The heart is an important organ of the cardiovascular system and plays the role of a pump, generating power through each beat of the heart to drive blood through the body, thus providing the body with the substances on which it depends and carrying away metabolites. The kidneys play a filtration role in the body system, producing urine, maintaining water balance, eliminating metabolites and toxic substances from the body, maintaining the acid-base balance of the body, secreting or synthesizing some substances, and regulating the physiological functions of the body. As two important organs in the human body, the heart and kidneys are inextricably linked to each other, and changes in the function of one will often have a serious impact on the other, never simply pumping and filtering. The kidneys can even be considered as part of the circulatory system, as they synthesize and release active substances such as renin, erythropoietin, kinins, prostaglandins, etc., which regulate cardiovascular function and metabolism. Thus, the regulation of hemodynamics and function by the heart and kidneys is a complex and dynamic system. The two organs establish a dialogue through nitric oxide, reactive oxygen clusters, systemic inflammation, activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS), and endothelin, prostaglandins, vasopressin, and natriuretic peptides as bridges. Accelerated cardiovascular atherosclerosis, left ventricular hypertrophy and remodeling, myocardial microangiopathy and vascular calcification can occur in the setting of renal hypoperfusion, while in the setting of cardiac insufficiency, a progressive decline in renal function results from factors such as reduced renal perfusion and RAAS activation. Moreover, many risk factors for cardiovascular disease are also risk factors for kidney disease, such as smoking, hypertension, hyperlipidemia, age and diabetes can contribute to the progression of kidney disease. In addition, both heart disease and kidney disease can cause anemia, and the latter in turn leads to the aggravation of both diseases, forming a vicious circle. First, the impact of renal lesions on the heart Renal blood flow accounts for about 20%-25% of cardiac output, and it plays a central role in water and electrolyte balance and blood pressure regulation. Some acute or chronic renal diseases can often lead to acute cardiac disease or affect cardiac function, and Johannes et al. found that cardiac remodeling occurs at very early stages of renal disease. In China, in the mid-1950s, acute nephritis complicated by heart failure was a common pediatric emergency, and the vast majority of patients who died from nephritis in the acute phase were due to heart failure. Richard Ashman reported that the percentage of acute nephritis complicated by congestive heart failure during this period was 17-71%, and similar data were available in China at that time. Among the 103 patients with acute nephritis reported by Dr. Yang Siyuan, 22 cases (21.4%) were complicated by heart failure. However, the current epidemiological trends at home and abroad show that the incidence of acute nephritis is significantly less than it was half a century ago, the reasons for which are not yet clear. For the mechanism of heart failure complicated by acute nephritis, the following three aspects are mostly considered: hypertension, myocardial injury, and water and sodium retention. Hypertension is an early sign of acute nephritis, and its mechanism is thought to be systemic small vessel spasm, but from clinical research data, hypertension is not the main cause of complicating heart failure. As for myocardial injury, although the hemolytic streptococcal infection that causes acute nephritis may also produce nonspecific myocardial lesions, and 60-100% of patients with acute nephritis have electrocardiographic changes, the production and extent of these changes are often not absolutely dependent on the complication rate and severity of heart failure, and therefore are not the main cause of heart failure. A large amount of clinical data shows that when heart failure symptoms are present in acute nephritis, cardiac function is approximately normal, while water and sodium retention due to reduced renal function increases circulating blood volume and congestion occurs in the venous and pulmonary circulation, resulting in symptoms of congestive heart failure. This is the same as those patients with heart disease, who first have reduced cardiac output and insufficient renal blood flow, followed by water and sodium retention causing congestive heart failure. Therefore, the main cause of heart failure complicated by acute nephritis is water and sodium retention. And in chronic kidney disease, the development to the end stage can lead to water retention, hypertension and myocardial dystrophy, all of which are the root causes of induced heart failure. Second, the impact of cardiac lesions on the kidney The deterioration of cardiac function caused by cardiac lesions often shows a decrease in cardiac output, redistribution of blood flow in the kidney, a decrease in renal blood flow and glomerular filtration rate, a decrease in sodium filtration, and an increase in renal tubular reabsorption, leading to water and sodium retention. In turn, redistribution of blood flow further decreases renal perfusion and activates the RAAS, increasing sodium and water retention, and such repeated amplification effects have potentially deleterious long-term cascading effects on the RAAS system. Angiotensin II secretion enhances the stimulation of vasoconstriction, including the persistence of strong constriction of the renal vasculature, and increases aldosterone secretion, which not only enhances sodium reabsorption from the distal renal tubules but also produces collagen deposition and fibrosis in the myocardium and vasculature. Since angiotensin II may be involved in the formation of vascular and myocardial hypertrophy, it promotes remodeling of the heart and peripheral vessels, which leads to a vicious cycle. In contrast, the release of renin increases the synthesis of angiotensin II, which in turn stimulates the secretion of antidiuretic hormone and triggers apoptosis. Aldosterone, in turn, synthesizes angiotensin II (which can be mediated by pro-adrenocorticotropic hormone, nitric oxide, free radicals, and other stimuli) that acts independently in the heart and blood vessels, producing deleterious effects in these organs. III. Cardiorenal syndrome The heart and kidneys are closely related, and the effects of both are mutual and multifaceted. Based on this understanding, the concept of cardiorenal syndrome has become widely used in recent years, although its pathogenesis is not fully understood so far. The narrow definition of cardiorenal syndrome: specifically refers to the progressive renal impairment that occurs in chronic heart failure and leads to renal insufficiency, which in turn affects the treatment of cardiac insufficiency and interferes with the prognosis. Broad definition of cardiorenal syndrome: pathophysiologic abnormalities of the heart and kidneys in which acute or chronic dysfunction of one organ leads to acute or chronic dysfunction of the other organ. At the World Congress of Nephrology in April 2007, Italian nephrologist Professor C. Ronco classified the simultaneous involvement of the heart and kidneys into 5 categories based on the primary cause and onset of the disease: Type I: acute cardiorenal syndrome. Sudden deterioration of cardiac function (such as acute cardiogenic shock or acute congestive heart failure) leads to acute kidney injury (AKI). Type II: Chronic cardiorenal syndrome. Chronic cardiac insufficiency (e.g., chronic congestive heart failure) leading to progressive and persistent chronic kidney disease (CKD). Type III: Acute renal-heart syndrome. Sudden deterioration of renal function (e.g., acute renal ischemia or nephritis) leading to acute cardiac disease (e.g., heart failure, arrhythmias, myocardial ischemia). Type IV: Chronic renal heart syndrome. Chronic kidney disease (e.g., glomerular or interstitial renal disease) leading to cardiac decompensation, ventricular hypertrophy, and/or increased risk of adverse cardiovascular events. Type V: Secondary cardiorenal syndrome. Cardiac and renal dysfunction due to systemic diseases (e.g., diabetes, sepsis). To prevent the occurrence of cardiorenal syndrome, strengthening the prevention and treatment of chronic heart failure is the fundamental measure, and some clinical treatment experiences also show that the application of diuretics, β-blockers, and angiotensin-converting enzyme inhibitors is effective in the treatment of cardiorenal syndrome. However, the connection between the heart and kidney is complex, variable and mutually constrained. Currently, people focus their research on the RAAS system, which is at the core, to achieve joint cardio-renal protection by finding suitable targets for intervention and blocking the links that affect the vicious cycle of cardio-renal function. Since the current therapeutic basis is mainly derived from information such as retrospective studies and clinical trials, and there is a lack of valid evidence-based medicine, it is yet to be clarified by multicenter prospective studies.