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TRANSLATIONAL PHYSIOLOGY

Evidence for increased postprandial distal nephron calcium delivery in hypercalciuric stone-forming patients

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

Submitted 8 July 2008 ; accepted in final form 19 August 2008

A main mechanism of idiopathic hypercalciuria (IH) in calcium stone-forming patients (IHSF) is postprandial reduction of renal tubule calcium reabsorption that cannot be explained by selective reduction of serum parathyroid hormone levels; the nephron site(s) responsible are not as yet defined. Using fourteen 1-h measurements of the clearances of sodium, calcium, and endogenous lithium during a three-meal day in the University of Chicago General Clinical Research Center, we found reduced postprandial proximal tubule reabsorption of sodium and calcium in IHSF vs. normal subjects. The increased distal sodium delivery is matched by increased distal reabsorption so that urine sodium excretions do not differ, but distal calcium reabsorption does not increase enough to match increased calcium delivery, so hypercalciuria results. In fact, urine calcium excretion and overall renal fractional calcium reabsorption both are high in IHSF vs. normal when adjusted for distal calcium delivery, strongly suggesting a distal as well as proximal reduction of calcium reabsorption. The combination of reduced proximal tubule and distal nephron calcium reabsorption in IHSF is a new finding and indicates that IH involves a complex, presumably genetic, variation of nephron function. The increased calcium delivery into the later nephron may play a role in stone formation via deposition of papillary interstitial apatite plaque.

nephrolithiasis; tubule reabsorption; lithium clearance; hypercalciuria; proximal tubule

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				K. J. Bergsland, F. L. Coe, D. L. Gillen, and E. M. Worcester A test of the hypothesis that the collecting duct calcium-sensing receptor limits rise of urine calcium molarity in hypercalciuric calcium kidney stone formers Am J Physiol Renal Physiol, October 1, 2009; 297(4): F1017 - F1023. [Abstract] [Full Text] [PDF]