Renal Calcium Reabsorption Caused by Bicarbonate and by Chlorothiazide in Patients with Hormone Resistant (Pseudo) Hypoparathyroidism*

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Abstract
The responses to infusion of parathyroid hormone (PTH), bicarbonate, PTH plus bicarbonate and chlorothiazide, were determined in 3 patients with pseudohypoparathyroidism and compared with responses of normal subjects to all 4 infusions, and of hyperparathyroid patients to PTH. A decrease in the ratio of Ca to Na clearances (CCa/CNa) was used as an index of renal Ca reabsorption. The patients with pseudohypoparathyroidism had negligible decreases in CCa/CNa in response to PTH. Infusion of bicarbonate, bicarbonate plus PTH and chlorothiazide resulted in greater decreases of CCa/CNa in each patient. In response to PTH infusion, the normal subjects had significantly greater responses than patients with pseudohypoparathyroidism, whereas normal subjects had a significantly lesser response to chlorothiazide. There was no significant difference in the decrease in CCa/CNa of normal subjects and patients with pseudohypoparathyroidism in response to bicarbonate or bicarbonate plus PTH. The impaired K and bicarbonate excretions observed in patients with pseudohypoparathyroidism infused with PTH were not observed after the infusion of PTH plus bicarbonate or of chlorothiazide. Patients with primary hyperparathyroidism had normal renal responses to PTH. The abnormal renal responses to PTH apparently were specific, since the elevated PTH level was not a factor and the abnormal renal responses were not observed with stimuli that did not act via a cyclic[c]AMP-mediated mechanism. The basic defect in pseudohypoparathyroidism probably is that PTH does not increase renal cAMP with the subsequent failure to increase tubular fluid bicarbonate which in turn leads to impaired renal Ca reabsorption.