Abstract
Cardiorenal syndrome (CRS), a clinical syndrome involving multiple pathological mechanisms, exhibits high morbidity and mortality. According to the primary activity of the disease, CRS can be divided into cardiorenal syndrome (type I and type II), renal heart syndrome (type III and type IV), and secondary heart and kidney disease (type V). The renin-angiotensin-aldosterone system (RAAS) is an important humoral regulatory system of the body that exists widely in various tissues and organs. As a compensatory mechanism, the RAAS is typically activated to participate in the regulation of target organ function. RAAS activation plays a key role in the pathogenesis of CRS. The RAAS induces the onset and development of CRS by mediating oxidative stress, uremic toxin overload, and asymmetric dimethylarginine production. Research on the mechanism of RAAS-induced CRS can provide multiple intervention methods that are of great significance for reducing end-stage organ damage and further improving the quality of life of patients with CRS.
Highlights
The incidence of heart and kidney disease, especially chronic heart failure (CHF) and chronic kidney disease (CKD), is increasing yearly with changes in lifestyle and increases in pressure
ADMA: asymmetric dimethylarginine; ED: endothelial dysfunction; Protein-Bound Uremic Toxin (PBUT): protein-bound uremic toxin; FGF-23: fibroblast growth factor-23; Figure 2: Schematic representation of renin-angiotensinaldosterone system (RAAS)-mediated Cardiorenal syndrome (CRS). 1 RAAS-mediated oxidative stress increases the preload and afterload of the heart by inducing renal fibrosis and atherosclerosis, respectively, and induces cardiac fibrosis, which further leads to cardiac dysfunction, reduced circulating blood volume, and renal insufficiency
ED in animal is a key process involved in the development of CRS, and it plays a vital role in the connection between cardiovascular disease and CKD (Figure 2) [68]
Summary
The incidence of heart and kidney disease, especially chronic heart failure (CHF) and chronic kidney disease (CKD), is increasing yearly with changes in lifestyle and increases in pressure. The increase in annual mortality related to dialysis is greater than 20%, and half of these deaths are cardiovascular related [3]. Comorbidities of these conditions are an indicator of poor prognosis, prolonged length of stay, and increased morbidity and mortality [4]. Type I and type II are referred to as cardiorenal syndrome, type III and type IV are called renal heart syndrome, and type V refers to heart and kidney involvement caused by simultaneous systemic diseases [7]. Excessive activation of the reninangiotensin-aldosterone system (RAAS) plays a key role in this process [9]
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