ON THE IMPAIRMENT OF RENAL CONCENTRATING ABILITY IN PROLONGED HYPERCALCEMIA AND HYPERCALCIURIA IN MAN*

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Abstract
Maximal urinary osmolality (Umax and TC H20 (solute free water reabsorbed) were measured in subjects with hypercalciuria, hypercalcemia, or both. Patients with "hyperabsorption hypercalciuria," hypervitaminosis D and hyper-parathyroidism were studied before and after treatment designed to lower urinary calcium. All subjects showed impairment in both Umax and Tc H2O and improvement in them with therapy. The data suggest that excess of Ca, rather than the agent or disease process producing it, is ultimately "responsible for the defect. The concentrating defect was not attributable to an increased solute excretion, which showed negligible changes with improvement. All subjects but one showed normal Na conservation with urinary Na less than 9 meq per day at this intake, suggesting that the concentrating defect does not depend upon gross failure of Na transport.