• 1 January 1984
    • journal article
    • research article
    • Vol. 53  (211) , 359-368
Abstract
The hypocalcemic response to salmon calcitonin was separated into its renal and skeletal components during the treatment of 21 patients with severe hypercalcemia complicating malignant disease. Inhibition of renal tubular Ca reabsorption by calcitonin may induce a rapid fall in serum Ca. The magnitude of this response depends in part upon the correction of volume depletion which is a common feature of hypercalcemia from any cause. The adequacy of rehydration can be assessed from the relationship between serum Ca and the Ca excretion rate expressed in .mu.mol/l glomerular filtrate (CaE). Not all patients show a good renal response to calcitonin and this may reflect secretions by the primary tumor of substances which inhibit the renal tubular actions of calcitonin. The response to rehydration may identify such patients and this has obvious practical implications for the choice of treatment.