Nephrology Dialysis Transplantation, Vol 13, Issue 10 2605-2611, Copyright © 1998 by Oxford University Press
F Caravaca, M Fernandez, R Ruiz-Calero, J Cubero, A Aparicio, F Jimenez and M Garcia
Background. Persistent hyperparathyroidism (HPT) is
frequently observed in kidney transplant recipients. Hypophosphataemia is a
common biochemical consequence of HPT. Theoretically, oral phosphorus
administration may induce negative effects on the control of HPT, though
this point has never been demonstrated in kidney-transplant recipients.
This study was designed to evaluate the effects of oral phosphorus
supplementation on the mineral metabolism of successful kidney transplant
recipients. Methods. Thirty-two kidney transplant
recipients with serum creatinine <2 mg/dl and serum phosphate levels
<3.5 mg/dl were included in the study. After a wash-out period in
which oral phosphorus supplementation was discontinued, the following
parameters were determined (F0 period): serum calcium, phosphate, alkaline
phosphatase, uric acid, bicarbonate, PTH, 1,25-dihydroxyvitamin D3
(1,25(OH)2D) and 25-hydroxyvitamin D3 (250HD). Creatinine clearance,
calcium, and phosphate excretion were determined from a 24-h urine sample.
The same determinations were repeated (F1 period) after all patients
received 1.5 g of oral phosphorus for 15 days. For data analysis, patients
were divided into two subgroups (optimal and suboptimal) according to
allograft function (Ccr>or<70 ml/min/1.73
m2). Results. In the F0 period,
only nine of 32 patients had PTH levels within the normal range (<65
pg/ml). The mean concentrations of PTH, 1,25(OH)2D and 25OHD were
132±97 pg/ml, 40.5+16 pg/ml and 12.5±8.2 ng/ml
respectively. Phosphorus supplementation led to significant reductions in
serum calcium and 1,25(OH)2D concentrations, as well as in urinary calcium
excretion in the whole group. On the contrary, serum phosphate, PTH, and
urinary phosphate excretion increased significantly. The percentage
increase in PTH concentrations after phosphorus supplementation were
similar in patients with optimal and suboptimal allograft function (33
vs 36%). The reduction of 1,25(OH)2D concentrations
after phosphorus supplementation was observed mainly in the subgroup with
optimal allograft function (21% reduction with respect to baseline values),
while the mean 1,25(OH)2D concentrations in patients with suboptimal
allograft function scarcely changed (1.4% increase). Changes in 1,25(OH)2D
concentrations after phosphorus supplementation, expressed as a percentage
of the initial concentrations, correlated positively with the percentage
changes in PTH concentrations for the whole group, as well as for each
subgroup. The best determinants for the percentage and the absolute
increase in PTH concentration after phosphorus supplementation was the
final serum 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.
Conclusions. Oral phosphorus supplementation led to a
significant increase in the PTH concentration of kidney transplant
recipients. The mean 1,25(OH)2D concentration decreased mainly in
recipients with optimal allograft function. The counterbalance effect of
PTH on 1,25(OH)2D production may account for the relative preservation of
1,25(OH)2D levels in recipients with suboptimal allograft function.
Keywords: kidney transplantation; phosphate; secondary
hyperparathyroidism; vitamin D
ORIGINAL ARTICLES
Effects of oral phosphorus supplementation on mineral metabolism of renal transplant recipients
S. Nefrologia, Hospital Universitario Infanta Cristina, 06080 Badajoz, Spain; Corresponding author
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