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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Colistin is essential against multidrug-resistant gram-negative infections but can cause acute kidney injury (AKI) in up to 70% of patients. Conventional colistin dosing based on creatinine clearance by the Cockcroft–Gault equation (eCrCl by CG) may overestimate kidney function in those with low muscle mass and increase drug toxicity. Cystatin C, unaffectedby muscle mass, offers improved glomerular filtration rate (GFR) estimation. The combined creatinine–cystatin C estimated glomerular filtration rate by CKD-EPI 2012 equation (eGFRcr-cys by CKD-EPI) may provide greater accuracy in colistin dose adjustment and potentially reduce colistin-associated AKI. This study evaluated whether colistin dosing guided by eGFRcr-cys by CKD-EPI could lower AKI incidence compared with eCrCl-by-CG-based dosing among patients with low muscle mass.
We conducted a single-center, randomized, controlled, superiority trial in hospitalized adults receiving intravenous colistin within 24 hours and at risk of low muscle mass, defined by a sarcopenia index <0.8 (serum creatinine/serum cystatin C) and excluded patients on dialysis, kidney transplants, severe AKI, and moribund state. Participants were randomized 1:1 to receive colistin dosing based on either eGFRcr-cys by CKD-EPI (intervention) or eCrCl by CG (control). The primary outcome was AKI incidence, defined by KDIGO 2012 criteria, within 14 days post-enrollment. Secondary outcomes included treatment duration, cumulative colistin exposure, kidney replacement therapy (KRT) use, hospital length of stay, and in-hospital mortality. The trial protocol was previously published in Thai Clinical Trial Registry (TCTR20240605006).
Of 120 randomized patients with mean sarcopenia index 0.48, 59 received eGFRcr-cys-by-CKD-EPI dosing and 61 eCrCl-by-CG dosing. Although treatment duration was comparable between groups, cumulative colistin exposure was significantly lower in the eGFRcr-cys group (835.17 vs. 1782.13 mg; absolute mean difference –947 mg, 95% CI –1268.6 to –625.2; p<0.001). However, AKI incidence at day 14 was similar between groups (59.3% vs. 60.7%; p=1.00). Other clinical outcomes, including KRT use, hospital length of stay, and mortality, did not differ significantly.
This trial, one of the first to test cystatin C–guided colistin dosing, demonstrated that although cystatin C-guided dosing could reduce colistin exposure without increasing serious adverse clinical outcomes, it did not lower AKI incidence compared to creatinine-based dosing. These findings suggest that cystatin C–guided dosing is feasible and safe, but its clinical benefit in preventing AKI remains unproven and warrants further study, particularly in patients with low muscle mass.
