Proximal tubular defects in idiopathic hypercalciuria: resistance to phosphate administration

Miner Electrolyte Metab. 1982;7(5):237-49.

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Absorption
  • Adult
  • Body Water / metabolism
  • Calcium / pharmacology
  • Calcium / urine*
  • Drug Resistance
  • Female
  • Glomerular Filtration Rate
  • Humans
  • Kidney Tubules, Proximal / metabolism*
  • Male
  • Parathyroid Hormone / blood
  • Phosphates / metabolism
  • Phosphates / pharmacology*
  • Sodium / metabolism

Substances

  • Parathyroid Hormone
  • Phosphates
  • Sodium
  • Calcium