Urine stone risk factors in nephrolithiasis patients with and without bowel disease

Parks, Joan H.; Worcester, Elaine M.; O’Connor, R. Corey; Coe, Fredric L.

doi:10.1046/j.1523-1755.2003.00725.x

Cited by 110 publications

(71 citation statements)

References 40 publications

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“…Details of the comparisons are in the figure legends. Overall, both the idiopathic-CaOxstone formers and the bypass patients are much like those we have described in previous reports (11,12).…”

Section: Urine Datasupporting

confidence: 76%

Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle

Evan¹,

Lingeman²,

Coe³

et al. 2003

J. Clin. Invest.

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490

279

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Section: Urine Datasupporting

confidence: 76%

Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle

Evan¹,

Lingeman²,

Coe³

et al. 2003

J. Clin. Invest.

Self Cite

490

279

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“…In this model, the absence of the Cl K exchanger converts the intestinal oxalate excretion in net oxalate absorption (20). The search for polymorphic variants rather than inactivating mutations of SLC26A6 gene in patients with PHPT was in accordance with the observation that PHPT patients generally show urine oxalate excretion levels similar to those reported in healthy subjects and well below the levels observed in idiopathic stone formers (21,22). Indeed, minimal changes in the intestinal and renal oxalate excretion potentially determined by SLC26A6 gene polymorphisms might have been associated with increased susceptibility to kidney stone formation in PHPT patients.…”

Section: Discussionsupporting

confidence: 64%

Analysis of the 206M polymorphic variant of the SLC26A6 gene encoding a Cl− oxalate transporter in patients with primary hyperparathyroidism

Corbetta¹,

Eller-Vainicher²,

Frigerio³

et al. 2009

European Journal of Endocrinology

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Objective: Primary hyperparathyroidism (PHPT) is often complicated by kidney stones. Hypercalciuria and urine oxalate excretion are considered risk factors for urolithiasis in PHPT as well as in idiopathic stone-formers. Recently, the anion-exchanger SLC26A6 has been involved in the oxalate metabolism.Design and methods: We tested the hypothesis that the 206M polymorphic variant of SLC26A6 gene might contribute to the risk of kidney stones in PHPT. DNA samples from 145 PHPT patients and 129 age-and sex-matched healthy subjects were genotyped. Results: The homozygous 206V genotype was the most frequent both in PHPT patients and controls (79.3 and 74.4%), while heterozygosity for the 206M allele was detected in 20.0 and 23.3% respectively. The homozygous 206M genotype was extremely rare, occurring in 0.7 and 2.3% of PHPT and healthy subjects respectively. In the PHPT cohort, the prevalence of urolithiasis did not differ between the V/V and V/MCM/M groups and urine oxalate excretions did not correlate with the genotype. Considering the subset of PHPT stone formers (nZ74), calciuria was lower in V/MCM/M patients with respect to V/V stone-formers (4.40G1.88 vs 5.92G2.62 mg/kg per 24 h; meanGS.D., PZ0.034). Finally, the SLC26A6 206M alleles were significantly related to the presence of hypertension (73.3 vs 47.8%), showing an OR of 4.8. Conclusions: Though the SLC26A6 206M polymorphism did not correlate with kidney stone development in PHPT patients, PHPT stone-formers harbouring the M allele had a lower hypercalciuria. This observation and the high prevalence of hypertension associated with the 206M polymorphism need further investigation.

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“…30 The permeability of the low capacity, size- Figure 6. Lack of effect of claudin-10a expression on oxalate and mannitol permeability.…”

Section: Discussionmentioning

confidence: 99%

Net Intestinal Transport of Oxalate Reflects Passive Absorption and SLC26A6-mediated Secretion

Knauf

Ko²,

Jiang³

et al. 2011

Journal of the American Society of Nephrology

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Mice lacking the oxalate transporter SLC26A6 develop hyperoxalemia, hyperoxaluria, and calciumoxalate stones as a result of a defect in intestinal oxalate secretion, but what accounts for the absorptive oxalate flux remains unknown. We measured transepithelial absorption of [14 C]oxalate simultaneously with the flux of [ 3 H]mannitol, a marker of the paracellular pathway, across intestine from wild-type and Slc26a6-null mice. We used the anion transport inhibitor DIDS to investigate other members of the SLC26 family that may mediate transcellular oxalate absorption. Absorptive flux of oxalate in duodenum was similar to mannitol, insensitive to DIDS, and nonsaturable, indicating that it is predominantly passive and paracellular. In contrast, in wild-type mice, secretory flux of oxalate in duodenum exceeded that of mannitol, was sensitive to DIDS, and saturable, indicating transcellular secretion of oxalate. In Slc26a6-null mice, secretory flux of oxalate was similar to mannitol, and no net flux of oxalate occurred. Absorptive fluxes of both oxalate and mannitol varied in parallel in different segments of small and large intestine. In epithelial cell lines, modulation of the charge selectivity of the claudin-based pore pathway did not affect oxalate permeability, but knockdown of the tight-junction protein ZO-1 enhanced permeability to oxalate and mannitol in parallel. Moreover, formation of soluble complexes with cations did not affect oxalate absorption. In conclusion, absorptive oxalate flux occurs through the paracellular "leak" pathway, and net absorption of dietary oxalate depends on the relative balance between absorption and SLC26A6-dependent transcellular secretion. 22: 224722: -225522: , 201122: . doi: 10.1681 Nephrolithiasis is the second most common chronic kidney condition after hypertension and demonstrates a rising prevalence and association with chronic kidney disease. 1 Calcium oxalate (CaOx) is the predominant component of most stones, and the level of urinary oxalate is an important risk factor for CaOx nephrolithiasis. 2,3 The amount of urinary oxalate depends on the net effect of metabolic production, intestinal absorption, and renal excretion. 4 The integral role of the intestine in oxalate homeostasis becomes most evident in diseases of intestine. Inflammatory bowel disease and small-bowel resections are conditions that are strongly associated with hyperoxaluria and CaOx nephrolithiasis. 5 New insight into the importance of the intestine in the pathogenesis of CaOx nephrolithiasis has come from studies of anion transporter SLC26A6. Slc26a6-null mice have a defect in in- J Am Soc Nephrol

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Urine stone risk factors in nephrolithiasis patients with and without bowel disease

Cited by 110 publications

References 40 publications

Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle

Randall’s plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle

Analysis of the 206M polymorphic variant of the SLC26A6 gene encoding a Cl− oxalate transporter in patients with primary hyperparathyroidism

Net Intestinal Transport of Oxalate Reflects Passive Absorption and SLC26A6-mediated Secretion

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