Hyperparathyroidism in kidney transplant candidates and postoperative parathyroid gland function in recipients

Abstract

Objective: to evaluate the effects of secondary hyperparathyroidism (HPT) in kidney transplantation (KT) candidates on recipients’ parathyroid gland function in the first postoperative year.Materials and methods. The retrospective cohort study included 210 patients (103 women, 107 men, age 45 ± 9 years) with stage 5 chronic kidney disease (stage 5 CKD, including dialysis-dependent patients), who had undergone cadaveric KT. Biochemical screening before kidney transplantation and in the postoperative period at 3 and 12 months determined serum levels of parathyroid hormone (PTH), calcium, phosphorus, alkaline phosphatase activity, albumin and creatinine using standard methods. PTH levels of 130–595 pg/mL and ≤130 pg/mL were taken as the target level in the pre- and post-transplant periods, respectively.Results. Fifty-six KT candidates (group 1) had HPT and 154 (group 2) had the target PTH levels. PTH level was 897 (722; 1136) and 301 (229; 411) pg/mL, respectively, p < 0.001. PTH decreased in all recipients at 3 months after KT: by 595 (420; 812) in group 1 and 148 (77; 230) pg/ mL in group 2, p < 0.001, to 254 (180; 455) and 150 (118; 212) pg/mL, respectively, p < 0.001; the target level was detected in 10.7% and 42.2% of recipients, respectively, p < 0.001. At 12 months, blood PTH was 171 (94; 239) pg/mL in group 1 and 112 (90; 135) pg/mL in group 2, p = 0.004; target level was found in 48.2% and 73.4% of recipients, respectively, p < 0.001. Kidney graft function was identical in both recipient groups: acute tubular necrosis in 41.1% and 54.5%; at 3 months, median glomerular filtration rates (GFR) of 60 and 65 mL/min (n.d.); at 12 months, 56 and 54 mL/min (n.d.). Post-transplant PTH levels correlated directly with preoperative levels in both groups and inversely with renal graft function in group 2 recipients.Conclusion. HPT in kidney transplant candidates is a major, graft function-independent predictor of excess PTH secretion in recipients, increasing the risk of persistent HPT 1.9-fold, one year after KT.