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NEIL BRESLAU, ARNOLD M. MOSES, Renal Calcium Reabsorption Caused by Bicarbonate and by Chlorothiazide in Patients with Hormone Resistant (Pseudo) Hypoparathyroidism, The Journal of Clinical Endocrinology & Metabolism, Volume 46, Issue 3, 1 March 1978, Pages 389–395, https://doi.org/10.1210/jcem-46-3-389
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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 calcium to sodium clearances (Cca/CNa) was used as an index of renal calcium reabsorption. The patients with pseudohypoparathyroidism had negligible decreases in CCO/CNO 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 potassium 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. These observations provide evidence that the abnormal renal responses to PTH are specific, since the elevated PTH level is not a factor and the abnormal renal responses are not observed with stimuli that do not act via a cyclic AMPmediated mechanism. They also support the possibility that the basic defect in pseudohypoparathyroidism is that PTH does not increase renal cyclic AMP with the subsequent failure to increase tubular fluid bicarbonate which in turn leads to impaired renal calcium reabsorption. (J Clin Endocrinol Metab46.389, 1978)
