Abstract
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 modified 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.
Highlights
Malfunction or absence of Sulfate Anion Transporter 1 (SAT-1) or Chloride/Formate EXchanger (CFEX) has been associated with hyperoxaluria and urolithiasis
Crystallisation occurs when the crystalforming materials, such as calcium oxalate (CaOx), calcium phosphate (CaP) or uric acid reach their upper metastable limits, which result in first solid phase precipitations, grow, aggregate, and form stones [4]
In another study [7], approx. 70,000 stones were analyzed during a 10-year period and nearly 80 % were built from CaOx and/or brushite, ~7 % mainly from carbonate and various apatites, ~5 % from urate, and ~1 % from cystine
Summary
Urolithiasis or kidney stone disease (KSD) is a health condition that is rarely life-threatening, but has severe morbidity with a potential lifetime risk for up to 13 % of the general population. Populations prone to disease have larger and coarser crystals, leading to haematuria, pain, and, if not diagnosed on time, formation of sand-like material, gravel, and stones. 70,000 stones were analyzed during a 10-year period and nearly 80 % were built from CaOx and/or brushite, ~7 % mainly from carbonate and various apatites, ~5 % from urate, and ~1 % from cystine. These data indicate that elevating the concentrations of certain compounds in urine can trigger the onset of KSD. While the majority of affected patients show no signs of metabolic disorders that could lead to CaOx supersaturation (idiopathic stone formers), others suffer from hyperparathyroidism or other Ca2+-related metabolic disorders, inflammatory bowel disease, or inherited disorders of oxalate metabolism [10]
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