Decreased phosphate reabsorption after renal transplantation: Evidence for a mechanism independent of calcium and parathyroid hormone

We studied a group or 73 transplant recipients who had had stable renal function for more than 6 months after their transplant surgery. Of these 73 patients, 23 had fasting plasma phosphate concentrations less than 2.5 mg/dl (normal, 3 to 5 mg/dl). The concentration of plasma phosphates was 2.1 ± 0.1 mg/dl in the hypophosphatemic transplant-recipient group compared with 3.0 ± 0.1 mg/dl in the total transplant-recipient population. The hypophosphatemic patients had similar fractional phosphate reabsorption when compared with the total transplant-recipient population, and their renal phosphate threshold (Tm(PO₄)/GFR) was reduced from 3.0 ± 0.1 mg/dl in the total population to 0.4 ± 0.2 mg/dl. Although PTH levels correlated inversely with the Tm(PO₄)/GFR in the total transplant-recipient group, the hypophosphatemic patients appeared to exhibit lower renal phosphate thresholds than did normophosphatemic transplant-recipients with similar PTH levels. To further evaluate the relationship between PTH and renal phosphate handling, we performed calcium infusion and phosphate titration studies on 11 hypophosphatemic transplant-recipients. The data revealed that 5 of the 11 patients with only mildly abnormal PTH levels failed to decrease their rate of phosphate excretion, their phosphate clearances, and their fractional excretion of phosphate during calcium infusion. The 5 nonresponders to calcium infusion also exhibited smaller increments in their plasma phosphate concentration and Tm(PO₄)/GFR than did the 6 patients who responded to calcium infusion with reductions in phosphate excretion rates. Before calcium infusion, cyclic 3',5'-adenosine monophosphate excretion rates were similar in both responders and nonresponders and were decreased to the same degree by the calcium infusions. These data indicate the presence of either a defect in phosphate reabsorption that is independent of the action of PTH and calcium or a heightened sensitivity to PTH with a decreased suppressibility of response to PTH.