Epidemiology: Open Access
Open Access

Epidemiology; Cardiorenal syndrome; Heart-kidney interaction; Clinical research; Acute dialysis

Introduction

Globally, ageing populations and rising rates of obesity, diabetes mellitus (DM), and hypertension are the results of changing demographic trends. The importance of rising heart disease and kidney disease rates, as well as the co-occurrence of both heart and kidney disease, have been brought to the public's notice by these burgeoning pandemics.

Almost 80 million people, or roughly 1 in 3 adults in the USA, have been diagnosed with a cardiovascular disease (CVD), such as hypertension, coronary heart disease (CHD), heart failure (HF), stroke, or congenital heart disease. According to recent estimates, 13% of adults in the USA have CKD in any stage, which equates to close to 30 million people. A significant and possibly modifiable predictor of CVD, including CHD, left ventricular hypertrophy, and HF, CKD has also recently come to light. There is growing awareness of the significant clinical overlap and intricate pathophysiology between CKD and CVD. Cardiovascular illness may be the cause of more than 50% of fatalities in CKD patients, with mortality rates ten- to twenty-fold higher than in the general non-CKD population. This epidemic of CKD has potential far-reaching economic repercussions, since patients with CKD are more likely to be hospitalised, demand greater health resources, and have higher expenditures of treatment, both of which are enhanced further following progression to ESKD [1].

Understanding the overall illness burden for each of the suggested CRS subtypes, as well as their natural history, risk factors, associated morbidity and mortality, and potential health resource implications, requires a description of the epidemiology of heart-kidney interactions. The design of upcoming observational studies and clinical trials as well as the assessment of whether there are significant information gaps require an understanding of the existing literature on the epidemiology and outcomes of CRS. The epidemiology and clinical results related to the CRS, stratified by its subtypes, are discussed in this work [2].

The immediate worsening of cardiac function those results in acute kidney injury (AKI) and/or dysfunction is known as the Acute Cardio Renal Syndrome (Type 1 CRS). Acute cardiac events that may lead to AKI include acute decompensated heart failure (ADHF), acute coronary syndrome (ACS), cardiogenic shock, and cardiac surgeryassociated low cardiac output syndrome.

Although there are various and intricate pathophysiologic mechanisms causing WRF in ADHF, they most likely include changes to cardiac output, systemic hemodynamics that impair kidney perfusion, and pathological compensatory neurohormonal activation. Having CKD and having baseline renal function are both significant risk factors. A research by Aronson et al. shown that people with worse baseline kidney function were more likely to experience persistent WRF after admission for ADHF. Few studies have examined the time course of WRF and the clinical outcomes associated with temporary WRF or sustained stepwise decreases in renal function following hospitalisation for ADHF [3]. Aronson et al. have looked into this problem in a sample of 467 individuals who were admitted with ADHF. WRF was defined as an absolute rise in SCr ≥ 44.2 μmol/L, whereas temporary was defined as return to baseline within 30 days and persistent WRF as a sustained increase in SCr ≥ 44.2 μmol/L beyond 30 days. Transient and persistent WRF occurred in 7.9% and 14.3%, respectively, of those who developed WRF (33.9%). Mortality rates at 6 months were 17.3%, 20.5%, and 46.1% for people with neither transient nor chronic WRF (P.0001 for persistent versus no WRF), strongly indicating that people with persistent reductions in kidney function have a worse prognosis [4].

Discussion

Acute heart failure syndrome (AHFS) patients are typically admitted due to severe systemic congestion, which frequently manifests as dyspnea. Congestion, which is a defining feature of AHFS, is mostly brought on by pulmonary venous hypertension (World Health Organization type 2). These patients may also manifest with poor cardiac output and/or systemic hypotension. Based on the series, this has fluctuated from 2% to 7.7% to 29%. The most typical sign of these individuals' raised pulmonary venous pressure, which is frequently accompanied by elevated central venous pressure (CVP) and/or peripheral edoema, is dyspnea. Systemic congestion is hence the most sensible treatment focus. There is strong evidence that volume overload is the primary cause of illness, mortality, and readmission to the hospital. Furthermore, it is widely known that patients who are admitted with renal failure and AHFS experience worse results. In this work, we explore the pathogenesis of AHFS and its relation to deterioration of kidney function. Finally, we discuss the information that is currently available for therapeutic approaches in AHFS patients with cardio renal syndrome [5, 6].

Congestion is the hallmark of AHFS, as was already mentioned. The cardiorenal axis controls how the heart and kidney interact with one another. The principal neurohormones that preserve the consistency of effective arterial blood volume are the sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), and arginine vasopressin (AVP), therefore the cardiorenal axis. A rise in left atrial pressure in a heart that is not failing activates a feedback mechanism that reduces the production of AVP from the posterior pituitary. Vagotomy eliminates this reflex. Additionally, the renal SNS stimulation is lessened by higher atrial pressure. Natriuretic peptides, on the other hand, are released as a result of myocardial stretching and dilatation. The combination of these pathways ultimately leads to an increase in salt and water excretion, which keeps the total blood volume stable and protects the integrity of the arterial circulation [7-9].

This physiological reaction is hampered when heart failure sets in, and the kidneys continue to retain sodium and water despite a raised total blood volume. The system in charge of supplying the body's critical organs with blood, however, is governed by the smaller arterial circulation, allowing it to react to even modest variations in body fluid volume. Just 15% of the total blood volume is made up of this fraction. Consequently, kidneys continue to retain sodium and water in a failing heart due to disturbed body fluid balance, despite higher total sodium and total water and substantial venous engorgement. Patients with high or poor cardiac output are affected by this [10].

Conclusions

There is substantial evidence from observational studies and clinical trials that acute or chronic heart illness can directly cause acute or chronic renal function deterioration, and vice versa. The different subtypes of cardiorenal syndrome are distinguished by significant heartkidney interactions that have some pathophysiological similarities but appear to have important distinguishing characteristics in terms of risk identification, predisposing or precipitating events, natural history, and outcomes. The Type 1 CRS is prevalent, with incidence estimates of AKI in ADHF or ACS between 24%-45% and 9%-19%, respectively. There is little doubt that type 1 CRS results in increased morbidity and poorer clinical outcomes.

CKD and chronic cardiac disease regularly coexist and are becoming more common. As a result, it is difficult to apply the suggested Type 2 and Type 4 CRS definitions "retrospectively" to the current literature when it is difficult to discern between the primary and secondary processes. More investigation is needed on the pace of CKD progression in patients with established cardiovascular illness as well as the impact of cardioprotective treatments on these renal endpoints. For a better understanding of Types 2 and 4 CRS, prospective research incorporating novel biomarkers of kidney-heart interaction is required, as well as studies of CKD-specific therapies in Type 4 CRS.

The incidence and outcome estimates linked to Type 3 CRS are very context- and disease-specific due to heterogeneity. On the pathophysiology or epidemiology of secondary Type 5 CRS, there is a paucity of information. There is a clear need for more prospective studies to characterise the epidemiology of heart-kidney interactions across the CRS subtypes in order to better understand the overall burden of disease as well as to identify risks and create potential targets for intervention. As a result, Type 5 CRS epidemiology is also largely disease- and context-specific.

Acknowledgement

None

Conflict of Interest

None

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