Persistent hyperparathyroidism and impaired tubular reabsorption of phosphate (P) are common after kidney transplantation. In order to assess the suppressibility of these abnormalities, we studied the effects of a single oral calcium (Ca) load (1 g) in 7 healthy subjects (HS) and in 14 normocalcemic long-term renal transplant recipients with good renal function (RT). In HS and RT, serum and urinary Ca were similar at baseline, and increased (p < 0.001) to the same extent after Ca ingestion. Serum parathyroid hormone (PTH) and nephrogenic cAMP (NcAMP) levels were higher at baseline in RT than HS (mean ± SEM; respectively, PTH 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/lGFRp < 0.01). After Ca, PTH (p < 0.001) and NcAMP (p < 0.01) decreased markedly in both RT and HS. Maximal changes 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 higher 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 higher phosphaturia than HS (246 ± 25 vs. 127 ± 19 µmol/l, p < 0.01), and Ca ingestion lowered phosphaturia to similar values in both RT and HS (116 ± 13 vs. 95 ± 7 µmol/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 summarize, in normocalcemic long-term kidney transplant recipients, a single oral Ca intake acutely blunted the excessive PTH secretion and increased tubular reabsorption of P up to a normal range. We conclude therefore, that PTH is a main factor of tubular P loss in these patients.