ArticleClinical science (London, England : 1979)2025
Persistent subclinical renal injury in female rats following renal ischemia-reperfusion injury.
Article in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Delayed conception or sildenafil prevents endothelial dysfunction in pregnant rats after renal ischemia-reperfusion.American journal of physiology. Renal physiology · 2026Article
- When the Heart Hurts the Kidneys: From Flow to Translational Future.Seminars in nephrology · 2025Review
- The death of a myth: Females are not resistant to acute kidney injury.Clinical science (London, England : 1979) · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The incidence of acute kidney injury (AKI) continues to rise in both men and women. Although creatinine levels return to normal quicker in females following AKI than in males, it remains unclear whether subclinical renal injury persists in young females post-AKI. This study tested the hypothesis that AKI results in subclinical renal injury in females despite plasma creatinine returning to sham levels. For the present study, 12-13-week-old female Sprague-Dawley (SD) rats were randomized to sham or 45-minute warm bilateral ischemia-reperfusion surgery as an experimental model of ischemic AKI. Rats were euthanized 1, 3, 7, 14, or 30 days post-AKI/sham. Plasma creatinine, cystatin C, kidney injury molecule 1 (KIM-1), and NGAL were quantified via assay kits or immunoblotting. Kidneys were processed for histological analysis to assess tubular injury and fibrosis, and for electron microscopy to examine mitochondrial morphology. Immunoblots on kidney homogenates were performed to determine oxidative stress and apoptosis. Plasma creatinine levels were increased 24 hours post-AKI but returned to sham control levels three days post-AKI. However, cystatin C, KIM-1, and NGAL were increased 30 days post-AKI compared with sham. Tubular injury, tubulointerstitial fibrosis, and mitochondrial dysfunction were all increased in 30-day post-AKI rats compared with sham. Additionally, 30-day post-AKI rats had higher p-JNK expression and lower antioxidant enzyme glutathione peroxidase and catalase levels compared with sham. AKI resulted in higher expression of cleaved caspase 3, TUNEL+ cells, and caspase 9 than sham. Despite the normalization of creatinine levels, our data support the hypothesis that subclinical renal injury persists following ischemia-reperfusion injury in young female rats.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.