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Abstract: FR-PO252

Gut Microbiota and Kidney Injury After Allogeneic Hematopoietic Cell Transplantation (allo-HCT)

Session Information

Category: Onconephrology

  • 1700 Onconephrology

Authors

  • Abramson, Matthew, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Jaffer Sathick, Insara, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Knezevic, Andrea, Memorial Sloan Kettering Cancer Center, New York, New York, United States
  • Jaimes, Edgar A., Memorial Sloan Kettering Cancer Center, New York, New York, United States
Background

Acute kidney injury (AKI) is a common complication of allo-HCT associated with an increase in non-relapse mortality. In contrast, higher diversity of gut microbiota at neutrophil engraftment is associated with lower mortality. We aimed to study the association of changes in gut microbiome diversity in an allo-HCT cohort who developed post-transplant AKI or CKD.

Methods

We performed a single-center study of 419 allo-HCT recipients from 2014-2017 at Memorial Sloan Kettering Cancer Center with analysis of gut microbiome diversity. We defined AKI and CKD based on KDIGO criteria and eGFR using the CKD-EPI equation. We defined gut microbiome diversity using Shannon and Simpson reciprocal diversity indices (DI), with higher levels indicating more diverse microbiota. We used Wilcoxon rank-sum test to compare baseline DI (within 7 days of HCT conditioning) between patients who did and did not develop AKI by 100 days post-HCT, and peri-engraftment DI (median DI in days 7-21 post-HCT) between those who did and did not develop CKD at 6 months.

Results

Simpson reciprocal and Shannon DI were 21.8 (IQR: 13.7, 35.2) and 3.7 (IQR: 3.2, 4.2) at baseline, and 6.3 (IQR: 3.7, 10.4) and 2.3 (IQR: 1.7, 2.8) at peri-engraftment, respectively. Of the 419 patients, 263 (63%) developed AKI; 114 (27%) was Stage 2+. CKD occurred in 68 patients (18%) at 6 months. There were no significant differences in microbiome DI at baseline or peri-engraftment in patients who developed AKI or CKD, compared to those who did not (all p>0.05, Figure 1).

Conclusion

Our findings do not support the existence of a link between baseline or peri-engraftment gut diversity and the risk for development of AKI or CKD in patients undergoing allo-HCT. This study highlights the complex and multifactorial etiology of AKI in allo-HCT recipients and the need for additional prospective and mechanistic studies.