Elevated calcium phosphate product after renal transplantation is a risk factor for graft failure

Abnormal mineral metabolism is not uncommon after renal transplant (TXP). In dialysis patients, elevated serum phosphorous (P), calcium (Ca), CaP product, and parathyroid hormone (PTH) are associated with increased morbidity and mortality. The effect of these abnormalities on recipient and graft survival after renal transplantation is unknown.

We retrospectively analyzed 422 kidney-only transplants performed between June 1996 and June 2003. Cases with graft or recipient survival less than three months, pre-TXP parathyroidectomy (PTX), cinacalcet therapy and incomplete records were excluded, leaving 303 cases for analysis using Cox models that included post-TXP PTX, levels of albumin-adjusted Ca(Ca(adj)), P, Ca(adj)P product and PTH.

There was an 11-25% prevalence of abnormal serum Ca(adj), P or Ca(adj)P product within the first year post-TXP. At least 24% of recipients not undergoing PTX with an equation estimated GFR of 40-60 mL/min had PTH levels >130 pg/mL at one yr post-TXP. This is above levels recommended by the U.S National Kidney Foundation kidney disease quality initiative for patients with stages I-IV chronic kidney disease. Adjusted Ca > 10.5 mg/dL at three months post-TXP was an independent risk for recipient death (OR 3.0; 95% CI: 1.2-7.4). A Ca(adj)P product >35 mg(2)/dL(2) at six months (OR 4.0; 95% CI: 1.2-13.1), and Ca >10.5 mg/dL at 12 months post-TXP (OR 4.0; 95% CI: 1.2-14) were independent risks for death-censored graft loss. Twenty-two recipients underwent PTX for severe hyperparathyroidism.

Abnormalities of mineral metabolism are common early after renal TXP. An elevated serum Ca(adj) at three months post-TXP increases the risk for recipient death, while an elevated Ca(adj)P and Ca(adj) later in the first post-TXP year increases the risk of long-term death-censored graft loss.