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Acute Cardiorenal Syndrome: Models and Heart-Kidney Connectors
Yoshio Funahashi1, Sheuli Chowdhury2, Mahaba B Eiwaz2
1Anesthesiology & Perioperative Medicine, Oregon Health & Science University, Portland, Oregon, USA, funahash@ohsu.edu.
Abstract:
Cardiorenal syndrome type 1 (CRS-1) is an acute kidney injury (AKI) due to acute worsening of cardiac function. More than 20% of patients with acute heart failure develop AKI, and AKI predicts poor outcome. Although a number of potential pathways have been suggested as heart-kidney connectors which might drive the syndrome, there are significant barriers to investigation, such as a paucity of animal models, a lack of specific biomarkers, and an inconsistent temporal and causal relationship between changes in cardiac flow and development of renal dysfunction. Thus, mechanisms of heart-kidney interaction are still unclear, and there is no specific or effective therapy for CRS-1. This review, therefore, focuses on mitigating these challenges in the investigation of CRS-1. We review the available models and focus on mechanistic insights gained from those models. In particular, we focus on non-flow and endocrine mediators of CRS-1 such as heart-derived messengers which alter renal function and which may represent targetable pathways in this syndrome. As precise connectors of heart-kidney interaction remain unclear, the establishment of animal and relevant cell-culture models and further investigation are required.
Insights
Cardiorenal syndrome type 1 (CRS-1), a form of acute kidney injury (AKI) from heart issues, lacks clear mechanisms and treatments. This review explores models and non-flow mediators to advance CRS-1 research.
Area of Science:
- Nephrology
- Cardiology
- Pathophysiology
Background:
- Cardiorenal syndrome type 1 (CRS-1) involves acute kidney injury (AKI) secondary to acute cardiac dysfunction.
- AKI affects over 20% of acute heart failure patients, predicting poor prognosis.
- Current understanding of heart-kidney interaction mechanisms in CRS-1 is limited by research barriers.
Purpose of the Study:
- To address challenges in investigating CRS-1.
- To review existing animal and cell-culture models for CRS-1 research.
- To explore non-flow and endocrine mediators of heart-kidney interaction in CRS-1.
Main Methods:
- Review of current literature on CRS-1 models and mechanisms.
- Focus on insights from available animal models.
- Analysis of non-flow and endocrine mediators, including heart-derived messengers.
Main Results:
- Significant barriers hinder CRS-1 investigation, including lack of models and biomarkers.
- Mechanisms of heart-kidney interaction remain unclear.
- Non-flow and endocrine mediators are potential targets for CRS-1 therapy.
Conclusions:
- Further development of animal and cell-culture models is crucial for CRS-1 research.
- Understanding non-flow and endocrine mediators may reveal targetable pathways.
- Effective therapies for CRS-1 are currently lacking and require further investigation.
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