Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration.
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.
D000042:Absorption; D000328:Adult; D001834:Body Water / Q000378:metabolism; D002118:Calcium / Q000494:pharmacology / Q000652:urine*; D004351:Drug Resistance; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D008297:Male; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000378:metabolism / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism
D010281:Parathyroid Hormone; D010710:Phosphates; D012964:Sodium; D002118:Calcium