Oxalate transport by proximal tubule of the rabbit kidney

Senekjian, H. O.; Weinman, Edward J.

doi:10.1152/ajprenal.1982.243.3.f271

Cited by 24 publications

(18 citation statements)

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“…However, these and other studies suggested that more than one secretory system, with different affi nities for oxalate, may be responsible for oxalate handling in mammalian kidneys (129, 137, and 138). The studies of oxalate transport in rabbit kidneys indicated proximal tubules as the main locus of net oxalate secretion, with the S1/S2 and S3 segments having a dominant and minor role, respectively (139). Subsequent experiments linked the Na + -independent transport of SO 4 2-and HCO 3 -in the proximal tubule cell BLM (140, 141) to oxalate, according to which one oxalate is exchanged for one SO 4 2-or two HCO 3 - (142).…”

Section: Figure 3 Transporters Along the Rodent Gastrointestinal Tracmentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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Oxalate urolithiasis (nephrolithiasis) is the most frequent type of kidney stone disease. Epidemiological research has shown that urolithiasis is approximately twice as common in men as in women, but the underlying mechanism of this sex-related prevalence is unclear. Oxalate in the organism partially originate from food (exogenous oxalate) and largely as a metabolic end-product from numerous precursors generated mainly in the liver (endogenous oxalate). Oxalate concentrations in plasma and urine can be modifi ed by various foodstuffs, which can interact in positively or negatively by affecting oxalate absorption, excretion, and/or its metabolic pathways. Oxalate is mostly removed from blood by kidneys and partially via bile and intestinal excretion. In the kidneys, after reaching certain conditions, such as high tubular concentration and damaged integrity of the tubule epithelium, oxalate can precipitate and initiate the formation of stones. Recent studies have indicated the importance of the SoLute Carrier 26 (SLC26) family of membrane transporters for handling oxalate. Two members of this family [Sulfate Anion Transporter 1 (SAT-1; SLC26A1) and Chloride/Formate EXchanger (CFEX; SLC26A6)] may contribute to oxalate transport in the intestine, liver, and kidneys. Malfunction or absence of SAT-1 or CFEX has been associated with hyperoxaluria and urolithiasis. However, numerous questions regarding their roles in oxalate transport in the respective organs and male-prevalent urolithiasis, as well as the role of sex hormones in the expression of these transporters at the level of mRNA and protein, still remain to be answered.

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Section: Figure 3 Transporters Along the Rodent Gastrointestinal Tracmentioning

confidence: 99%

Oxalate: From the Environment to Kidney Stones

Brzica

Breljak

Burckhardt

et al. 2013

Archives of Industrial Hygiene and Toxicology

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“…Perfused segments of the proximal tubule in rabbit demonstrate net oxalate secretion [35]. Anion exchange proteins in the proximal tubule mediate transcellular oxalate excretion and recycling at the brush-border membrane.…”

Section: Renal Handling Of Calcium Phosphate and Oxalatementioning

confidence: 99%

Nephrocalcinosis: molecular insights into calcium precipitation within the kidney

2004

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Nephrocalcinosis may be defined as a generalized increase in the calcium content of the kidneys. This renal calcification may occur at a molecular, microscopic or macroscopic level leading to progressive amounts of renal damage. The major causes include those associated with an increase in urinary levels of calcium, oxalate and phosphate. Under these conditions, urine concentration and supersaturation leads to calcium crystal precipitation, which may be an intratubular event or initiate within the renal interstitium. The focus of discussion concerning renal calcification is often limited to factors that lead to renal stones (calculi and nephrolithiasis); however, nephrocalcinosis is a more sinister event, and often implies a serious metabolic defect. This review will discuss the hypotheses concerning initiating lesions of nephrocalcinosis using available laboratory and clinical studies and will examine whether new understanding of the molecular basis of tubulopathies, that lead to nephrocalcinosis, has given further insights.

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“…The latter transporter functions in multiple exchange modes using oxalate, chloride, formate, sulfate, or bicarbonate as substrates [2,16]. The distal tubule has a minor role in oxalate secretion in rats [19,46] and rabbits [44].…”

Section: Introductionmentioning

confidence: 99%

The liver and kidney expression of sulfate anion transporter sat-1 in rats exhibits male-dominant gender differences

Brzica

Breljak

Krick

et al. 2008

Pflugers Arch - Eur J Physiol

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The sulfate anion transporter (sat-1, Slc26a1) has been cloned from rat liver, functionally characterized, and localized to the sinusoidal membrane in hepatocytes and basolateral membrane (BLM) in proximal tubules (PT). Here, we confirm previously described localization of sat-1 protein in rat liver and kidneys and report on gender differences (GD) in its expression by immunochemical, transport, and excretion studies in rats. The ∼85-kDa sat-1 protein was localized to the sinusoidal membrane in hepatocytes and BLM in renal cortical PT, with the maledominant expression. However, the real-time reversetranscription polymerase chain reaction data indicated no GD at the level of sat-1 mRNA. In agreement with the protein data, isolated membranes from both organs exhibited the male-dominant exchange of radiolabeled sulfate for oxalate, whereas higher oxalate in plasma and 24-h urine indicated higher oxalate production and excretion in male rats. Furthermore, the expression of liver, but not renal, sat-1 protein was: unaffected by castration, upregulated by ovariectomy, and downregulated by estrogen or progesterone treatment in males. Therefore, GD (males > females) in the expression of sat-1 protein in rat liver (and, possibly, kidneys) are caused by the female sexhormone-driven inhibition at the posttranscriptional level. The male-dominant abundance of sat-1 protein in liver may conform to elevated uptake of sulfate and extrusion of oxalate, causing higher plasma oxalate in males. Oxalate is then excreted by the kidneys via the basolateral sat-1 (males > females) and the apical CFEX (Slc26a6; GD unknown) in PT and eliminated in the urine (males > females), where it may contribute to the male-prevailing development of oxalate urolithiasis.

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Oxalate transport by proximal tubule of the rabbit kidney

Cited by 24 publications

References 0 publications

Oxalate: From the Environment to Kidney Stones

Oxalate: From the Environment to Kidney Stones

Nephrocalcinosis: molecular insights into calcium precipitation within the kidney

The liver and kidney expression of sulfate anion transporter sat-1 in rats exhibits male-dominant gender differences

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