Abstract: SA-PO0267
Developmental Timing of Neonatal AKI Determines Renal Functional Reserve: Increased Vulnerability During Nephrogenesis
Session Information
- AKI: Mechanisms - Cell Signaling
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Soranno, Danielle Elise, Indiana University School of Medicine, Indianapolis, Indiana, United States
- Harshman, Lyndsay, University of Iowa Health Care, Iowa City, Iowa, United States
Background
Neonatal acute kidney injury (AKI) coincides with active nephrogenesis and is associated with increased risk of chronic kidney disease (CKD). Renal functional reserve (RFR), a physiologic stress test of kidney capacity, may detect subclinical dysfunction not evident at baseline. However, the impact of injury timing on long-term RFR remains unclear.
Methods
Using a translational rat pup model of ischemia-reperfusion AKI (IR-AKI), injury was induced at postnatal day 5 (P5; active nephrogenesis) or postnatal day 15 (P15; post-nephrogenesis), with sham controls. At 10 weeks, transdermal GFR (tGFR) was measured at baseline and following protein loading (oral gavage of meat extract, 5 mg/g) to assess RFR (ΔtGFR%). Data include combined male and female animals (n=4–8/group) and are not sex-stratified due to power limitations.
Results
Baseline tGFR was similar across groups. In contrast, RFR differentiated injury effects: IR-AKI reduced RFR compared to sham (p<0.01), with a greater reduction in P5 versus P15 cohorts (p<0.05). Sham animals demonstrated a consistent increase in tGFR following protein loading, whereas IR-AKI animals exhibited a blunted response. This suggests that early-life AKI results in persistent renal reserve impairment that is not detected by traditional measures.
Conclusion
Neonatal AKI is associated with long-term impairment in renal functional reserve, with greater vulnerability during active nephrogenesis. RFR may serve as a sensitive functional biomarker to detect subclinical kidney dysfunction following AKI. This model provides a platform for defining mechanisms and evaluating interventions targeting AKI-to-CKD progression.