Disease relevance of oxalic acid

• We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones [1].
• Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6 [2].
• BACKGROUND: Patients with cystic fibrosis have an increased risk of hyperoxaluria, and of subsequent nephrocalcinosis and calcium-oxalate urolithiasis [3].
• Calcium oxalate microcrystalline-associated arthritis in end-stage renal disease [4].
• Thus, radiographically typical chondrocalcinosis may be due to calcium oxalate [4].

Psychiatry related information on oxalic acid

• Dietary habits, particularly a high sodium intake, may commonly contribute to hypercalciuria in patients with calcium oxalate stones [5].
• OBJECTIVE: To evaluate the circadian fluctuations in the risk of urinary calcium oxalate stone formation with regard to critical periods of crystallization [6].

High impact information on oxalic acid

• A new study shows that Slc26a6-null mice manifest calcium-oxalate nephrolithiasis accompanied by enhanced net intestinal oxalate absorption [7].
• In a double-blind study, we examined the efficacy of allopurinol in the prevention of recurrent calcium oxalate calculi of the kidney [8].
• Saturation-inhibition index as a measure of the risk of calcium oxalate stone formation in the urinary tract [9].
• Intermittent peritoneal dialysis may be less efficient than hemodialysis in clearing oxalate, and physicians should now consider calcium oxalate-associated arthritis in patients undergoing peritoneal dialysis who are not receiving large doses of ascorbic acid [10].
• Pulverized calcium oxalate renal stones were extracted with 0.05 M EDTA, pH 8.0; nephrocalcin eluted in five peaks using DEAE-cellulose column chromatography, and each peak was further resolved by Sephacryl S-200 column chromatography [11].

Chemical compound and disease context of oxalic acid

• We have determined that the organic matrix of calcium oxalate kidney stones contains a glycoprotein inhibitor of calcium oxalate crystal growth (nephrocalcin) that resembles nephrocalcin present in the urine of patients with calcium oxalate stones and differs from nephrocalcin from the urine of normal people [11].
• This paper reports the presence of Gla in the EDTA-soluble, nondialyzable proteins of calcium-containing renal calculi including calcium oxalate, hydroxyapatite, and mixed stores of apatite and struvite (MgNH4PO4) [12].
• Isolation from human calcium oxalate renal stones of nephrocalcin, a glycoprotein inhibitor of calcium oxalate crystal growth. Evidence that nephrocalcin from patients with calcium oxalate nephrolithiasis is deficient in gamma-carboxyglutamic acid [11].
• Piridoxilate-associated calcium oxalate urinary calculi: a new metabolic drug-induced nephrolithiasis [13].
• A variety of factors influence the formation of calcium oxalate kidney stones, including gender, diet, and urinary excretion of calcium, oxalate, and uric acid [14].

Biological context of oxalic acid

• In the presence of the inhibitor, the kinetics of calcium oxalate monohydrate crystal growth inhibitor showed that the macromolecule binds to the crystal surface according to a Langmuir adsorption isotherm with a dissociation constant, Kd = 5.3 X 10(-7) M [15].
• A low level of endogenous casein kinase II activity was found in crude preparations of cardiac SR but did not co-purify with SR vesicles after calcium oxalate loading, suggesting that casein kinase II phosphorylation in vivo occurs at a site other than the SR [16].
• 0. Ca2+ ions, which were transported into vesicles under conditions resulting in low coupling ratios, were retained as the calcium oxalate precipitate, following complete hydrolysis of substrate [17].
• Once present on the cell surface, calcium oxalate monohydrate, calcium oxalate dihydrate, and hydroxyapatite crystals are quickly internalized by renal cells; alterations in gene expression and initiation of proliferation may then ensue [18].
• It is characterized by an elevated anion gap metabolic acidosis, osmolal gap, calcium oxalate crystals in the urine, and a well-defined clinical picture [19].

Anatomical context of oxalic acid

• The buoyant density of the sarcoplasmic reticulum (SR) microsomes was increased after loading them with calcium oxalate [20].
• The concave microsomal fracture faces of purified microsomes which did not load calcium oxalate had particle distributions nearly identical to the distributions of intact P-face T tubules [20].
• The factors influencing accumulation of calcium in the endoplasmic reticulum were evaluated by a semiquantitative approach based on determining the relative frequency of calcium oxalate crystals under varying conditions [21].
• In one patient, calcium oxalate crystals were also identified within synovium and cartilage [4].
• We report the identification of calcium oxalate crystals in the synovial fluid of three patients with chronic renal failure [4].

Associations of oxalic acid with other chemical compounds

• The uptake is augmented by oxalate and, based on identification of calcium oxalate crystals by electron microscopy and electron probe analysis, is localized to the sarcoplasmic reticulum (SR) [22].
• To isolate protein(s) that may participate in crystal attachment, apical membranes of cultured renal inner medullary collecting duct were biotinylated, the cells were lysed with detergent, the lysate was subjected to hydroxyapatite chromatography, and fractions were incubated with calcium oxalate monohydrate [23].
• Moreover, citrate inhibited calcium oxalate crystallization by complexing calcium and lowering calcium oxalate saturation [24].
• These proteins function as Kunitz-type serine protease inhibitors and appear capable of inhibiting calcium oxalate (CaOx) crystallization in vitro [25].
• Dissolved urate salts out calcium oxalate in undiluted human urine in vitro: implications for calcium oxalate stone genesis [26].

Gene context of oxalic acid

• Increased expression of monocyte chemoattractant protein-1 (MCP-1) by renal epithelial cells in culture on exposure to calcium oxalate, phosphate and uric acid crystals [27].
• Associations between calcium oxalate stone disease and the CAG repeats in AR gene and TA repeats in ER gene were then evaluated [28].
• Both Ox and CaOx crystals selectively activate p38 mitogen-activated protein kinase (MAPK) in exposed tubular cells [29].
• Vascular endothelial growth factor gene polymorphism is associated with calcium oxalate stone disease [30].
• Arginine form of p21 gene codon 31 is less prominent in patients with calcium oxalate stone [31].

Analytical, diagnostic and therapeutic context of oxalic acid

• Under the same conditions of dietary and fluid intake the urine samples of the patients with stone formation were more supersaturated with calcium oxalate (P less than 0.001) and had lower concentrations of protective inhibitors of crystallization (P less than 0.001) than those of the controls [9].
• Arthritis associated with calcium oxalate crystals in an anephric patient treated with peritoneal dialysis [10].
• Second, the concentration product ratio (CPR), the ratio of the measured calcium oxalate concentration product before to that after incubation of the sample with calcium oxalate monohydrate crystal, was measured in seven uremic and seven normal serum ultrafiltrates [32].
• We describe 4 patients who, during the course of long-term hemodialysis, developed calcium oxalate crystal deposits in the synovium and skin [33].
• Using ryanodine-mediated calcium oxalate loading of SR vesicles followed by density gradient centrifugation, we have shown that calnexin is a bona fide SR protein and an integral constituent of both junctional and free SR vesicles [34].

References