251. Secondary hyperparathyroidism and acute tubular necrosis following renal transplantation.
- Author
-
Traindl O, Längle F, Reading S, Franz M, Watschinger B, Klauser R, Woloszczuk W, and Kovarik J
- Subjects
- Adult, Calcium metabolism, Creatinine blood, Female, Humans, Hyperparathyroidism, Secondary blood, Kidney Transplantation physiology, Kidney Tubular Necrosis, Acute blood, Male, Middle Aged, Parathyroid Hormone blood, Hyperparathyroidism, Secondary etiology, Kidney Transplantation adverse effects, Kidney Tubular Necrosis, Acute etiology
- Abstract
In the present study we investigated the relationship between secondary hyperparathyroidism in renal graft recipients and post-transplantation acute tubular necrosis (ATN). Patients were divided into two groups according to graft function: group A consisted of 28 patients who had an uneventful postoperative period and did not require haemodialysis. Group B comprised 26 patients with primary non-function of the graft due to biopsy-proven ATN who required continued haemodialysis for the first postoperative week or longer (mean 14.2 +/- 8.7 days). Both groups had comparable donor characteristics, HLA-matching and ischaemia times. All patients were given cyclosporin and low-dose prednisolone for immunosuppression. Pretransplant levels of intact PTH were significantly greater in group B than in group A (203.5 +/- 193.1 pg/ml versus 81.7 +/- 45.2 pg/ml, P < 0.01). Group B patients had more transplant biopsies (50 versus 7) and a longer hospitalization time (33.4 +/- 10.9 days versus 21.9 +/- 11.9 days, P < 0.01), although serum creatinine on the day of discharge was higher in group B (1.77 +/- 0.51 mg/dl versus 1.5 +/- 0.45 mg/dl, P < 0.05). We conclude that patients with secondary hyperparathyroidism as assessed by measuring circulating levels of intact PTH have an increased incidence of ATN.
- Published
- 1993