ROLE OF SECONDARY HYPERPARATHYROIDISM IN THE DEVELOPMENT OF POSTTRANSPLANT ACUTE TUBULAR-NECROSIS

Post-transplant cure tubular necrosis (ATN) represents the most freque nt cause of delayed graft function in the immediate post-transplant pe riod. Several causes have been associated with the development of post -transplant ATN such as donor and recipient ages, cold-warm ischemia t imes, HLA mismatches, and postoperative hypotension. In the present st udy, we retrospectively evaluated the role of secondary hyperparathyro idism and high parathyroid hormone (PTHi) blood levels in the developm ent of post-transplant ATN. One hundred patients submitted to cadaveri c renal transplant between January 1992 and March 1993 in our unit wer e included. Twenty-seven patients (27%) developed post-transplant ATN and seventy-three (73%) did not. Post-transplant ATN was significantly associated with gender (p < 0.01), recipient age (p < 0.01), number o f transplantations (p < 0.01), time on hemodialysis (p < 0.001), cold ischemia time (p < 0.05) and PTHi levels (p < 0.001). The bivariate an d multivariate statistical analyses demonstrated that the development of post-transplant ATN was significantly more frequent in females; ret ransplanted patients, patients with a time on dialysis of more than 5 years, recipients over 60 years old, patients with a PTHi blood level higher than 240 pg/ml (4 times normal level) and a cold ischemia time of more than 18 h. Based on these results, we conclude that high PTHi blood levels in the renal transplant recipients represent a relevant f actor in the development of post-transplant ATN. The administration of intravenous pulsed of 1,25(OH)(2)D-3 and/or a calcium channel blocker in the perioperative period could be useful to decrease the incidence and severity of post-transplant ATN in these patients.