Parathyroid hormone (PTH) has been proposed as an important inhibitor of renal bicarbonate reabsorption, so metabolic acidosis should occur in patients with primary hyperparathyroidism. Systemic acid-base status and serum PTH levels were studied in 13 patients, ten of whom were studied again after curative parathyroidectomy. Two patients, one with reduced glomerular filtration rate, were acidotic; the remainder were normal. Chloride concentration fell and CO2 content rose after parathyroidectomy, but serum PTH level was not correlated significantly with either. Since PTH does not uniformly cause acidosis when elevated to a level 10 to 20 times above normal, it is unlikely to be an important regulator of renal acid excretion.