TY - JOUR
T1 - Calcium and phosphate changes after renal transplantation
AU - Messa, Piergiorgio
AU - Cafforio, Cosimo
AU - Alfieri, Carlo
PY - 2010
Y1 - 2010
N2 - 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).
AB - 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).
KW - Calcium phosphorus
KW - Hyperparathyroidism
KW - Renal transplant
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M3 - Article
C2 - 21170877
AN - SCOPUS:79952278677
VL - 23
JO - Journal of Nephrology
JF - Journal of Nephrology
SN - 1121-8428
IS - SUPPL.16
ER -