Abstracts of the 18th Annual Meeting of the American Society of Transplantation (AST), May 15-19, 1999, Chicago, Illinois
THE DEVELOPMENT OF POST TRANSPLANT ERYTHROCYTOSIS IN HYPERCALCEMIC RENAL TRANSPLANT PATIENTS
Kurella, M; Smith, S R; Butterly, D W
Duke University Medical Center, Durham NC 27710.
Abstract 650
Post transplant erythrocytosis (PTE) is a common complication following renal transplantation, estimated to occur in 10-20% of patients receiving transplants. The pathogenesis of this common complication remains unclear. Previous studies have produced conflicting data regarding the role of erythropoietin in PTE, leading to suggestions that factors other than erythropoietin may be involved in the pathogenesis of PTE. We studied 299 consecutive patients who underwent renal transplantation from August 1994 to January 1998 at Duke University Medical Center. All patients were treated with standard triple immunossuppresion therapy of cyclosporine, prednisone and azathioprine or mycophenylate mofetil. Of the 299 patients studied, 74 patients (25%) developed PTE, defined as a HCT ≥ 50%. Of these 74 patients, 46 patients (62%) also had hypercalcemia post transplant, defined as Ca++ ≥ 10.2 mg/dl. Hypercalcemia occurred in 91/225 patients (40%) without PTE. (Table)
The association was highly significant (p = 0.001) by the chi square test. Linear regression analysis confirmed that the maximum calcium post transplant was a univariate predictor of the maximum Hct (p = 0.015). In the 46 patients who had both hypercalcemia and PTE, 40 patients developed hypercalcemia prior to or concurrent with the development of PTE. The mean time from transplant to the development of hypercalcemia was 4.7 months, and from transplant to the development of PTE was 8.9 months. Our results suggest that hypercalcemia, or factors leading to the development of hypercalcemia, may be involved in the pathogenesis of PTE in a subgroup of renal transplant recipients who develop erythrocytosis.
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