Relationship between Cardiovascular Disorder and Chronic Kidney Disease

Abstract

Cardiovascular and renal diseases are common and often co-occur, which significantly increases mortality, morbidity, complexity, and cost of treatment [1,2]. Comorbidities such as heart failure and renal failure exist. The term “cardio-renal syndrome” (CRS) refers to acute or chronic dysfunction of one organ that leads to the acute or chronic failure of another (Table 1) [3,4]. Moreover, renal failure in heart failure can result in reduced diuretic effect, increased blockage, and further loss of renal function, resulting in a vicious cycle. CRS was long assumed to be caused by renal hypoperfusion as a result of inadequate cardiac output and hyper-diuresis. Nevertheless, research has gradually revealed a link between Venous Thrombo Embolism (VTE) and CRS rather than insufficient cardiac output, which has been linked to CRS in right-sided heart problems in the latest generations. In contrast to a single cardiorenal illness, both Right heart failure (RHF) and CRS have complicated and interrelated pathogen physiological pathways that can impact various organs and systems. The most severe type of cardiorenal regulations is referred to be “CRS,” and treatment of obstructed symptoms is confined to impaired renal function. This physiological notion is distinct from the Acute Dialysis Quality Initiative [5] categorization systems, which specify main organ failure (cardiac or renal) and total duration (acute or chronic), with an extra category for clinical syndrome impacting both organs at the same time. Additionally, there are few quantifiable assessments of cardiac or renal function to characterize these subtypes; hence, their clinical use is mostly descriptive and cardiopulmonary. CRS occurs when people who have heart failure develop renal failure while being treated for heart failure. Renal failure in heart failure patients is complicated and generally multivariate in nature; nonetheless, the illness may be curable in certain people. Reducing angiotensin II levels with angiotensin-converting enzyme medications can help to avoid glomerular hyperfiltration and, in the long run, preserve kidney function.