Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration.
Publication/Presentation Date
1-1-1982
Abstract
Of 100 consecutive patients with recurrent renal calculi, 43 had idiopathic hypercalciuria (IH) on outpatient evaluation. Hypercalciuria was classified as diet-dependent or fasting; all patients had normal serum iPTH and urinary cyclic AMP, and serum phosphate and TmPO4/GFR were reduced in IH compared to normocalciuric stone formers. In 16 patients with IH, clearance studies revealed an elevated urine flow are factored for GFR (V/GFR) as compared with normal controls (p less than 0.05). In 12 patients, serum PTH was normally suppressed by calcium infusion but TmPO4/GFR was persistently reduced. Acute and chronic phosphate administration significantly reduced urine calcium excretion but did not correct the abnormal V/GFR. We conclude that in IH of both the fasting and the diet-dependent type, there is a defect in the proximal tubular reabsorption of sodium and fluid as well as PTH-independent tubular phosphate wasting. The proximal tubular defect is not a consequence of hypercalciuria nor of phosphate depletion but may be a cause of these abnormalities.
Volume
7
Issue
5
First Page
237
Last Page
249
ISSN
0378-0392
Published In/Presented At
Lau, Y. K., Wasserstein, A., Westby, G. R., Bosanac, P., Grabie, M., Mitnick, P., Slatopolsky, E., Goldfarb, S., & Agus, Z. S. (1982). Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration. Mineral and electrolyte metabolism, 7(5), 237–249.
Disciplines
Medicine and Health Sciences
PubMedID
7169988
Department(s)
Department of Medicine
Document Type
Article