A Jörres, C Chiabrando, O Kordonouri, A Schiessler, S Hess, S Farke, G M Gahl, C Müller, L Rivoltella, R Djurup
{"title":"Thromboxane B2 urinary metabolites in patients undergoing cardiopulmonary bypass.","authors":"A Jörres, C Chiabrando, O Kordonouri, A Schiessler, S Hess, S Farke, G M Gahl, C Müller, L Rivoltella, R Djurup","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>The urinary excretion of selected markers for renal injury and thromboxane metabolites was studied in 16 patients undergoing cardiopulmonary bypass (CPB). Excretion of both tubular and glomerular markers sharply increased on day 1 after CPB and remained elevated throughout the observation period (five days). Immunoreactive thromboxane B2 (i-TXB2, mainly reflecting 2,3-dinor-TXB2) and immunoreactive 11-keto-thromboxane B2 (i-11-keto-TXB2) were measured by direct enzyme immunoassays. TXB2, 2,3-dinor-TXB2 and 11-keto-TXB2 were also measured in selected samples by GC-MS. Urinary excretion rates of both i-TXB2 and i-11-keto-TXB2 markedly increased on day 1 after surgery and decreased thereafter. Following CPB, excretion rates of 2,3-dinor-TXB2 and TXB2 displayed parallel changes, suggesting that in these patients most urinary TXB2 derives from blood platelets rather than the kidney. Taken together, our observations do not support the hypothesis that acute renal injury observed after CPB is caused by exaggerated thromboxane biosynthesis in the kidney.</p>","PeriodicalId":11520,"journal":{"name":"Eicosanoids","volume":"5 3-4","pages":"147-51"},"PeriodicalIF":0.0000,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Eicosanoids","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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Abstract
The urinary excretion of selected markers for renal injury and thromboxane metabolites was studied in 16 patients undergoing cardiopulmonary bypass (CPB). Excretion of both tubular and glomerular markers sharply increased on day 1 after CPB and remained elevated throughout the observation period (five days). Immunoreactive thromboxane B2 (i-TXB2, mainly reflecting 2,3-dinor-TXB2) and immunoreactive 11-keto-thromboxane B2 (i-11-keto-TXB2) were measured by direct enzyme immunoassays. TXB2, 2,3-dinor-TXB2 and 11-keto-TXB2 were also measured in selected samples by GC-MS. Urinary excretion rates of both i-TXB2 and i-11-keto-TXB2 markedly increased on day 1 after surgery and decreased thereafter. Following CPB, excretion rates of 2,3-dinor-TXB2 and TXB2 displayed parallel changes, suggesting that in these patients most urinary TXB2 derives from blood platelets rather than the kidney. Taken together, our observations do not support the hypothesis that acute renal injury observed after CPB is caused by exaggerated thromboxane biosynthesis in the kidney.
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