Hyperphosphataemia, but not hypercalcaemia, predicts cardiovascular risk after kidney transplantation

Kidney transplant recipients (KTRs) face a heightened risk of cardiovascular disease but the impact of post-transplant mineral and bone disorders on this risk remains unclear. This study investigated the association between serum calcium, phosphate and calcium-phosphate (Ca × P) product levels and cardiovascular outcomes.

In this retrospective cohort study, adult KTRs transplanted between 2005 and 2014 at a large centre were analysed. The primary outcome was major adverse cardiovascular events (MACE). Secondary outcomes included all-cause mortality and a composite of MACE and mortality. Cumulative exposure to abnormal mineral levels was assessed using time-weighted average calculations. Cox proportional hazards models were used to evaluate associations adjusting for confounders, including estimated glomerular filtration rate (eGFR). Mineral abnormalities were analysed both as continuous variables and by quartiles.

The study included 649 KTRs (median follow-up 2943 days), with 109 patients (16.8%) experiencing MACE. Over time, calcium exposure decreased, while phosphate and Ca × P product exposure increased. Hypercalcaemia was not significantly associated with MACE, all-cause mortality or the composite outcome. In contrast, hyperphosphataemia remained significantly associated with an increased risk of MACE {hazard ratio [HR] 1.414 [95% confidence interval (CI) 1.044-1.916]) and the composite outcome [HR 1.353 (95% CI 1.064-.721)] even after adjustment for eGFR. Elevated, Ca × P product levels were similarly associated with increased cardiovascular risk [HR 1.055/mg²/dl² (95% CI 1.015-1.096) and HR 1.043/mg²/dl² (95% CI 1.013-1.075), respectively].

While hypercalcaemia does not independently predict cardiovascular outcomes post-transplant, sustained hyperphosphataemia and elevated Ca × P product are significant risk factors for adverse cardiovascular events in KTRs.