ArticleKidney international2020
The acute kidney injury to chronic kidney disease transition in a mouse model of acute cardiorenal syndrome emphasizes the role of inflammation.
Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 47 citations in OpenAlex.
- Cardiac LIM Protein, Kidney Fibrosis, and Vascular Change after Acute Cardiorenal Syndrome.Journal of the American Society of Nephrology : JASN · 2025Article
- Kidney cell response to acute cardiorenal and isolated kidney ischemia-reperfusion injury.Physiological genomics · 2025Article
- Persistent subclinical renal injury in female rats following renal ischemia-reperfusion injury.Clinical science (London, England : 1979) · 2025Article
- Acute kidney injury through a metabolic lens: pathological reprogramming mechanisms and clinical translation potential.Frontiers in physiology · 2025Review
- Chronic kidney disease activates the HDAC6-inflammatory axis in the heart and contributes to myocardial remodeling in mice: inhibition of HDAC6 alleviates chronic kidney disease-induced myocardial remodeling.Basic research in cardiology · 2024Article
- Nanotherapeutic kidney cell-specific targeting to ameliorate acute kidney injury.Kidney international · 2024Article
- An early and stable mouse model of polymyxin-induced acute kidney injury.Intensive care medicine experimental · 2024Article
- Article
- STING/ACSL4 axis-dependent ferroptosis and inflammation promote hypertension-associated chronic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- KIM-1 augments hypoxia-induced tubulointerstitial inflammation through uptake of small extracellular vesicles by tubular epithelial cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Experimental models of acute kidney injury for translational research.Nature reviews. Nephrology · 2022Review
- Renal injury in cardiorenal syndrome type 1 is mediated by albumin.Physiological reports · 2022Article
- LncRNA MALAT1-deficiency restrains lipopolysaccharide (LPS)-induced pyroptotic cell death and inflammation in HK-2 cells by releasing microRNA-135b-5p.Renal failure · 2021Article
- Ibrutinib does not prevent kidney fibrosis following acute and chronic injury.Scientific reports · 2021Article
- Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction.American journal of physiology. Renal physiology · 2021Article
- Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.Journal of inflammation (London, England) · 2021Article
- Chronic Secondary Cardiorenal Syndrome: The Sixth Innovative Subtype.Frontiers in cardiovascular medicine · 2021Article
- Single-Cell Profiling of AKI in a Murine Model Reveals Novel Transcriptional Signatures, Profibrotic Phenotype, and Epithelial-to-Stromal Crosstalk.Journal of the American Society of Nephrology : JASN · 2020Article
- Deficit of resolution receptor magnifies inflammatory leukocyte directed cardiorenal and endothelial dysfunction with signs of cardiomyopathy of obesity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- A two-stage bilateral ischemia-reperfusion injury-induced AKI to CKD transition model in mice.American journal of physiology. Renal physiology · 2020Article
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10 authors at 1 institution in 2 countries.
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Abstract
Acute cardiorenal syndrome is a common complication of acute cardiovascular disease. Studies of acute kidney injury (AKI) to chronic kidney disease (CKD) transition, including patients suffering acute cardiovascular disease, report high rates of CKD development. Therefore, acute cardiorenal syndrome associates with CKD, but no study has established causation. To define this we used a murine cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) model or sham procedure on male mice. CA was induced with potassium chloride while CPR consisted of chest compressions and epinephrine eight minutes later. Two weeks after AKI was induced by CA/CPR, the measured glomerular filtration rate (GFR) was not different from sham. However, after seven weeks the mice developed CKD, recapitulating clinical observations. One day, and one, two, and seven weeks after CA/CPR, the GFR was measured, and renal tissue sections were evaluated for various indices of injury and inflammation. One day after CA/CPR, acute cardiorenal syndrome was indicated by a significant reduction of the mean GFR (649 in sham, vs. 25 μL/min/100g in CA/CPR animals), KIM-1 positive tubules, and acute tubular necrosis. Renal inflammation developed, with F4/80 positive and CD3-positive cells infiltrating the kidney one day and one week after CA/CPR, respectively. Although there was functional recovery with normalization of GFR two weeks after CA/CPR, deposition of tubulointerstitial matrix proteins α-smooth muscle actin and fibrillin-1 progressed, along with a significantly reduced mean GFR (623 in sham vs. 409 μL/min/100g in CA/CPR animals), proteinuria, increased tissue transforming growth factor-β, and fibrosis establishing the development of CKD seven weeks after CA/CPR. Thus, murine CA/CPR, a model of acute cardiorenal syndrome, causes an AKI-CKD transition likely due to prolonged renal inflammation.
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