoxicity) and severity of posttransplant ARF and Child-Pugh score. CNI toxicity and focal segmental sclerosis, but not immune-complex disease, were revealed as significant contributors to CKD after LTx in HBV recipients.
CONCLUSION: Judicious use of CNIs should be applied to liver recipients to prevent kidney dysfunction.
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