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TRANSLATIONAL PHYSIOLOGY

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

¹Department of Medicine and ⁴General Clinical Research Center, University of Chicago, Chicago, Illinois; ²Department of Statistics, University of California, Irvine, California; and ³Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana

Submitted 11 April 2006 ; accepted in final form 11 June 2006

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.

idiopathic hypercalciuria; urine calcium excretion; parathyroid hormone

This article has been cited by other articles:

				T. Isakova, O. Gutierrez, A. Shah, L. Castaldo, J. Holmes, H. Lee, and M. Wolf Postprandial Mineral Metabolism and Secondary Hyperparathyroidism in Early CKD J. Am. Soc. Nephrol., March 1, 2008; 19(3): 615 - 623. [Abstract] [Full Text] [PDF]

				G. Gambaro and C. Abaterusso Pathophysiology of hypercalciuria Am J Physiol Renal Physiol, November 1, 2007; 293(5): F1758 - F1758. [Full Text] [PDF]

				D. L. Gillen, E. M. Worcester, and F. L. Coe Reply to Gambaro and Abaterusso Am J Physiol Renal Physiol, November 1, 2007; 293(5): F1759 - F1759. [Full Text] [PDF]