Oxalate as a potent promoter of kidney stone formation

Abstract

Kidney stones are among the most prevalent urological diseases, with a high incidence and recurrence rate. Treating kidney stones has been greatly improved by the development of various minimally invasive techniques. Currently, stone treatment is relatively mature. However, most current treatment methods are limited to stones and cannot effectively reduce their incidence and recurrence. Therefore, preventing disease occurrence, development, and recurrence after treatment, has become an urgent issue. The etiology and pathogenesis of stone formation are key factors in resolving this issue. More than 80% of kidney stones are calcium oxalate stones. Several studies have studied the formation mechanism of stones from the metabolism of urinary calcium, but there are few studies on oxalate, which plays an equally important role in stone formation. Oxalate and calcium play equally important roles in calcium oxalate stones, whereas the metabolism and excretion disorders of oxalate play a crucial role in their occurrence. Therefore, starting from the relationship between renal calculi and oxalate metabolism, this work reviews the occurrence of renal calculi, oxalate absorption, metabolism, and excretion mechanisms, focusing on the key role of SLC26A6 in oxalate excretion and the regulatory mechanism of SLC26A6 in oxalate transport. This review provides some new clues for the mechanism of kidney stones from the perspective of oxalate to improve the understanding of the role of oxalate in the formation of kidney stones and to provide suggestions for reducing the incidence and recurrence rate of kidney stones.

Solid Electrochemiluminescence Sensor by Immobilization of Emitter Ruthenium(II)tris(bipyridine) in Bipolar Silica Nanochannel Film for Sensitive Detection of Oxalate in Serum and Urine

“…In patients with gout, abnormal metabolism or insufficient excretion of oxalate ions leads to an elevated level of oxalate ions in the blood, triggering the deposition of oxalate crystals in the joints, causing arthritis. The concentration of oxalate ions in urine is also associated with the formation of urinary stones [ 7 , 8 , 9 ]. As oxalate ions are primarily excreted through the kidneys, the level of oxalate ions in the blood is closely related to renal function.…”

Mechanism of Porphyra Yezoensis Polysaccharides in Inhibiting Hyperoxalate-Induced Renal Injury and Crystal Deposition

“…Kidney stone is a globally prevalent disease, and its incidence and recurrence rates are increasing year by year. , The incidence and prevalence of kidney stones was up to 14.8% and a recurrence rate of up to 50% within the first 5 years of the initial stone episode . Oxalate is a common metabolic end product and a key component of most clinically detected calcium oxalate (CaOx) kidney stones. , …”

“…3 Oxalate is a common metabolic end product and a key component of most clinically detected calcium oxalate (CaOx) kidney stones. 4,5 Oxidative stress injury to renal epithelial cells serves as the initiating factor and underlying lesion for the formation of calcium oxalate (CaOx) stones. Prolonged exposure of renal tubular epithelial cells to high levels of oxalate and the presence of CaOx microcrystals lead to excessive production of reactive oxygen species (ROS), which contributes further to oxidative stress damage in the cells.…”

Estrogen’s Tissue-Specific Regulation of the SLC26A6 Anion Transporter Reveal a Phenotype of Kidney Stone Disease in Estrogen-Deficient Females: A Systematic Review

“…Studies have shown that a defect in the PAT1 can lead to hyperoxalemia, hyperoxaluria, and the formation of oxalate stones [ 13 ]. This occurs because the deficiency of PAT1-mediated oxalate secretion in the intestine leads to an increase in the net absorption of oxalate, which results in an increase in the concentration of oxalate in the plasma and a higher level of oxalate excreted in the urine.…”

“…This occurs because the deficiency of PAT1-mediated oxalate secretion in the intestine leads to an increase in the net absorption of oxalate, which results in an increase in the concentration of oxalate in the plasma and a higher level of oxalate excreted in the urine. In contrast, the overexpression of PAT1 in the intestine can reduce the oxalate concentration in the urine and prevent kidney stone formation [ 13 ]. Therefore, regulating PAT1 expression could be a potential target for treating and preventing kidney stones.…”