Parathyroid Hormone Resistance in Renal Allograft Recipients
Hypophosphatemia is common after renal transplantation and has been variously ascribed to persistent hyperparathyroidism, to tubular damage from rejection, or to the effect of corticosteroid or immunosuppressive therapy (1–3). To learn more about the mechanisms, we measured TmP/GFR, nephrogenous cyclic AMP (NcAMP) and immunoreactive PTH in 25 renal transplant patients with stable renal function (Ccr≥70 ml/min/1.73 m2,≥6 months post-transplant), 21 healthy control subjects and 5 uninephrectomized renal transplant donors. On the basis of the parathyroid function tests, we divided the patients into three groups. In Group 1 (5 patients) serum calcium, NcAMP and PTH were all normal; these patients had resolved hyperparathyroidism. In Group 2 (6 patients) serum calcium, NcAMP and PTH. were all raised; these patients had persistent hypercalcemic hyperparathyroidism. In Group 3 (14 patients) serum calcium was normal but either NcAMP or iPTH or both were raised; these patients had persistent normocalcemic hyperparathyroidism. These three groups did not differ significantly in duration of graft survival, creatinine clearance, type or dose of immunosuppressive therapy, or serum levels of vitamin D metabolites.
KeywordsSerum Calcium Renal Transplant Patient Renal Allograft Recipient Phosphate Reabsorption Single Kidney
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