ABSTRACT
Introduction: The term cardiorenal syndrome (CRS) describes the progressive pathology and interactions that develop upon heart and kidney failure. The definition of CRS is not firmly established and has evolved gradually during the last decade. The main clinical challenges associated with CRS are the lack of tools for early disease diagnosis and the inability to predict the development of cardiorenal pathophysiology. Currently several biomarkers have been proposed for improving CRS patient management. However, validation studies are needed to implement these initial findings to the clinical setting.
Areas covered: In this review the database PubMed was used for a literature search on the definition and classification of CRS as well as biomarkers for CRS diagnosis and prognosis.
Expert opinion: A universally acceptable classification system for CRS is not available. Thus, acquiring mechanistic insights relative to the pathophysiology of the disease is challenging. Reported biomarkers include well-established markers for heart/renal dysfunction and inflammation. Some proteins expressed in both organs have also been associated with CRS, yet their link to disease pathophysiology and organ cross-talk is missing. Establishing the link between deregulated molecular pathways and CRS phenotypes is required to define biological relevance of existing findings and ultimately biology-driven markers and targets.
Article highlights
Cardiorenal Syndrome describes the complex cross-talk between heart and kidney malfunction.
The definition of the cardiorenal syndrome evolved gradually and two classification systems have been proposed.
Reported protein biomarkers include well-established renal and cardiac specific markers (such as NGAL, KIM1, troponins) but also proteins expressed in both organs thus of higher chance to be linked to the CRS underlying pathology.
Adopting a more systematic approach in CRS research, starting with more clear clinical definitions of its types to allow for larger trials and facilitate data comparability appears to be needed for validation of the existing markers in parallel, better characterization of the disease molecular phenotype.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviews disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.
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