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Pathophysiology of the cardiorenal syndromes: executive summary from the eleventh consensus conference of the Acute Dialysis Quality Initiative (ADQI)

McCullough PA, Kellum JA, Haase M, et al, Contrib Nephrol. 2013;182:82-98.

Authors list: McCullough PA, Kellum JA, Haase M, Müller C, Damman K, Murray PT, Cruz D, House AA, Schmidt-Ott KM, Vescovo G, Bagshaw SM, Hoste EA, Briguori C,Braam B, Chawla LS, Costanzo MR, Tumlin JA, Herzog CA, Mehta RL, Rabb H, Shaw AD, Singbartl K, Ronco C.

St. John Providence Health System, Warren, Mich., Providence Hospitals and Medical Centers, Southfield and Novi, MI 48374 , USA. [email protected]

Abstract

Cardiorenal syndromes (CRS) have been recently classified into five distinct entities, each with different major pathophysiologic mechanisms. CRS type 1 most commonly occurs in the setting of acutely decompensated heart failure where approximately 25% of patients develop a rise in serum creatinine and a reduction of urine output after the first several doses of intravenous diuretics. Altered cardiac and renal hemodynamics are believed to be the most important determinants of CRS type 1. CRS type 2 is the hastened progression of chronic kidney disease (CKD) in the setting of chronic heart failure. Accelerated renal cell apoptosis and replacement fibrosis is considered to be the dominant mechanism. CRS type 3 is acutely decompensated heart failure after acute kidney injury from inflammatory, toxic, or ischemic insults. This syndrome is precipitated by salt and water overload, acute uremic myocyte dysfunction, and neurohormonal dysregulation. CRS type 4 is manifested by the acceleration of the progression of chronic heart failure in the setting of CKD. Cardiac myocyte dysfunction and fibrosis, so-called ‘CKD cardiomyopathy’, is believed to be the predominant pathophysiologic mechanism. Type 5 CRS is simultaneous acute cardiac and renal injury in the setting of an overwhelming systemic insult such as sepsis. In this scenario, the predominant pathophysiological disturbance is microcirculatory dysfunction as a result of acutely abnormal immune cell signaling, catecholamine cellular toxicity, and enzymatic activation which result in simultaneous organ injury often extending beyond both the heart and the kidneys. This paper will summarize these and other key findings from an international consensus conference on the spectrum of pathophysiologic mechanisms at work in the CRS.

Copyright © 2013 S. Karger AG, Basel.

 

 

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Additional Information:

Pathophysiology of the Cardiorenal Syndromes:  Executive Summary from the Eleventh Consensus Conference of the Acute Dialysis Quality Initiative (ADQI), McCullough PA, et al. The Acute Dialysis Quality Initiative (ADQI) is a leading consensus group that operates worldwide in establishing common ground upon which future research is planned in the domain of cardiorenal syndromes.  These syndromes occur in a variety of clinical scenarios and result in acute or chronic organ failure in the heart, kidneys, or both.  Acute Cardio-Renal Syndrome (Type 1) is considered as acute worsening of heart function leading to kidney injury and/or dysfunction.  This is a syndrome of worsening renal function that frequently complicates acutely decompensated heart failure in hospitalized patients.  Chronic Cardiorenal Syndrome (Type 2) refers to chronic abnormalities in heart function leading to kidney injury or dysfunction. This subtype indicates that chronic heart failure can hasten the progression of chronic kidney disease with loss of renal filtration function and the development of proteinuria. Acute Reno-Cardiac Syndrome (Type 3) highlights acute worsening of kidney function leading to heart injury and/or dysfunction. Little is known about the frequency of this syndrome where acute heart failure develops as a consequence of AKI.  It was inferred from the literature that subclinical heart failure or significant myocardial disease is an important determinant of the phenotypic expression of this syndrome.  Chronic Reno-Cardiac Syndrome (Type 4) occurs when chronic kidney disease leads to heart injury, disease and/or dysfunction.  Chronic kidney disease is an accepted independent determinant for the progression of heart failure to hospitalization, pump failure death, and sudden death.  Secondary Cardio-Renal Syndromes (Type 5) is defined by systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney. Although this subtype does not have a primary and secondary organ dysfunction in temporal sequence, situations do arise where both organs simultaneously are targeted by systemic illnesses, the prototype being acute sepsis.  The ADQI process has identified key targets for in vitro diagnostics as well as targets for drug and device development in all five syndromes.  With agreed upon terminology and definitions, ADQI has established a platform for biotechnology market development that will bring new products to this space and advance our knowledge and ability to care for patients with these high-risk and often fatal syndromes.

 

 

Pathophysiology of the cardiorenal syndromes: executive summary from the eleventh consensus conference of the Acute Dialysis Quality Initiative (ADQI). Global Medical Discovery