Disease relevance of oxalic acid

• BACKGROUND: Human urine is known to inhibit growth, aggregation, nucleation, and cell adhesion of calcium oxalate monohydrate (COM) crystals, the main solid phase of human kidney stones [1].
• After the optimal parameters were determined we studied the disintegrative efficacy of THSWL for 3 types of human urinary calculi, including COM, calcium hydrogen phosphate (brushite) and cystine [2].
• BACKGROUND: Deposition of crystals within tubular lumens is a feature of many kidney stone diseases, including crystals of calcium oxalate monohydrate (COM) in primary hyperoxaluria and of 2,8-dihydroxyadenine (DHA) in adenine phosphoribosyltransferase deficiency [3].

High impact information on oxalic acid

• In summary, inhibiting activation of p38 MAPK pathway abrogated the DNA synthesis in response to COM crystals [4].
• Interaction of calcium oxalate monohydrate (COM) crystals with renal cells has been shown to result in altered gene expression, DNA synthesis, and cell death [4].
• The nucleation and growth of calcium oxalate monohydrate (COM) crystals were studied using the constant composition kinetics technique, in solution supersaturated with respect to COM (sigmaCOM = 1.44) [5].
• The initial growth rate of COM on pure HAP particles, Rm approximately/= 0.56 X 10(-7) mol/min per m2, was slower than that for HAP surfaces preadsorbed with albumin, 2.14 x 10(-7) mol/min per m2 [5].
• Coated COM crystals from male controls contained 3.5-fold more Tamm-Horsfall protein (THP) than SF subjects (P < 0.01) [6].

Biological context of oxalic acid

• Exposure of cells to COM crystals (20 microg/cm(2)) rapidly stimulated strong phosphorylation and activation of p38 mitogen-activated protein kinase (p38 MAP kinase) and re-initiation of DNA synthesis [4].
• However, isoforms C and D act as promotors for COM crystal growth-kidney stone formation [7].
• For instance, calcium oxalate dihydrate (COD) was more frequent in men than in women, with a sex ratio of 4.97 versus 2.57 for calcium oxalate monohydrate (COM) [8].
• They were heat sensitive, showed antibiotic resistance and accelerated COM crystallization [9].

Anatomical context of oxalic acid

• These data are the first demonstrations of activation of the p38 MAPK signaling pathway by COM crystals and suggest that, in response to COM crystals, this pathway transduces critical signals governing the re-initiation of DNA synthesis in renal epithelial cells [4].
• Whereas to our knowledge the binding molecules for COM at the surface of LLC-PK1 cells are still unknown, crystals adhere to the hyaluronan (HA) rich pericellular matrix transiently expressed by mobile MDCK-I cells [10].

Associations of oxalic acid with other chemical compounds

• Patients who form COM stones produce abnormal NC molecules that lack gamma-carboxyglutamic acid and fail to inhibit COM crystallizations normally [11].
• CONCLUSIONS: Decreased THP and citrate excretions were found in CaOx stone-forming patients [12].
• METHODS: Quantitative determination of THP in calcium oxalate (CaOx) stone-forming patients and healthy subjects was carried out according to the enzyme-linked immunosorbent assay method [12].
• Saponins (aescin and glycyrrhinic acid) only exhibited important inhibitory effects of COM crystallization on the hydrophobic wax substrate but in no case the formation of COM crystals was totally prevented [13].
• BACKGROUND: Renal tubular fluid in the distal nephron is supersaturated with calcium and oxalate ions that nucleate to form crystals of calcium oxalate monohydrate (COM), the most common crystal in renal stones [14].

Gene context of oxalic acid

• COM crystal coating by urinary prothrombin fragment 1 (UPTF1, P < 0.05) and crystal adhesion inhibitor (CAI) (P= 0.09) correlated with decreased crystal binding to cells, whereas coating with osteopontin (OPN) correlated with increased adhesion tendency (P < 0.05) [6].
• CONCLUSION: Urinary macromolecules >10 kD coat COM crystals and block their adhesion to renal cells [6].

Analytical, diagnostic and therapeutic context of oxalic acid

• In order to identify responsible macromolecule(s), calcium oxalate monohydrate (COM) crystals were coated with U(conc) and adherent proteins then released and probed by Western blot [6].
• Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis were performed to assess whether the crystals became coated with urine derived proteins RESULTS: Western blot analysis demonstrated that pretreated COM crystals were covered with protein inhibitors of crystallization [10].
• RESULTS: The COM-coated stent mineralized upon immersion in the supersaturated solutions [15].
• In these experiments SEM and X-ray crystallography showed a high percentage of CaOx in the precipitate [16].
• The aim of this paper is to clarify some of these questions by studying the regrowth achieved by real spontaneously passed post-extracorporeal shock wave lithotripsy (post-ESWL) fragments of calcium oxalate monohydrate (COM) renal calculi [17].

References