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

BACKGROUND: 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 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. 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 nonoliguric AKI. Smoking, no acetylsalicylic acid use, and lower diastolic blood pressure are the clinical risk factors for AKI during iloprost treatment.

The Effect of Hepatitis B Virus on Graft and Overall Survival in Kidney Transplant Patients.

OBJECTIVES: We investigated the effect of hepatitis B virus in kidney transplant patients in terms of patient care and survival. MATERIALS AND METHODS: We retrospectively analyzed kidney transplant patients from 1993 to 2013. A control group with negative serology was selected. The hepatitis B virus-positive group was divided into 2 subgroups based on serologic status, treatments, and treatment responses. Group A had viral suppression, and group B had hepatitis B virus DNA persistence. Overall and allograft survival rates were compared. RESULTS: We identified 32 hepatitis B virus-positive and 74 hepatitis B virus-negative patients. Positive group was treated with lamivudine (n = 23), lamivudine plus entecavir (n = 4), lamivudine plus tenofovir (n = 4), or lamivudine plus entecavir and tenofovir (n = 1). In group A (n = 15), antiviral treatment was given based on the presence of either hepatitis B surface antigen with negative hepatitis B virus DNA (n = 11) or hepatitis B virus DNA positivity (n = 4). Group B patients (n = 17) received antiviral treatment for persistence of hepatitis B virus DNA (n = 7) or for viral reactivation (ie, recurrence of hepatitis B virus DNA) (n = 10). Groups A and B did not differ significantly in terms of graft or overall survival. Liver biopsy was performed in 17 patients; 3 patients had high-grade fibrosis or cirrhosis, and 14 patients had normal histology or mild hepatitis. Median graft survival time was longer in positive group (69.5 mo vs 54 mo; P = .007). Five- and 10-year overall survival rates were comparable (89%-84% vs 96%-96%; P = .107). CONCLUSIONS: Hepatitis B virus-positive kidney transplant patients have increased liver transaminase levels, longer graft survival times, and similar median overall survival rates compared with hepatitis B virus-negative patients.