Control of Renal Tubular Phosphate Reabsorption by Parathyroid Hormone in Man

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Abstract
The maximum tubular reabsorption capacity for phosphate relative to glomerular filtration rate (Tm,P/GFR) apparently ranged from 0.8-1.5 mmol/l in 32 normal fasting subjects. In 14 patients with primary hyperparathyroidism and 5 patients with hyperparathyroidism secondary to vitamin D deficiency or malabsorption, values ranged from 0.2-0.8 mmol/l. Plasma parathyroid hormone [PTH] concentrations measured by an immunoradiometric technique ranged from < 0.15-0.9 ng/ml in normal subjects and from 0.5-10 ng/ml in patients with hyperparathyroidism. There was no correlation between plasma PTH and Tm,P/GFR in normal or abnormal groups. Plasma PTH was lower in 11 out of 13 patients with primary hyperparathyroidism 3 or 4 wk after tumor removal than immediately before the operation. In all cases there was a rise in Tm,P/GFR, though not all values were normalized. Changes in plasma PTH, Tm,P/GFR and plasma and urinary cyclic[c]AMP concentrations were measured during infusion of bovine PTH into normal fasting subjects. Phosphate reabsorption fell markedly in response to low doses of PTH (0.5 IU h-1 kg-1), higher doses (4 IU h-1 kg-1) producing little additional change in Tm,P/GFR despite large changes in cAMP excretion. At the highest doses used (8 IU h-1 kg-1) apparent saturation of the renal adenylate cyclase occurred. During an infusion of hormone, 0.25 IU h-1 kg-1 over 3 h, a fall in Tm,P/GFR was recorded at concentrations of immunoreactive PTH within the normal range for endogeneous hormone. At such concentrations it was not possible to detect significant changes in plasma or urine cAMP. PTH probably is an important regulator of renal phosphate handling under normal physiological conditions. Such a regulatory process was implicated in control of vitamin D metabolism.

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