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Abstract Details
Scientific Research Abstract
Research in AKI (basic, translational, clinical, trials)
N/A
Author & Affiliation
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Heng‑Chih Pan hengchihpan0107@gmail.com Keelung Chang Gung Memorial Hospital Division of Nephrology Keelung Taiwan *
Chih-Hsiang Chang franwisandsun@gmail.com Linkou Chang Gung Memorial Hospital Division of Nephrology Taoyuan Taiwan -
Ya‑Fei Yang yangyafe@gamil.com China Medical University Hsinchu Hospital Division of Nephrology Zhubei Taiwan -
Tao‑Min Huang taominhuang@ntu.edu.tw National Taiwan University Hospital Division of Nephrology Taipei Taiwan -
Che-Yi Chou cychou.chou@gmail.com Asia University Hospital Division of Nephrology Taichung Taiwan -
Chun-Te Huang huangchunte@gmail.com Taichung Veterans General Hospital Department of Critical Care Taichung Taiwan -
Chiao‑Yin Sun Fish3970@gmail.com Keelung Chang Gung Memorial Hospital Division of Nephrology Keelung Taiwan -
Vin‑Cent Wu dr.vincentwu@gmail.com National Taiwan University Hospital Division of Nephrology Taipei Taiwan -
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Presenting Author
Heng‑Chih
Pan
hengchihpan0107@gmail.com
Taiwan
Abstract Content
Post-AKI Gut Microbiota and Kidney Recovery: A Feasibility Study With Preliminary MAKE30-Based Microbiome Analysis
Acute kidney injury (AKI) may progress to acute kidney disease and chronic kidney disease. The gut-kidney axis has been implicated in inflammation and renal recovery, but human data linking post-AKI stool microbiota with subsequent kidney outcomes remain limited. We established a post-AKI stool microbiome cohort and performed a preliminary analysis of microbiota profiles according to adverse kidney recovery.
We enrolled patients who experienced AKI and returned for outpatient follow-up after hospital discharge. Stool samples were collected after AKI and analyzed using 16S rRNA sequencing with amplicon sequence variant-based taxonomic profiling. The preliminary outcome was MAKE30, defined as death, dialysis, or a ≥30% decrease in eGFR from baseline to 3 months. Microbiome analyses included alpha and beta diversity, principal coordinate analysis, PERMANOVA/adonis, ANOSIM, MRPP, and ANCOM.
A total of 80 post-AKI stool samples were included. The mean age was 65.2 ± 13.5 years, 70.0% were male, baseline eGFR was 52.9 ± 30.7 mL/min/1.73 m², and discharge eGFR was 38.9 ± 28.1 mL/min/1.73 m². RAAS inhibitor use was observed in 51 patients (63.7%). eGFR decline ≥20% occurred in 31 patients (38.8%), while MAKE30 occurred in 18 patients (22.5%). No death or dialysis events occurred within 3 months; therefore, MAKE30 events were driven by the eGFR decline component. Beta diversity analysis showed no clear clustering by MAKE30 status. PERMANOVA showed limited explanatory variation (R² = 0.0118, p = 0.631), and ANOSIM (R = 0.0474, p = 0.1970) and MRPP (p = 0.648) were not significant. ANCOM identified no significantly differentially abundant taxa.
Post-AKI stool microbiome profiling is feasible in an outpatient follow-up cohort. In this preliminary MAKE30-based analysis, gut microbiota profiles did not identify a distinct microbial signature associated with adverse kidney recovery. More kidney-specific recovery outcomes, such as eGFR decline ≥20%, along with persistent AKI phenotypes and covariate-adjusted analyses, may better capture microbiome-associated renal recovery trajectories after AKI.
Acute kidney injury; Gut microbiota; Kidney recovery; Post-AKI outcomes; 16S rRNA sequencing; Gut–kidney axis
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