Abstract
Cardiorenal syndrome (CRS) is a multi-organ disease characterized by the complex interaction between heart and kidney during acute or chronic injury. The pathogenesis of CRS involves metabolic, hemodynamic, neurohormonal, and inflammatory mechanisms, and atherosclerotic degeneration. In the process of better understanding the bi-directional pathophysiological aspects of CRS, the need to find precise and easy-to-use markers has also evolved. Based on the new pathophysiological standpoints and an overall vision of the CRS, the literature on renal, cardiac, metabolic, oxidative, and vascular circulating biomarkers was evaluated. Though the effectiveness of different extensively applied biomarkers remains controversial, evidence for several indicators, particularly when combined, has increased in recent years. From new aspects of classic biomarkers to microRNAs, this review aimed at a 360-degree analysis of the pathways that balance the kidney and the heart physiologies. In this delicate system, different markers and their combination can shed light on the diagnosis, risk, and prognosis of CRS.
Highlights
Definition of Cardiorenal SyndromePublisher’s Note: MDPI stays neutralThere is a close link between the heart and kidney: cardiovascular damage drives a worsening of kidney function; in turn kidney failure worsens cardiovascular injury [1].Heart Failure (HF) affects 5.8 million people within the USA, and over 23 million worldwide [2]
It contributes to Cardiorenal syndrome (CRS) development in several ways: reduced oxygen delivery, reduced antioxidants synthesized from red blood cells, activation of sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), arginine vasopressin (AVP) because of tissue ischemia that leads to vasoconstriction, salt-water retention, and venous congestion
The significant interaction (p = 0.002 unadjusted; p = 0.03 adjusted) between decrease in eGFR value and change in NT-proBNP confirmed that reduction of renal function during therapy for acute decompensated HF is linked to better outcomes if associated with a decline in NT-proBNP levels
Summary
There is a close link between the heart and kidney: cardiovascular damage drives a worsening of kidney function; in turn kidney failure worsens cardiovascular injury [1]. Cardiorenal syndrome (CRS) is a multi-organ disease that includes a spectrum of disorders resulting from the close interaction between the heart and kidney during acute or chronic dysfunction of one of these organs. It was described for the first time by Robert Bright, in 1836, who found cardiac structural changes in a patient with advanced renal failure [5]. CRS patients into two groups based on the primary organ failure driving the disease process OnThis the classification primary organ failure driving the disease process into (cardiorenal or renocardiac) was further elaborated and arranged five groups accorddiac). Lated but,aon the contrary, portion of larger multifaceted and complex pathophysiological pathways
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