Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392525 (nephrolithiasis)
2,669 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Immediate and long-term effects of extracorporeal shock-wave lithotripsy (ESWL) on urine enzymes were studied in 200 patients with nephrolithiasis (NL). The patients had abnormally high urine excretion of AP, GGT, APA, LDH and NAG, whereas aminotransferases excretion was low. Pathobiochemical and diagnostic implications of these findings are discussed. Immediately after its conduction ESWL entails a mild injury to tubular portion of the nephron. The causes of long-term stay of enzymuria after ESWL in NL patients are discussed.
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PMID:[The effect of extracorporeal shockwave lithotripsy on the indices of urinary enzymes in nephrolithiasis patients]. 938 10

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

Increasing intracellular calcium ion concentration in the cytoplasm is the starting point in the activation of cell death. Regulation of these pathological processes in various organs and tissues is possible using agents from the group of calcium antagonists. This study was aimed at assessing the level of urinary excretion of two enzymes, lactate dehydrogenase (LDH, EC 1.1.1.27) and y-glutamyltransferase (GGT, EC 2.3.2.2), calcium antagonists in an experimental model of nephrolithiasis and finding ways to pharmacological protection of the kidneys. It established that the use of calcium antagonists can reduce the excretion of LDH by 20% and the excretion of GGT by more than 40%.
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PMID:[Experimental nephrolithiasis: nephroprotective effect of calcium antagonists]. 2370 Jun 64