ACUTE ORAL CALCIUM LOAD DECREASES PARATHYROID SECRETION AND SUPPRESSES TUBULAR PHOSPHATE LOSS IN LONG-TERM RENAL-TRANSPLANT RECIPIENTS

Persistent hyperparathyroidism and impaired tubular reabsorption of ph osphate (P) are common after kidney transplantation. In order to asses s the suppressibility of these abnormalities, we studied the effects o f a single oral calcium (Ca) load(1 g) in 7 healthy subjects (HS) and in 14 normocalcemic longterm renal transplant recipients with good ren al function (RT). In HS and RT, serum and urinary Ca were similar at b aseline, and increased (p < 0.001) to the same extent after Ca ingesti on. Serum parathyroid hormone (PTH) and nephrogenic cAMP (NcAMP) level s were higher at baseline in RT than HS (mean +/- SEM; respectively, P TH 7.8 +/- 0.8 vs. 3.5 +/- 0.6 pmol/l, p < 0.001, and NcAMP 24.8 +/- 2 .3 vs. 13.9 +/- 2.3 nmol/l GFR, p < 0.01). After Ca, PTH (p < 0.001) a nd NcAMP (p < 0.01) decreased markedly in both RT and HS. Maximal chan ges in PTH and NcAMP were larger in RT than HS (PTH -3.3 +/- 0.4 vs. - 2.1 +/- 0.03 pmol/l, p < 0.01, and NcAMP -18.2 +/- 3.3 vs. -8.1 +/- 2. 6 nmol/l GFR, p < 0.05). Although PTH levels remained significantly hi gher in RT than HS from baseline to the end of the study (p < 0.001), PTH decreased to the normal range in RT after Ca load. Moreover, NcAMP reached similar values in RT and HS after Ca (16.0 +/- 3.2 vs. 13.2 /- 2.8 nmol/l GFR at the end of the survey, NS). At baseline, RT had h igher phosphaturia than HS (246 +/- 25 vs. 127 +/- 19 mu mol/l, p < 0. 01), and Ca ingestion lowered phosphaturia to similar values in both R T and HS (116 +/- 13 vs. 95 +/- 7 mu mol/l GFR, NS). Renal P threshold expressed as TmP/GFR and tubular reabsorption rate of P were lower in RT than HS at baseline, and resumed normal values after Ca. To summar ize, in normocalcemic long-term kidney transplant recipients, a single oral Ca intake acutely blunted the excessive PTH secretion and increa sed tubular reabsorption of P up to a normal range. We conclude theref ore, that PTH is a main factor of tubular P loss in these patients.