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. 2009 Dec 25;31(6):703–711. doi: 10.1093/eurheartj/ehp507

Table 1.

Cardio-renal syndromes: classification, definitions, and work group statements

Syndromes Acute cardio-renal (type 1) Chronic cardio-renal (type 2) Acute reno-cardiac (type 3) Chronic reno-cardiac (type 4) Secondary CRS (type 5)
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Definition Acute worsening of heart function (AHF–ACS) leading to kidney injury and/or dysfunction Chronic abnormalities in heart function (CHF-CHD) leading to kidney injury or dysfunction Acute worsening of kidney function (AKI) leading to heart injury and/or dysfunction Chronic kidney disease (CKD) leading to heart injury, disease and/or dysfunction Systemic conditions leading to simultaneous injury and/or dysfunction of heart and kidney
Primary events Acute heart failure (AHF) or acute coronary syndrome (ACS) or cardiogenic shock Chronic heart disease (LV remodelling and dysfunction, diastolic dysfunction, chronic abnormalities in cardiac function, cardiomyopathy) AKI CKD Systemic disease (sepsis, amyloidosis, etc.)
Criteria for primary events ESC, AHA/ACC ESC, AHA/ACC RIFLE–AKIN KDOQI Disease-specific criteria
Secondary events AKI CKD AHF, ACS, arrythmias, shock CHD (LV remodelling and dysfunction, diastolic dysfunction, abnormalities in cardiac function), AHF, ACS AHF, ACS, AKI, CHD, CKD
Criteria for secondary events RIFLE–AKIN KDOQI ESC, AHA/ACC ESC, AHA/ACC ESC, AHA/ACC, RIFLE/AKIN ESC, AHA/ACC KDOQI
Cardiac biomarkers Troponin, CK-MB, BNP, NT-proBNP, MPO, IMA BNP, NT-proBNP, C-reactive protein BNP, NT-proBNP BNP, NT-proBNP, C-reactive protein C-reactive protein, procalcitonin, BNP
Renal biomarkers Serum cystatine C, creatinine, NGAL. Urinary KIM-1, IL-18, NGAL, NAG Serum creatinine, cystatin C, urea, uric acid, C-reactive protein, decreased GFR Serum creatinine, cystatin C, NGAL. Urinary KIM-1, IL-18, NGAL, NAG Serum creatinine, cystatin C, urea, uric acid, decreased GFR Creatinine, NGAL, IL-18, KIM-1, NAG
Prevention strategies Acutely decompensated heart failure and acute coronary syndromes are most common scenariosInciting event may be acute coronary ischaemia, poorly controlled blood pressure, and noncompliance with medication and dietary sodium intakeRandomized trials improving compliance with heart failure care management have reduced rates of hospitalization and mortality, and a reduction in the rates of acute cardio-renal syndrome (type 1) can be inferred A common pathophysiology (neurohumoral, inflammatory, oxidative injury) could be at work to create organ dysfunctionDrugs that block the renin–angiotensin system reduce the progression of both heart failure and CKDIt is unknown whether other classes of drugs can prevent chronic cardio-renal syndrome (type 2) Acute sodium and volume overload are part of the pathogenesisIt is unknown whether sodium and volume overload is prevented with different forms of renal replacement therapy and if this will result in lower rates of cardiac decompensation The chronic processes of cardiac and renal fibrosis, left ventricular hypertrophy, vascular stiffness, chronic Na and volume overload, and other factors (neurohumoral, inflammatory, oxidative injury) could be at work to create organ dysfunctionA reduction in the decline of renal function and albuminuria has been associated with a reduction in cardiovascular eventsThe role of chronic uraemia, anaemia, and changes in CKD-mineral and bone disorder on the cardiovascular system is known in chronic reno-cardiac syndrome Potential systemic factors negatively impact function of both organs acutelyIt is uncertain if reduction/elimination of the key factors (immune, inflammatory, oxidative stress, thrombosis) will prevent both cardiac and renal decline.
Management strategies Specific—depends on precipitating factorsGeneral supportive—oxygenate, relieve pain & pulmonary congestion, treat arrhythmias appropriately, differentiate left from right heart failure, treat low cardiac output or congestion according to ESC guidelines(a); avoid nephrotoxins, closely monitor kidney function. Treat CHF according to ESC guidelinesa, exclude precipitating pre-renal AKI factors (hypovolaemia and/or hypotension), adjust therapy accordingly and avoid nephrotoxins, while monitoring renal function and electrolytesExtracorporeal ultrafiltration Follow ESC guidelines for acute CHFa specific management may depend on underlying aetiology, may need to exclude renovascular disease and consider early renal support, if diuretic resistant Follow KDOQI guidelines for CKD management, exclude precipitating causes (cardiac tamponade). Treat heart failure according to ESC guidelinesa, consider early renal replacement support Specific—according to etiology. General—see CRS management as advised by ESC guidelines* 2008

AKI, acute kidney injury; CKD, chronic kidney disease; NGAL, neutrophil gelatinase-associated lipocalin; NAG, N-acetyl-β-(d)glucosaminidase.

aAs advised by ESC guidelines 2008.