Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The consumption of oxygen by slices of kidney tissue of dogs made hypertensive by the Goldblatt technique was studied manometrically. The respiration of the ischemic kidney tissue was found to be much less than that of the normal kidney. Further, a marked reduction in oxidizing ability, as measured by the oxygen uptake and ammonia formation in the presence of the added amines and amino acids, tyramine, isoamylamine, dl-alanine, and l-aspartic acid, was observed. Extracts of the kidneys were made and tested for amine oxidase, amino acid oxidase, and polyphenol oxidase activity by measuring the increased oxygen consumption and ammonia formation in the presence of the substrates listed above with the addition of l-epinephrine, histamine, and dl- and l-dihydroxyphenylalanine. The preparations from ischemic kidneys of dogs and rabbits showed much lower activity. Animals with varying degrees of constriction of the renal arteries and therefore varying degrees of renal ischemia were prepared and studied. The results with these animals suggested a direct relationship between the degree of renal ischemia and the decrease in oxidizing power of the tissue. The product of the enzymic oxidation of tyramine was identified as p-hydroxyphenylacetaldehyde by isolation as the dinitrophenylhydrazone of p-hydroxyphenylacetaldehyde.
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PMID:THE METABOLISM OF THE ISCHEMIC KIDNEY : I. THE RESPIRATION AND THE OXIDASE ACTIVITY OF THE ISCHEMIC KIDNEY. 1987 11

Elevated levels of plasma catecholamines accompany ischemic AKI, possibly contributing the inflammatory response. Renalase, an amine oxidase secreted by the proximal tubule, degrades circulating catecholamines and reduces myocardial necrosis, suggesting that it may protect against renal ischemia reperfusion injury. Here, mice subjected to renal ischemia reperfusion injury had significantly lower levels of renalase in the plasma and kidney compared with sham-operated mice. Consistent with this, plasma NE levels increased significantly after renal ischemia reperfusion injury. Furthermore, renal tubular inflammation, necrosis, and apoptosis were more severe and plasma catecholamine levels were higher in renalase-deficient mice subjected to renal ischemia reperfusion compared with wild-type mice. Administration of recombinant human renalase reduced plasma catecholamine levels and ameliorated ischemic AKI in wild-type mice. Taken together, these data suggest that renalase protects against ischemic AKI by reducing renal tubular necrosis, apoptosis, and inflammation, and that plasma renalase might be a biomarker for AKI. Recombinant renalase therapy may have potential for the prevention and treatment of AKI.
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PMID:Renalase protects against ischemic AKI. 2339 18