The renal response to exogenous parathyroid hormone in treated pseudohypoparathyroidism

Resistance to the renal actions of parathyroid hormone (PTH) in pseudohypoparathyroidism (PsH) may be improved after treatment with vitamin D or its metabolites, but reports conflict. We have examined the renal response to infusion of 35 μg of 1–38 PTH in patients with PsH type I ( n = 8) and PsH type II ( n = 1) during treatment and related this to prevailing endogenous serum PTH and calcium levels. Nine patients with postsurgical or idiopathic hypoparathyroidism (HP) served as controls. The urinary cAMP increase (ΔcAMP) was lower ( p < 0.001) in the PsH type I (175 ± 6.4 nmol/l glomerular filtrate) than in the HP group (3251 ± 515 nmol/l glomerular filtrate). ΔcAMP in the PsH type I subjects was dependent on endogenous PTH concentrations ( r = − 0.76; p = 0.046) and serum calcium ( r = 0.74; p = 0.037). Phosphaturic responses (expressed as % decrease in TmPO 4/ glomerular filtration rate) were lower ( p = 0.013) in the PsH type I (28.8 ± 3.75) compared with those of the HP patients (43 ± 3.48). The phosphaturic responses in the PsH type I patients were strongly dependent on endogenous PTH ( r = 0.94; p < 0.001) and serum calcium levels ( r = 0.94; p < 0.001) so that the responses of subjects with normal or low PTH levels were no different ( p = 0.16) from the HP group. Renal handling of calcium and sodium in response to exogenous PTH was identical in patients with PsH (types I and II) and HP. Renal tubular reabsorption during a calcium infusion was normal in all patients with PsH. These results emphasise the importance of the modulatory effects due to associated biochemical abnormalities in PsH on the responses to exogenous PTH. They also confirm that renal handling of calcium and sodium is probably normal in treated PsH.