EFFECTS OF ORAL PHOSPHORUS SUPPLEMENTATION ON MINERAL METABOLISM OF RENAL-TRANSPLANT RECIPIENTS

Background. Persistent hyperparathyroidism (HPT) is frequently observe d in kidney transplant recipients. Hypophosphataemia is a common bioch emical consequence of HPT. Theoretically, oral phosphorus administrati on may induce negative effects on the control of HPT, though this poin t has never been demonstrated in kidney-transplant recipients. This st udy was designed to evaluate the effects of oral phosphorus supplement ation on the mineral metabolism of successful kidney transplant recipi ents. Methods. Thirty-two kidney transplant recipients with serum crea tinine <2 mg/dl and serum phosphate levels <3.5 mg/dl were included in the study. After a washout period in which oral phosphorus supplement ation was discontinued, the following parameters were determined (F0 p eriod): serum calcium, phosphate, alkaline phosphatase, uric acid, bic arbonate, PTH, 1,25-dihydroxyvitamin D3 (1,25(OH)(2)D) and 25-hydroxyv itamin D3 (25OHD). Creatinine clearance, calcium, and phosphate excret ion were determined from a 24-h urine sample. The same determinations were repeated (F1 period) after all patients received 1.5 g of oral ph osphorus for 15 days. For data analysis, patients were divided into tw o subgroups (optimal and suboptimal) according to allograft function ( Ccr> or < 70 ml/min/1.73 m(2)). Results. In the F0 period, only nine o f 32 patients had PTH levels within the normal range (< 65 pg/ml). The mean concentrations of PTH, 1,25(OH)(2)D and 25OHD were 132+/-97 pg/m l, 40.5+/-16 pg/ml and 12.5+/-8.2 ng/ml respectively. Phosphorus suppl ementation led to significant reductions in serum calcium and 1,25(OH) (2)D concentrations, as well as in urinary calcium excretion in the wh ole group. On the contrary, serum phosphate, PTH, and urinary phosphat e excretion increased significantly. The percentage increase in PTH co ncentrations after phosphorus supplementation were similar in patients with optimal and suboptimal allograft function (33 vs 36%). The reduc tion of 1,25(OH)(2)D concentrations after phosphorus supplementation w as observed mainly in the subgroup with optimal allograft function (21 % reduction with respect to baseline values), while the mean 1,25(OH)( 2)D concentrations in patients with suboptimal allograft function scar cely changed (1.4% increase). Changes in 1,25(OH)(2)D concentrations a fter phosphorus supplementation, expressed as a percentage of the init ial concentrations, correlated positively with the percentage changes in PTH concentrations for the whole group, as well as for each subgrou p. The best determinants for the percentage and the absolute increase in PTH concentration after phosphorus supplementation was the final se rum phosphate concentration (F=4.84, r=0.37, P=0.035) and the increase in serum phosphate (F=7.69, r=0.45, P= 0.009) respectively. Conclusio ns. Oral phosphorus supplementation led to a significant increase in t he PTH concentration of kidney transplant recipients. The mean 1,25(OH )(2)D concentration decreased mainly in recipients with optimal allogr aft function. The counterbalance effect of PTH on 1,25(OH)(2)D product ion may account for the relative preservation of 1,25(OH)(2)D levels i n recipients with suboptimal allograft function.