title: Cardiorenal syndrome type 4: insights on clinical presentation and pathophysiology from the eleventh consensus conference of the Acute Dialysis Quality Initiative (ADQI).
abstract: In developed countries, the continuing rise in the prevalence of hypertension, hyperlipidemia and diabetes has contributed to an overall increase in the incidence of both cardiovascular disease (CVD) and chronic kidney disease (CKD). The observation that even modest reductions in renal function correlate with increased CVD morbidity and mortality has led to the recognition that CKD is an independent risk factor for CVD. Conversely, there is a growing recognition that many pathologic conditions that contribute to CVD, including coronary artery disease, left ventricular hypertrophy and diastolic dysfunction, can accelerate the decline in renal function. In addition, physiologic mechanisms designed to compensate for reduced glomerular filtration rate including activation of the renin-angiotensin-aldosterone axis, the release of fibroblastic growth factor 23 and other mechanisms for calcium-phosphate homeostasis as well as and the pathophysiologic effects of uremic toxins can also directly contribute to CVD. The end result of the interaction between changes in pressure and volume overload and the physiologic compensation for the loss of function in both the heart and the kidney leads to accelerated decline in both organ systems. This complex physiologic and pathophysiologic interplay between the cardiovascular and renal systems is collectively referred to as the cardiorenal syndrome. The discussion which follows is aimed at outlining the pathophysiologic mechanisms linking advanced CKD (4 and 5) to the development of cardiac abnormalities which occur with unique frequency and severity in patients with severe impairment of renal function.
authors.affiliation: Department of Medicine, College of Medicine, University of Tennessee, Chattanooga, TN 37408, USA. jamestumlinmd@nephassociates.com
authors.forename: James A
authors.initials: JA
authors.lastname: Tumlin
authors.forename: Maria R
authors.initials: MR
authors.lastname: Costanzo
authors.forename: Lakhmir S
authors.initials: LS
authors.lastname: Chawla
authors.forename: Charles A
authors.initials: CA
authors.lastname: Herzog
authors.forename: John A
authors.initials: JA
authors.lastname: Kellum
authors.forename: Peter A
authors.initials: PA
authors.lastname: McCullough
authors.forename: Claudio
authors.initials: C
authors.lastname: Ronco
mesh_terms: D059347:Cardio-Renal Syndrome / Q000145:classification / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000453:epidemiology; D003324:Coronary Artery Disease / Q000453:epidemiology; D000089703:Fibroblast Growth Factor-23; D005346:Fibroblast Growth Factors / Q000502:physiology; D005355:Fibrosis; D037502:Galectin 3 / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000453:epidemiology; D009206:Myocardium / Q000473:pathology; D006435:Renal Dialysis / Q000592:standards*; D051436:Renal Insufficiency, Chronic / Q000150:complications; D061205:Vascular Calcification / Q000453:epidemiology
chemical_list: D037502:Galectin 3; D005346:Fibroblast Growth Factors; D000089703:Fibroblast Growth Factor-23