Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis

Elaine M. Worcester, Daniel L. Gillen, Andrew P. Evan, Joan H. Parks, Katrina Wright, Linda Trumbore, Yasushi Nakagawa, Fredric L. Coe

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

Idiopathic hypercalciuria (IH) is common among calcium stone formers (IHSF). The increased urinary calcium arises from increased intestinal absorption of calcium, but it is unclear whether increased filtered load or decreased renal tubular reabsorption of calcium is the main mechanism for the increased renal excretion. To explore this question, 10 IHSF and 7 normal subjects (N) were studied for 1 day. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, and calories. Fasting and fed, ultrafiltrable calcium levels, and filtered load of calcium did not differ between N and IHSF. Urine calcium rose with meals, and fractional reabsorption fell in all subjects, but the change was significantly higher in IHSF. The changes in calcium excretion were independent of sodium excretion. Serum parathyroid hormone levels did not differ between N and IHSF, and they could not account for the greater fall in calcium reabsorption in IHSF. Serum magnesium and phosphorus levels in IHSF were below N throughout the day, and tubule phosphate reabsorption was lower in IHSF than N after meals. The primary mechanism by which kidneys ferry absorbed calcium into the urine after meals is via reduced tubule calcium reabsorption, and IHSF differ from N in the magnitude of the response. Parathyroid hormone is not likely to be a sufficient explanation for this difference.

Original languageEnglish (US)
Pages (from-to)F66-F75
JournalAmerican Journal of Physiology - Renal Physiology
Volume292
Issue number1
DOIs
StatePublished - Jan 1 2007

Fingerprint

Hypercalciuria
Nephrolithiasis
Calcium
Meals
Urine
Parathyroid Hormone
Phosphorus
Renal Reabsorption
Fasting
Sodium
Intestinal Absorption
Serum
Magnesium

Keywords

  • Idiopathic hypercalciuria
  • Parathyroid hormone
  • Urine calcium excretion

ASJC Scopus subject areas

  • Physiology

Cite this

Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis. / Worcester, Elaine M.; Gillen, Daniel L.; Evan, Andrew P.; Parks, Joan H.; Wright, Katrina; Trumbore, Linda; Nakagawa, Yasushi; Coe, Fredric L.

In: American Journal of Physiology - Renal Physiology, Vol. 292, No. 1, 01.01.2007, p. F66-F75.

Research output: Contribution to journalArticle

Worcester, Elaine M. ; Gillen, Daniel L. ; Evan, Andrew P. ; Parks, Joan H. ; Wright, Katrina ; Trumbore, Linda ; Nakagawa, Yasushi ; Coe, Fredric L. / Evidence that postprandial reduction of renal calcium reabsorption mediates hypercalciuria of patients with calcium nephrolithiasis. In: American Journal of Physiology - Renal Physiology. 2007 ; Vol. 292, No. 1. pp. F66-F75.
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