Iloprost as an acute kidney injury-triggering agent in severely atherosclerotic patients.

Abstract

SummaryBackgroundIloprost, 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.MethodsEighty-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 μmol/l) increase in creatinine levels from baseline within 48 hours.Results:Cr2 (1.46 ± 0.1 mg/dl) (129.06 ± 8.84 μmol/l) and Cr3 (1.53 ± 0.12 mg/dl) (135.25 ± 10.61 μmol/l) creatinine levels were significantly higher compared to the initial value (1.15 ± 0.6 mg/dl) (101.66 ± 53.04 μmol/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 cm3) and diastolic blood pressure significantly decreased (70.07 ± 15.50 vs 74.14 ± 9.42 mmHg) from their initial values.ConclusionWhile iloprost treatment is effective in patients with PAD who are not suitable for surgery, severe systemic vasodilatation can cause renal ischaemia, resulting in nonoliguric AKI. Smoking, no acetylsalicylic acid use, and lower diastolic blood pressure are the clinical risk factors for AKI during iloprost treatment.