Kidney Week

Abstract: FR-PO0923

White Matter Microstructure on Diffusion MRI After AKI in Preterm Infants

Session Information

• Pediatric Nephrology: Genetic Diseases, Development, Neonatal Nephrology, Glomerular Diseases, and More
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Pediatric Nephrology

• 1800 Pediatric Nephrology

Authors

• Zhou, Melissa S., Stanford University School of Medicine, Stanford, California, United States

Melissa S. Zhou, MD, MS

• Travis, Katherine Elizabeth, Stanford University School of Medicine, Stanford, California, United States

Katherine Elizabeth Travis, PhD

• Menon, Shina, Stanford University School of Medicine, Stanford, California, United States

Shina Menon, MD, FASN

• Chock, Valerie, Stanford University School of Medicine, Stanford, California, United States

Valerie Chock, MD

• Feldman, Heidi M., Stanford University School of Medicine, Stanford, California, United States

Heidi M. Feldman, MD, PhD

Background

Preterm infants are vulnerable to inflammation-related white matter (WM) injury. Acute kidney injury (AKI) is pro-inflammatory and often co-occurs with inflammation but its association with WM microstructure is unclear.

Methods

Retrospective single-center cohort study of infants born <32 weeks' gestation (2016-2023) with near-term diffusion MRI. Infants stratified by inflammation (sepsis, necrotizing enterocolitis, or bronchopulmonary dysplasia) and creatinine-based neonatal KDIGO AKI, with No Inflammation/No AKI as the normative reference group. WM tract-specific fractional anisotropy (FA) and mean diffusivity (MD) were converted to normative z-scores by standardizing observed-minus-expected residuals from reference-group models adjusted for postmenstrual age at MRI, sex, and coil type. Primary analyses used linear regression to compare tract-specific FA and MD normative z-scores between Inflammation/AKI and Inflammation/No AKI, with Benjamini-Hochberg correction for multiple comparisons (q<0.05).

Results

186 infants included (Fig1). Compared to Inflammation/No AKI, Inflammation/AKI showed higher superior cerebellar peduncle MD (β=1.17, 95% CI 0.32 to 2.02, q=0.04) and lower anterior frontal corpus callosum MD (β=−1.54, 95% CI −2.57 to −0.52, q=0.04). Both inflammation groups had reduced FA and altered MD across multiple tracts versus reference, with larger effects in Inflammation/AKI (Fig2).

Conclusion

AKI-associated WM microstructural differences beyond common inflammatory conditions of prematurity suggest AKI may independently contribute to regional brain vulnerability.

Funding

• Other NIH Support