Abstract
Cardiorenal syndrome (CRS) is defined as a disorder resulting from the abnormal interaction between the heart and kidney, in which acute or chronic dysfunction of one organ may lead to acute and/or chronic dysfunction of the other. The functional interplay between the heart and kidney is characterized by a complex bidirectional symbiotic interaction, regulated by a wide array of both genetic and environmental mechanisms. There are at least five known subtypes of CRS, based on the severity of clinical features and the degree of heart/renal failure. The fourth subtype (cardiorenal syndrome type 4 (CRS4)) is characterized by a primary chronic kidney disease (CKD), which in turn leads to a decreased cardiac function. Impairment of renal function is among the most important pathophysiological factors contributing to heart failure (HF) in the pediatric age group, and cardiovascular complications could be one of the most important causes of mortality in pediatric patients with advanced CKD. In this context, a loss of glomerular filtration rate directly correlates with both the progression of cardiovascular complications in CRS and the risk of HF. This review describes the interaction pathways between the heart and kidney and the recently identified pathophysiological mechanisms underlying pediatric CRS, with a special focus on CRS4, which encompasses both primary CKD and cardiovascular disease (CVD).
Highlights
The heart and kidneys interact through several intricate cellular and subcellular processes and molecular pathways [1]
cardiorenal syndrome (CRS) type 1 reflects an acute worsening of cardiac function affecting the kidneys, type 2 encompasses chronic cardiac disorders worsening the kidney’s function, type 3 comprises acute renal abnormalities causing acute heart failure, type 4 reflects a chronic kidney disorder leading to decreased cardiac function and heart failure, and, type 5 describes a systemic insult leading to cardiorenal dysfunction
Type 1 CRS is relatively prevalent. It is usually present in the setting of acute decompensated heart failure (ADHF), often after an ischemic or nonischemic heart disease, which may be divided into four subtypes: hypertensive pulmonary edema with preserved left ventricular systolic function, acutely decompensated chronic HF, cardiogenic shock, and predominant right ventricular failure
Summary
The heart and kidneys interact through several intricate cellular and subcellular processes and molecular pathways [1]. A clear definition of these interactions and a better knowledge of organ cross-talk are required to establish an effective treatment for individuals affected with CRS This is important in pediatric patients in whom cardiovascular disease (CVD) can be regarded as a major risk of premature death in the context of advanced chronic kidney disease (CKD) [3]. Next-generation sequencing technologies, including exome and mRNA sequencing studies, have shed new light on the complex molecular mechanisms underlying CRS [4,5] This has led to a better understanding of the intricate subcellular mechanisms underlying these conditions and promoting the risk of both CRS and CVS, including several regulatory networks and transcriptional factors, such as the interferon regulatory factor 1 [6]. Many novel molecular factors have been identified with consequent benefits in terms of refining clinical phenotypes, valuable prognostic information, detailed imaging studies, and targeted therapies for the affected children [11,12,13,14,15]
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