Hypercalcemia and hypophosphatemia are frequently observed in recipients of a kidney transplant (KTx). Hypercalcemia has been reported in up to 66% of KTx patients. Many factors have been suggested as the putative causal factors; however, the persistence of moderate-severe secondary hyperparathyroidism, associated with a change in the set-point of the Cacontrolled parathyroid hormone (PTH) secretion, is considered to play a prominent role. Hypercalcemia can negatively impact on both the graft and patient outcome, increasing the incidence of nephrocalcinosis, which can induce a worse graft outcome, inducing vascular calcifications, and increasing the incidence of pancreatitis. In addition, severe hypercalcemia after KTx often requires parathyroidectomy, which is not universally considered a safe medical solution in this clinical setting. After KTx, phosphate levels often fall below the normal range, with hypophosphatemia being observed in up to 40% of patients. The putative causal factors for this metabolic alteration are persistent hyperparathyroidism, increased levels of FGF- 23, tubular damage secondary to the immunological effects, and toxic and vascular effectors. Hypophosphatemia can negatively impact on either skeletal or muscular systems, contributing to the increased incidence of bone fractures in KTx patients. The current therapeutic options should take into account an accurate pretransplant treatment and screening of the waiting-list patient and should also evaluate the efficacy and safety profile of the new pharmacological tools (calcimimetics) in comparison with the classical surgical approach (parathyroidectomy).
|Journal||Journal of Nephrology|
|Publication status||Published - 2010|
- Calcium phosphorus
- Renal transplant
ASJC Scopus subject areas