412.7: Pre-transplant Hyperparathyroidism and Adverse Posttransplant Outcomes in Kidney Transplant Recipients

Abstract

Introduction: Whether correction of severe hyperparathyroidism (HPT) is required before kidney transplantation is subject of debate, as previous studies investigating the impact of pretransplant HPT on graft and patient outcomes showed conflicting results. We aimed to assess whether pretransplant serum PTH levels are associated with the risk of delayed graft function (DGF), death censored graft failure (DCGF), or mortality. Additionally, we focused on a subgroup of patients with very high pre-transplant PTH levels (≥81 pmol/L; ≥764 pg/mL). Methods: We performed a single-center cohort study including patients who underwent kidney transplantation between 1986 and 2020. Donor and recipient demographic data, medical information and routine laboratory measurements were extracted from the local transplant registry. We performed multivariable logistic regression and Cox regression analyses to study associations between PTH and DGF (persisting dialysis requirement for up to 7 days post-transplant), DCGF (return to dialysis or re-transplantation), or all-cause mortality, respectively. We also compared these outcomes for patients in the highest vs. lowest PTH decile for each endpoint. Results: A total of 1576 kidney transplant recipients (KTRs) (51.6 ± 14.0 years-old, 42.7% male) were included. Donor age was 51.2 ± 13.5 years, 785 (49.8%) patients received a graft from a living donor, and 535 (33.9%) patients underwent a pre-emptive transplantation. Median (IQR) pretransplant serum PTH concentration was 24.3 (12.8 – 44.6) pmol/L. Corrected calcium increased while PTH and corrected phosphate decreased within the first 3 months post-transplant, even in patients with pre-transplant PTH >81 pmol/L (Figure 1A-C). Pre-transplant PTH was not associated with DGF (Table 1). During median follow-up of 5.0 (2.2 – 8.4) years, 201 (12.8%) patients developed DCGF. In fully adjusted Cox regression analyses, PTH was not associated with DCGF (Table 1). Additionally, patients with PTH >81 pmol/L (N=121) did not have an increased risk of DGF (HR 1.67 [95% CI 0.62 – 4.55], P=0.65) or DCGF (HR 0.86 [95% CI 0.47 – 1.61], P=0.65), compared with those in the lowest PTH decile. During median follow-up of 5.2 (2.9 – 9.0) years, 474 (30.1%) patients deceased. In age- and sex-adjusted analyses, a higher serum PTH was associated with an increased risk of all-cause mortality, but this association lost significance upon multivariable adjustment (Table 1). When comparing KTRs with PTH levels in the highest vs. lowest decile, there was also no association with mortality (HR 0.96 [95% CI 0.62 – 1.48], P=0.65). Conclusion: In this cohort study, pre-transplant serum PTH was not associated with an increased risk of DGF, DCGF or mortality after transplantation. Subgroup analyses in patients with severe HPT yielded similar results. Our data do not support the requirement of pre-transplant parathyroidectomy in patients with (severe) hyperparathyroidism to improve graft or patient survival.