The effects of intravenously administered parathyroid extract and of a purified parathyroid hormone on urinary acidification and on solute excretion were measured in six thyroparathyroidectomized dogs, in three normal women, and in a patient with diabetes insipidus. Parathyroid extract and the purified parathyroid hormone produced an immediate rise in urinary pH and bicarbonate with a fall in titratable-acid-minus-bicarbonate and in ammonia in all subjects. This was usually associated with a rise in urinary sodium and potassium. The changes in urinary acidification usually preceded any rise in glomerular filtration rate, and were associated with no increase in serum bicarbonate concentration. They also preceded a rise in the excretion of phosphate in most experiments, and thus did not depend on a rise in urinary buffer content. It is postulated that parathyroid hormone inhibits sodium-for-hydrogen ion exchange in the renal tubules, perhaps by interfering directly with the ability of the kidney to maintain a hydrogen ion gradient between the body fluids and the tubular urine.

Medullary carcinoma (MC) of the thyroid, in contrast to papillary-follicular carcinoma, fails to concentrate iodine and thus has not been treated with radioactive iodine. We have successfully treated a 16-yr-old Mexican-American girl with residual MC after maximal thyroidectomy (Tx), utilizing radioiodine (131I) to deliver radiation to residual follicular cells in the tumor bed. Immediately after Tx, plasma thyrocalcitonin levels before and during calcium infusion were all elevated (640--1200 pg/ml). 131I (150 mCi) was administered 12 days after Tx after four daily im injections of bovine TSH. Three months after 131I therapy, thyrocalcitonin levels before and during calcium infusion were all normal (less than 50 pg/ml). Ten months after 131I therapy, thyrocalcitonin levels before and after iv pentagastrin were all normal (less than 60 pg/ml). These results suggest that parafollicular cells are radiosensitive, and that therapeutic levels of radiation can be delivered to these cells after Tx if iodine trapping by the remaining follicular cells is enhanced by high levels of circulating TSH. 131I may be the therapy of choice for MC after Tx, if disease has not spread beyond the area proximate to the thyroid gland.