http://medlib.yu.ac.kr/eur_j_oph/sem_nephrol/sem_n_pdf/SemNep_28_2_120.pdf

New Insights into the Pathogenesis of Idiopathic Hypercalciuria

Nephrolithiasis, with a lifetime incidence of up to 13% ([1–9][1] [⇓][2] [⇓][3] [⇓][4] [⇓][5] [⇓][6] [⇓][7] [⇓][8] [⇓][9]), results in significant morbidity as well as substantial economic costs, not only directly from medical treatment but also indirectly through time lost from

Molecular Mechanisms of Primary Hypercalciuria

The fine tuning of Ca2+ excretion in the kidney takes place in the distal nephron, which consists of the distal convoluted tubule, connecting tubule, and initial portion of the cortical collecting ...

Toward a comprehensive molecular model of active calcium reabsorption

The estimated lifetime risk of nephrolithiasis is growing nowadays, and the formation of kidney stones is frequently promoted by hypercalciuria. Vitamin D, and especially its active metabolite calcitriol, increase digestive calcium absorption—as urinary calcium excretion is directly correlated with digestive calcium absorption, vitamin D metabolites could theoretically increase calciuria and promote urinary stone formation. Nevertheless, there was, until recently, low evidence that 25-hydroxyvitamin D serum levels would be correlated with kidney stone formation, even if high calcitriol concentrations are frequently observed in hypercalciuric stone formers. Low 25-hydroxyvitamin D serum levels have been associated with a broad spectrum of diseases, leading to a huge increase in vitamin D prescription in the general population. In parallel, an increased frequency of kidney stone episodes has been observed in prospective studies evaluating vitamin D alone or in association with calcium supplements, and epidemiological studies have identified an association between high 25-hydroxyvitamin D serum levels and kidney stone formation in some groups of patients. Moreover, urinary calcium excretion has been shown to increase in response to vitamin D supplements, at least in some groups of kidney stone formers. It seems likely that predisposed individuals may develop hypercalciuria and kidney stones in response to vitamin D supplements.

https://www.mdpi.com/2072-6643/10/3/366/pdf/1

Vitamin D, Hypercalciuria and Kidney Stones.

The epithelial Ca(2+) channels TRPV5 and TRPV6 represent a new family of Ca(2+) channels that belongs to the superfamily of transient receptor potential channels. TRPV5 and TRPV6 constitute the apical Ca(2+) entry mechanism in active Ca(2+) transport in kidney and intestine. The central role of TRPV5 and TRPV6 in active Ca(2+) (re)absorption makes it a prime target for regulation to maintain Ca(2+) balance. This review covers the hormonal regulation, interaction with accessory proteins and (patho)physiological implications of these epithelial Ca(2+) channels.

/pdf/the-epithelial-calcium-channels-trpv5-and-trpv6-regulation-36qxlxwp4o.pdf

The epithelial calcium channels TRPV5 and TRPV6 : regulation and implications for disease

Absorptive hypercalciuria (a stone-forming condition) is characterized by gut hyperabsorption of calcium, hypercalciuria, and reduced bone density. Inasmuch as these features implicate enhanced calcitriol action in gut and bone, we analyzed the vitamin D receptor (VDR) gene to ascertain whether an abnormality of this gene marks patients with intestinal hyperabsorption of calcium. We have compared the frequency of a restriction fragment length polymorphism (Bsm I) associated with different alleles of the VDR gene in a group of 33 well characterized absorptive hypercalciuric patients and a group of 36 normal race- and age-matched control subjects. There was no difference between the distribution of the VDR alleles in the patient population when compared with the normal population. The coding region of VDR messenger RNA was also normal, as determined by both DNA sequence analysis and chemical mismatch cleavage analysis of copy DNA from 11 index absorptive hypercalciuric patients. On the basis of these result...

Evidence for normal vitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria.

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Evidence for normal vitamin D receptor messenger ribonucleic acid and genotype in absorptive hypercalciuria.