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dc.contributor.authorUyar, Mehtap Erkmen
dc.contributor.authorYucel, Piril
dc.contributor.authorIlin, Sena
dc.contributor.authorBal, Zeynep
dc.contributor.authorYildirim, Saliha
dc.contributor.authorUyar, Ahmet Senol
dc.contributor.authorAkay, Tankut
dc.contributor.authorTutal, Emre
dc.contributor.authorSezer, Siren
dc.date.accessioned2019-06-21T11:06:30Z
dc.date.available2019-06-21T11:06:30Z
dc.date.issued2016
dc.identifier.issn1995-1892
dc.identifier.urihttp://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC5101430&blobtype=pdf
dc.identifier.urihttp://hdl.handle.net/11727/3673
dc.description.abstractBackground: Iloprost, a stable prostacyclin analog, is used as a rescue therapy for severe peripheral arterial disease (PAD). It has systemic vasodilatory and anti-aggregant effects, with severe vasodilatation potentially causing organ ischaemia when severe atherosclerosis is the underlying cause. In this study, we retrospectively analysed renal outcomes after iloprost infusion therapy in 86 patients. Methods: Eighty-six patients with PAD who received iloprost infusion therapy were retrospectively analysed. Clinical and biochemical parameters were recorded before (initial, Cr1), during (third day, Cr2), and after (14th day following the termination of infusion therapy, Cr3) treatment. Acute kidney injury (AKI) was defined according to KDIGO guidelines as a >= 0.3 mg/dl (26.52 mu mol/l) increase in creatinine levels from baseline within 48 hours. Results: Cr2 (1.46 +/- 0.1 mg/dl) (129.06 +/- 8.84 mu mol/l) and Cr3 (1.53 +/- 0.12 mg/dl) (135.25 +/- 10.61 mu mol/l) creatinine levels were significantly higher compared to the initial value (1.15 +/- 0.6 mg/dl) (101.66 +/- 53.04 mu mol/l). AKI was observed in 36 patients (41.86%) on the third day of iloprost infusion. Logistic regression analysis revealed smoking and not using acetylsalicylic acid as primary predictors (p = 0.02 and p = 0.008, respectively) of AKI during iloprost treatment. On the third infusion day, patients' urinary output significantly increased (1813.30 +/- 1123.46 vs 1545.17 +/- 873.00 cm(3)) and diastolic blood pressure significantly decreased (70.07 +/- 15.50 vs 74.14 +/- 9.42 mmHg) from their initial values. Conclusion: While iloprost treatment is effective in patients with PAD who are not suitable for surgery, severe systemic vasodilatation can cause renal ischaemia, resulting in non-oliguric AKI. Smoking, no acetylsalicylic acid use, and lower diastolic blood pressure are the clinical risk factors for AKI during iloprost treatment.en_US
dc.language.isoengen_US
dc.relation.isversionof10.5830/CVJA-2015-051en_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectIloprosten_US
dc.subjectAcute kidney injuryen_US
dc.subjectSevere atherosclerosisen_US
dc.titleIloprost as an acute kidney injury-triggering agent in severely atherosclerotic patientsen_US
dc.typearticleen_US
dc.relation.journalCARDIOVASCULAR JOURNAL OF AFRICAen_US
dc.identifier.volume27en_US
dc.identifier.issue3en_US
dc.identifier.startpage128en_US
dc.identifier.endpage133en_US
dc.identifier.wos000384800800007


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