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Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under severe hyperoxaluric conditions calcium oxalate crystals often deposit in the renal interstitium and produce localized inflammation. We have proposed that renal epithelial cells exposed to CaOx crystals produce chemoattractants such as monocyte chemoattractant protein-1 (MCP-1). MCP-1 synthesis is mediated by reactive oxygen species (ROS). HK-2 cells of human renal epithelial line were exposed to CaOx crystals for different lengths of time. The culture media was tested for cell injury marker LDH, and subjected to enzyme-linked immunosorbent assay to determine the secretion of MCP-1 protein. Cell expression of MCP-1 was assessed by Western blot analysis. Gene expression was determined by reverse transcriptase-polymerase chain reaction. The data clearly showed that the HK-2 cells express MCP-1 gene and protein. The MCP-1 mRNA expression was increased following exposure to CaOx crystals, which was reduced upon treatment with free radical scavengers, catalase and superoxide dismutase. Results indicate that CaOx crystals strongly induce MCP-1 synthesis and secretion by the HK-2 cells and production is mediated by intracellular ROS production. Based on these and other data, antioxidant therapy and blockade of rennin-angiotensin system may prove beneficial for the prevention of end stage renal disease caused by hyperoxaluria and CaOx crystal deposition.
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PMID:Reactive oxygen species mediated calcium oxalate crystal-induced expression of MCP-1 in HK-2 cells. 1639 73

Experimental animal model studies suggest that calcium oxalate (CaOx) crystal deposition in the kidneys is associated with the development of oxidative stress, epithelial injury and inflammation. There is increased production of inflammatory molecules including osteopontin (OPN), monocyte chemoattractant protein-1 (MCP-1) and various subunits of inter-alpha-inhibitor such as bikunin. What does the increased production of such molecules suggest? Is it a cause or consequence of crystal deposition? We hypothesized that over-expression and increased production of MCP-1 is a result of the interaction between renal epithelial cells and CaOx crystals after their deposition in the renal tubules. We induced hyperoxaluria in MCP-1 null as well as wild type mice and examined pathological changes in their kidneys and urine. Both wild type and MCP-1 null male mice became hyperoxaluric and demonstrated CaOx crystalluria. Neither of them developed crystal deposits in their kidneys. Both showed some morphological changes in their renal proximal tubules. Significant pathological changes such as cell death and increased urinary excretion of LDH were not seen. Results suggest that at least in mice (1) Increase in oxalate and decrease in citrate excretion can lead to CaOx crystalluria but not CaOx nephrolithiasis; (2) MCP-1 does not play a role in crystal retention within the kidneys; (3) Expression of OPN and MCP-1 is not increased in the kidneys in the absence of crystal deposition; (4) Crystal deposition is necessary for significant pathological changes and movement of monocytes and macrophages into the interstitium.
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PMID:Experimentally induced hyperoxaluria in MCP-1 null mice. 2116 47