Cardiorenal syndrome: pathophysiology, preclinical models, management and potential role of uraemic toxins.
Cardiorenal syndrome (CRS) describes the primary dysfunction in either the kidney or heart that initiates the combined impairment of both organs. The heart and kidney exert reciprocal control of the respective function to maintain constant blood volume and organ perfusion under continuously changing conditions. The pathophysiology of CRS is not fully understood, but appears to be caused by a complex combination of haemodynamic, neurohormonal, immunological and biochemical feedback pathways. Of these pathways, the contributory role of uraemic toxins that accumulate in CRS has been underexplored. One such toxin, namely indoxyl sulphate, has been found to have direct adverse effects on relevant cardiac cells. Early diagnosis by assessing cardiac and renal injury biomarkers may be critical for timely therapeutic intervention. Such therapies are directed at attenuation of neurohormonal activation, control of elevated blood pressure, correction of anaemia and relief of hypervolaemia. Reduction of non-dialysable uraemic toxins is a further potentially beneficial therapeutic strategy.
Centre for Cardiovascular Research and Education in Therapeutics, Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Victoria, Australia.
Shan
S
Liu
Suree
S
Lekawanvijit
Andrew R
AR
Kompa
Bing H
BH
Wang
Darren J
DJ
Kelly
Henry
H
Krum
D000818:Animals; D015415:Biomarkers; D059347:Cardio-Renal Syndrome / Q000150:complications / Q000453:epidemiology / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology; D009392:Nephrectomy; D014511:Uremia / Q000503:physiopathology*
D015415:Biomarkers