Antioxidant Signal and Kidney Injury Molecule-1 Levels in Shockwave Lithotripsy Induced Kidney Injury

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dc.contributor.authorHatipoglu, Namik Kemal
dc.contributor.authorEvliyaoglu, Osman
dc.contributor.authorIsik, Birgul
dc.contributor.authorBodakci, Mehmet Nuri
dc.contributor.authorBozkurt, Yasar
dc.contributor.authorSancaktutar, Ahmet Ali
dc.contributor.authorSoylemez, Haluk
dc.date.accessioned2024-04-24T17:08:01Z
dc.date.available2024-04-24T17:08:01Z
dc.date.issued2014
dc.departmentDicle Üniversitesien_US
dc.description.abstractPurpose: Shockwave lithotripsy (SWL) induces acute kidney injury (AKI) that extends from the papilla to the outer cortex by causing ischemia and the production of nephrotoxic agents. Direct ischemic damage and the generation of free radicals cause injury to the proximal tubular cells. Kidney injury molecule-1 (KIM-1) is a transmembrane glycoprotein that is upregulated in proximal tubular cells after ischemic or nephrotoxic injury and is not expressed in healthy kidneys. We evaluated the extent of free radical production in response to SWL by measuring urinary total antioxidant capacity (TAC) and total oxidant status (TOS). Furthermore, we investigated the severity of SWL-induced kidney injury by measuring KIM-1 expression levels. Patients and Methods: The study population comprised 30 patients who were carefully selected and 30 age and sex matched control subjects. All patients received the same SWL procedure. Midstream urine samples were collected from patients before SWL and at 120 minutes after SWL. Urine KIM-1 levels were measured by enzyme-linked immunosorbent assay, and TAC and TOS were measured via spectrophotometry. Results: Mean levels of TAC (2.880.56mmolTxEq/L),TOS (8.27 +/- 1.57molH(2)O(2)Eq/L), and KIM-1 (0.55 +/- 0.08ng/mL) before SWL were not significantly different from mean TAC, TOS, and KIM-1 levels measured from the control group at 2.81 +/- 0.42mmolTxEq/L, 10.73 +/- 1.4molH(2)O(2)Eq/L, and 0.51 +/- 0.07ng/mL, respectively. Two hours after SWL, mean urine TAC levels (2.81 +/- 0.85mmolTxEq/L, P=0.02) were decreased and mean KIM-1 expression (0.85 +/- 0.11ng/mL, P=0.01) was significantly increased, but there was no significant difference in mean TOS levels (11.24 +/- 1.9molH(2)O(2)Eq/L, P=0.627) compared with the control group. Conclusions: The increased burden of free radical oxidants in the setting of decreasing antioxidant capacity may be one of the initial indicators of AKI after SWL. Moreover, KIM-1 demonstrates great potential as an early and noninvasive biomarker of SWL-induced kidney injury.en_US
dc.identifier.doi10.1089/end.2013.0535
dc.identifier.endpage228en_US
dc.identifier.issn0892-7790
dc.identifier.issn1557-900X
dc.identifier.issue2en_US
dc.identifier.pmid24044353
dc.identifier.scopus2-s2.0-84893469539
dc.identifier.scopusqualityQ1
dc.identifier.startpage224en_US
dc.identifier.urihttps://doi.org/10.1089/end.2013.0535
dc.identifier.urihttps://hdl.handle.net/11468/17158
dc.identifier.volume28en_US
dc.identifier.wosWOS:000330312200020
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherMary Ann Liebert, Incen_US
dc.relation.ispartofJournal of Endourology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subject[No Keyword]en_US
dc.titleAntioxidant Signal and Kidney Injury Molecule-1 Levels in Shockwave Lithotripsy Induced Kidney Injuryen_US
dc.titleAntioxidant Signal and Kidney Injury Molecule-1 Levels in Shockwave Lithotripsy Induced Kidney Injury
dc.typeArticleen_US

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