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Mechanisms Underlying Calcium Nephrolithiasis

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Alexander R.T., Fuster D.G., Dimke H.,
Project Mechanisms of thiazide-induced glucose intolerance
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Original article (peer-reviewed)

Journal Annual Review of Physiology
Volume (Issue) 84(1)
Page(s) 559 - 583
Title of proceedings Annual Review of Physiology
DOI 10.1146/annurev-physiol-052521-121822

Open Access

URL www.boris.unibe.ch
Type of Open Access Repository (Green Open Access)

Abstract

Nephrolithiasis is a worldwide problem with increasing prevalence, enormous costs, and significant morbidity. Calcium-containing kidney stones are by far the most common kidney stones encountered in clinical practice, and thus, hypercalciuria is the greatest risk factor for kidney stone formation. Hypercalciuria can result from enhanced intestinal absorption, increased bone resorption, or altered renal tubular transport. Kidney stone formation is complex and driven by high concentrations of calcium-oxalate or calcium-phosphate in the urine. After discussing the mechanism mediating renal calcium salt precipitation, we review recent discoveries in renal tubular calcium transport from the proximal tubule, thick ascending limb, and distal convolution. Furthermore, we address how calcium is absorbed from the intestine and mobilized from bone. The effect of acidosis on bone calcium resorption and urinary calcium excretion is also considered. Although recent discoveries provide insight into these processes, much remains to be understood in order to provide improved therapies for hypercalciuria and prevent kidney stone formation.
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