ArticleCardiorenal medicine2015
The Role of Congestion in Cardiorenal Syndrome Type 2: New Pathophysiological Insights into an Experimental Model of Heart Failure.
Article in Cardiorenal medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
- A Comprehensive Review on the Cardioprotective and Nephroprotective Effects of Semaglutide, and Its Therapeutic Efficacy and Mechanisms in Cardiorenal Syndrome.Drug design, development and therapy · 2026Review
- Assessment of Cardiorenal Involvement in Systemic Sclerosis Patients.Biomolecules · 2025Article
- Urinary NGAL as an Early Marker of Renal Dysfunction in Dogs with Heartworm Disease and Pulmonary Hypertension.Animals : an open access journal from MDPI · 2025Article
- Cardiac and Renal Fibrosis, the Silent Killer in the Cardiovascular Continuum: An Up-to-Date.Journal of cardiovascular development and disease · 2024Review
- The Association Between Intra-abdominal Pressure and Diuretic Response in Heart Failure.Current heart failure reports · 2023Review
- The Review of Current Knowledge on Neutrophil Gelatinase-Associated Lipocalin (NGAL).International journal of molecular sciences · 2023Review
- Improvement of cardiac function after coronary artery bypass grafting surgery reduces the risk of postoperative acute kidney injury.Clinical cardiology · 2022Article
- Mitochondrial Dysfunction: An Emerging Link in the Pathophysiology of Cardiorenal Syndrome.Frontiers in cardiovascular medicine · 2022Review
- SGLT2 inhibitors in the treatment of type 2 cardiorenal syndrome: Focus on renal tubules.Frontiers in nephrology · 2022Review
- Poly(lipoic acid)-Based Nanoparticles as Self-Organized, Biocompatible, and Corona-Free Nanovectors.Biomacromolecules · 2021Article
- Grb2 Induces Cardiorenal Syndrome Type 3: Roles of IL-6, Cardiomyocyte Bioenergetics, and Akt/mTOR Pathway.Frontiers in cell and developmental biology · 2021Article
- Small animal models of heart failure.Cardiovascular research · 2019Review
- Current animal models for the study of congestion in heart failure: an overview.Heart failure reviews · 2019Review
- Data on the stem cells paracrine effects on apoptosis and cytokine milieu in an experimental model of cardiorenal syndrome type II.Data in brief · 2018Article
- Preoperative right heart hemodynamics predict postoperative acute kidney injury after heart transplantation.Intensive care medicine · 2018Article
- Reversible preoperative renal dysfunction does not add to the risk of postoperative acute kidney injury after cardiac valve surgery.Therapeutics and clinical risk management · 2017Article
- Cellular apoptosis in the cardiorenal axis.Heart failure reviews · 2016Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn cardiorenal syndrome type 2 (CRS2), the role of systemic congestion in heart failure (HF) is still obscure. We studied a model of CRS2 [monocrotaline (MCT)-treated rats] secondary to pulmonary hypertension and right ventricular (RV) failure in order to evaluate the contribution of prevalent congestion to the development of kidney injury.
methodsTen animals were treated with MCT for 4 weeks until they developed HF. Eleven animals were taken as controls. Signs of hypertrophy and dilatation of the right ventricle demonstrated the occurrence of HF. Brain natriuretic peptide (BNP), serum creatinine (sCreatinine), both kidney and heart neutrophil gelatinase-associated lipocalin (NGAL), matrix metallopeptidase 9 (MMP9), serum cytokines as well as kidney and heart cell death, as assessed by TUNEL, were studied.
resultsRats with HF showed higher BNP levels [chronic HF (CHF) 4.8 ± 0.5 ng/ml; controls 1.5 ± 0.2 ng/ml; p < 0.0001], marked RV hypertrophy and dilatation (RV mass/RV volume: CHF 1.46 ± 0.31, controls 2.41 ± 0.81; p < 0.01) as well as pleural and peritoneal effusions. A significant increase in proinflammatory cytokines and sCreatinine was observed (CHF 3.06 ± 1.3 pg/ml vs. controls 0.54 ± 0.23 pg/ml; p = 0.04). Serum (CHF 562.7 ± 93.34 ng/ml vs. controls 245.3 ± 58.19 ng/ml; p = 0.02) as well as renal and heart tissue NGAL levels [CHF 70,680 ± 4,337 arbitrary units (AU) vs. controls 32,120 ± 4,961 AU; p = 0.001] rose significantly, and they were found to be complexed with MMP9 in CHF rats. A higher number of kidney TUNEL-positive tubular cells was also detected (CHF 114.01 ± 45.93 vs. controls 16.36 ± 11.60 cells/mm(2); p = 0.0004).
conclusionIn this model of CHF with prevalent congestion, kidney injury is characterized by tubular damage and systemic inflammation. The upregulated NGAL complexed with MMP9 perpetuates the vicious circle of kidney/heart damage by enhancing the enzymatic activity of MMP9 with extracellular matrix degradation, worsening heart remodeling.
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