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Cardiorenal syndrome: acute kidney injury secondary to cardiovascular disease and role of protein‐bound uraemic toxins
Author(s) -
Lekawanvijit Suree,
Krum Henry
Publication year - 2014
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2014.273078
Subject(s) - cardiorenal syndrome , acute kidney injury , medicine , heart failure , kidney disease , disease , kidney , lipocalin , intensive care medicine , myocardial infarction , cardiology , bioinformatics , biology
Abstract Cardiovascular disease (CVD) and kidney disease are closely interrelated. Disease of one organ can induce dysfunction of the other, ultimately leading to failure of both. Clinical awareness of synergistic adverse clinical outcomes in patients with coexisting CVD and kidney disease or ‘cardiorenal syndrome (CRS)’ has existed. Renal dysfunction, even mild, is a strong independent predictor for poor prognosis in CVD patients. Developing therapeutic interventions targeting acute kidney injury (AKI) has been limited due mainly to lack of effective tools to accurately detect AKI in a timely manner. Neutrophil gelatinase‐associated lipocalin and kidney injury molecule‐1 have been recently demonstrated to be potential candidate biomarkers in patients undergoing cardiac surgery. However, further validation of AKI biomarkers is needed in other CVD settings, especially acute decompensated heart failure and acute myocardial infarction where AKI commonly occurs. The other concern with regard to understanding the pathogenesis of renal complications in CVD is that mechanistically oriented studies have been relatively rare. Pre‐clininal studies have shown that activation of renal inflammation–fibrosis processes, probably triggered by haemodynamic derangement, underlies CVD‐associated renal dysfunction. On the other hand, it is postulated that there still are missing links in the heart–kidney connection in CRS patients who have significant renal dysfunction. At present, non‐dialysable protein‐bound uraemic toxins (PBUTs) appear to be the main focus in this regard. Evidence of the causal role of PBUTs in CRS has been increasingly demonstrated, mainly focusing on indoxyl sulfate (IS) and p ‐cresyl sulfate ( p CS). Both IS and p CS are derived from colonic microbiotic metabolism of dietary amino acids, and hence the colon has become a target of treatment in addition to efforts to improve dialysis techniques for better removal of PBUTs. Novel therapy targeting the site of toxin production has led to new prospects in early intervention for predialysis patients with chronic kidney disease.