31 - A Prospective Study on Colistin Plasma Concentration and Risk of Acute Kidney Injury(AKI) in Sick Neonates

Poster Number: 31
Publication Number: 31.1824

Background: Colistin is a vital antibiotic used in sick newborns, and it is associated with acute kidney injury (AKI), which is an important contributor to neonatal morbidity and mortality. As there is a paucity of studies on colistin levels in neonates, this study would be the first such study which helps us to understand the correlation of steady-state concentrations of colistin with the development of nephrotoxicity in newborns.

Objective: To study colistin-induced AKI and explore the correlation of steady-state plasma concentration of colistin with the development of AKI in sick neonates.

Design/Methods: In this prospective study, sick neonates who received colistin within the first 28 days of life admitted in a level 3, tertiary center over one year were studied. Major congenital malformations, neonates surviving ≤ 72 hours, and renal malformations were excluded. WHO-UMC (World Health Organization-Uppsala Monitoring Center) criteria was used for the causality assessment of colistin-induced AKI. Steady-state colistin levels were collected after 6 doses of colistin administration and measured by LCMS (liquid chromatographic-mass spectrometry). AKI was defined as per KDIGO guidelines. Neonatal sickness details were recorded.

Results: Forty sick neonates were enrolled, mean (SD) gestational age was 29.3 (3.08) weeks, and AKI was seen in 28/40(70%) cases. Colistin-induced nephrotoxicity as assessed by WHO causality criteria, “Possible” colistin-induced AKI was seen in 10/28(35%), cases were categorized as “unlikely” if the neonate had AKI prior to starting of colistin or developed AKI after 1 week of stopping colistin, 16/28 (57%) were categorized as unlikely. Median (IQR) steady state colistin level was 1.08mg/L (0.53,2.53). It was higher in “possible” (2.1 mg/L) compared to “unlikely” (0.9 mg/L) and non-AKI groups (1.1 mg/L). The time between completion of colistin infusion and sampling was a median of 1.5 hours and a median of 6 doses were completed before sampling. The mean duration of colistin use was 10 days. Urea and creatinine for 19 cases were assessed after 5 days of stopping colistin, and 2/19 (10%) of them had Azotemia even after discontinuation of colistin. Death was seen in 13/40 (33%) cases.

Conclusion(s): “Possible” colistin-induced AKI was seen in 10/28 (35%) cases. Median steady-state colistin levels were higher in the “possible” group compared to unlikely/Unassessable and non-AKI groups.