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10.1113/jphysiol.2014.273078 http://scihub22266oqcxt.onion/10.1113/jphysiol.2014.273078 C4198008!4198008 !24907309     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24907309 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cardiorenal syndrome: acute kidney injury secondary to cardiovascular disease and role of protein-bound uraemic toxins |pdf=|usr=}}{{24907309 }} gab.com Text Cardiorenal syndrome: acute kidney injury secondary to cardiovascular disease and role of protein-bound uraemic toxins JO: J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24907309 #FOAvip 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 (pCS). Both IS and pCS 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. Twit Text FOAVip Cardiorenal syndrome: acute kidney injury secondary to cardiovascular disease and role of protein-bound uraemic toxins ????J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=24907309 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24907309 #FOAvip English Wikipedia <ref>{{Cite pmid|24907309 }}</ref> Cardiorenal syndrome: acute kidney injury secondary to cardiovascular disease and role of protein-bound uraemic toxins #MMPMID24907309 Lekawanvijit S ; Krum H J Physiol 2014[Sep]; 592 (18 ): 3969-83 PMID24907309 show ga 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 (pCS). Both IS and pCS 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. |Animals [MESH] |Biomarkers/blood [MESH] |Cardio-Renal Syndrome/*blood/etiology/physiopathology [MESH] |Humans [MESH] |Toxins, Biological/*blood [MESH]Cardiorenal syndrome: acute kidney injury secondary to cardiovascular (epmc).pdf DeepDyve Pubget Overpricing