Hypercalcemia is a relatively common finding after kidney transplant, and when correctly evaluated has been reported to be present in around 5-15% of patients. The peak of its incidence can be found after the third month from
transplantation and it usually maintains relatively constant levels, even though a moderate attenuation of the phenomenon can be expected in the long term. Many factors have been claimed to cause
hypercalcemia after kidney transplant. However, the main recognized factor is the degree of persistent
hyperparathyroidism deriving from a long previous history of
uremia. It has been suggested that
hypercalcemia can be damaging to both graft (induction of
nephrocalcinosis, reduction of graft survival) and other organ or system functions (
vascular calcification,
erythrocytosis,
pancreatitis, etc.). However, there is no definitive demonstration of a cause-effect relationship between
hypercalcemia and the above-mentioned clinical events. Furthermore, it is not possible to establish to what extent these effects are due to
hypercalcemia per se or also to increased PTH levels, which are often associated with
hypercalcemia. In addition, there is no definitive evidence that correction of
hypercalcemia might solve the above-mentioned clinical events. The best way to reduce the incidence of
hypercalcemia is considered to be the optimization of
therapy for
secondary hyperparathyroidism during the pretransplant period. It has long been thought that
parathyroidectomy was the only way to solve the problem of stabilized
hypercalcemia associated with moderate-severe persistent
hyperparathyroidism after kidney transplant. The introduction of calcimimetics, which have substantially changed the therapeutic approach to
secondary hyperparathyroidism in dialysis patients, seems to be promising also in this field. However, many issues need to be clarified before its definitive inclusion into the therapeutic armamentarium of the transplant patient who is already burdened by so many medications.