HYPERTENSION: THE PREDICTOR OF CHRONIC RENAL IMPAIRMENT POST CARDIAC TRANSPLANTATION?
J. Webb*, B. Levvey, G. Perry, P. Bergin, M. Rabinov, D. Esmore, N. Thomson.
Heart & Lung Transplant Service and Renal Unit, Alfred Hospital, Prahran, Victoria.
Background: Renal impairment following heart transplantation (Tx) is well described. This partially relates to cyclosporin nephrotoxicity. However, the contribution of hypertension (HT) to development of renal impairment has not been clearly defined.
Methods: retrospective review of up to five years was obtained for 84 consecutive recipients who had Tx between February 1989 and October 1991 and survived more than 6 months. Renal complications were recorded and serum creatinine, creatinine clearance and blood pressure were reviewed.
Results: Seven patients developed acute renal failure, requiring temporary renal replacement therapy at the time of Tx in the setting of multi-organ failure. Transient peri-operative renal impairment not requiring renal replacement therapy occurred in 26% of patients. Acute Cyclosporine toxicity was found in 24%. Chronic renal failure was present after 5 years in 38%. No patient progressed to end-stage renal failure. Mean serum creatinine increased over time from a pre-transplant value of 115±3 to 147±5mmd/1 at 5 years post-transplant (p<0.001). Creatinine clearance improved initially post-transplant then steadily declined. A history of HT pre-Tx was present in 14% whereas 93% had HT post-Tx with 59% of all patients refractory to treatment. By univariate analysis, significant predictors of chronic renal impairment at 5 years were: poor history of Ht (p=0.002), older age at time of Tx (p=0.003) and refractory HT post-Tx (p=0.01). By multivariate analysis, pre-Tx HT (p=0.03) and refractory HT between the end of the first and fifth year post-Tx (p=0.05) were the only significant predictors of renal dysfunction. Pre-operative renal impairment was not a significant factor. The relationship between renal impairment and cyclosporin levels was not possible to interpret due to alterations in dose in response to rises in serum creatinine.
Conclusion: HT is an important factor in the development of renal impairment following Tx. Tighter control of HT may delay or prevent progression of renal impairment.
