
Volume Overload and Cardiorenal Syndromes
Author(s) -
Ronco Claudio,
Maisel Alan
Publication year - 2010
Publication title -
congestive heart failure
Language(s) - English
Resource type - Journals
eISSN - 1751-7133
pISSN - 1527-5299
DOI - 10.1111/j.1751-7133.2010.00176.x
Subject(s) - cardiorenal syndrome , medicine , heart failure , volume overload , kidney disease , intensive care medicine , disease , renal function , acute kidney injury , cardiology , sepsis , population , pathophysiology , bioinformatics , environmental health , biology
To include the vast array of interrelated derangements and to stress the bidirectional nature of the heart‐kidney interactions, the classification of the cardiorenal syndrome today includes 5 subtypes whose terminology reflects their primary and secondary pathology, time frame, and the presence of concomitant cardiac and renal dysfunction. Cardiorenal syndromes (CRSs) are pathophysiologic disorders of the heart and kidneys whereby acute or chronic dysfunction of one organ may induce acute or chronic dysfunction of the other. Type 1 CRS reflects an abrupt worsening of cardiac function leading to acute kidney injury. Type 2 CRS describes chronic abnormalities in cardiac function causing progressive chronic kidney disease. Type 3 CRS consists in an abrupt worsening of renal function causing acute cardiac disorder. Type 4 CRS describes a state of chronic kidney disease contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (eg, sepsis) simultaneously causing both cardiac and renal dysfunction. Biomarkers can help characterize the subtypes of CRS as well as suggest the timing of treatment initiation and its likely effectiveness. The identification of patients and the pathophysiologic mechanisms underlying each syndrome subtype, including fluid overload or, in general, altered conditions of fluid status, can help physicians understand clinical derangements, provide the rationale for management strategies, and allow the design of future clinical trials with more accurate selection and stratification of the population under investigation. Congest Heart Fail. 2010;16(4)(suppl 1):Si–Siv. © 2010 Wiley Periodicals, Inc.