ArticleAmerican journal of physiology. Renal physiology2019
Capillary rarefaction is more closely associated with CKD progression after cisplatin, rhabdomyolysis, and ischemia-reperfusion-induced AKI than renal fibrosis.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 51 citations in OpenAlex.
- Chronic Radiation-Induced Wounds: Pathogenesis, Current Therapeutic Strategies, and Emerging Regenerative Approaches.International journal of molecular sciences · 2026Review
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- Recent advances in stimuli-responsive nanomaterials for the treatment of acute kidney injury.Journal of nanobiotechnology · 2026Review
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Inflammation: The Pathological Axis of Cisplatin-Induced Renal Injury.Journal of inflammation research · 2026Review
- Vitamin B12 Protects the Exacerbated Ischemia-Reperfusion Injury-Induced Chronic Kidney Disease in Mice with Genetically Increased Elmo1.Antioxidants (Basel, Switzerland) · 2025Article
- INHBA knockdown inhibits renal fibrosis in mice following ischemia-reperfusion injury by suppressing activation of the TGF-β/Smad signaling pathway.BMC nephrology · 2025Article
- Nfkb1 Removal from Proximal Tubule Cells Improves Renal Tubular Outcomes Following Ischemia Reperfusion Injury.Kidney360 · 2025Article
- Altered renal vascular patterning reduces ischemic kidney injury and limits age-associated vascular loss.American journal of physiology. Renal physiology · 2025Article
- Alterations to peritubular capillary structure in a rat model of kidney interstitial fibrosis: Implications for oxygen diffusion.Anatomical record (Hoboken, N.J. : 2007) · 2025Article
- Adding insult to injury: the spectrum of tubulointerstitial responses in acute kidney injury.The Journal of clinical investigation · 2025Review
- Resazurin dye is an in vivo sensor of kidney tubular function.Kidney international · 2025Article
- Lymphocytes and innate immune cells in acute kidney injury and repair.Nature reviews. Nephrology · 2024Review
- Development of a Model of Tubulointerstitial Fibrosis Using Transient Unilateral Renal Ischemia and Delayed Contralateral Nephrectomy in Domesticated Cats.Comparative medicine · 2024Article
- miR-486-5p protects against rat ischemic kidney injury and prevents the transition to chronic kidney disease and vascular dysfunction.Clinical science (London, England : 1979) · 2024Article
- Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024Review
- Endothelial Glycocalyx of Peritubular Capillaries in Experimental Diabetic Nephropathy: A Target of ACE Inhibitor-Induced Kidney Microvascular Protection.International journal of molecular sciences · 2023Article
- Reconfiguration and loss of peritubular capillaries in chronic kidney disease.Scientific reports · 2023Article
- Inhibition of retinoic acid signaling in proximal tubular epithelial cells protects against acute kidney injury.JCI insight · 2023Article
- Anemia and Hypoxia Impact on Chronic Kidney Disease Onset and Progression: Review and Updates.Cureus · 2023Review
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7 authors at 1 institution in 1 country.
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Abstract
Acute kidney injury (AKI) is a strong independent predictor of mortality and often results in incomplete recovery of renal function, leading to progressive chronic kidney disease (CKD). Many clinical trials have been conducted on the basis of promising preclinical data, but no therapeutic interventions have been shown to improve long-term outcomes after AKI. This is partly due to the failure of preclinical studies to accurately model clinically relevant injury and long-term outcomes on CKD progression. Here, we evaluated the long-term effects of AKI on CKD progression in three animal models reflecting diverse etiologies of AKI: repeat-dose cisplatin, rhabdomyolysis, and ischemia-reperfusion injury. Using transdermal measurement of glomerular filtration rate as a clinically relevant measure of kidney function and quantification of peritubular capillary density to measure capillary rarefaction, we showed that repeat-dose cisplatin caused capillary rarefaction and decreased renal function in mice without a significant increase in interstitial fibrosis, whereas rhabdomyolysis-induced AKI led to severe interstitial fibrosis, but renal function and peritubular capillary density were preserved. Furthermore, long-term experiments in mice with unilateral ischemia-reperfusion injury showed that restoration of renal function 12 wk after a contralateral nephrectomy was associated with increasing fibrosis, but a reversal of capillary rarefaction was seen at 4 wk. These data demonstrate that clear dissociation between kidney function and fibrosis in these models of AKI to CKD progression and suggest that peritubular capillary rarefaction is more strongly associated with CKD progression than renal fibrosis.
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