Table 1.

Classification of CRS^1,23,25

Type	Definition	Major mechanisms
Type I	Acute CRS Abrupt worsening of heart function (e.g., ACS or acute HF) resulting in AKI	Neurohormonal, abnormal cell signaling, hemodynamic abnormalities
Type II	Chronic CRS Chronic abnormalities in heart function (e.g., chronic HF) resulting in progressive and permanent CKD	Chronic neurohormonal hyperactivation
Type III	Acute renocardiac syndrome Abrupt worsening of kidney function (e.g., AKI caused by volume overload, inflammatory surge, or metabolic disturbances in uremia; glomerulonephritis) resulting in acute heart disorder (e.g., acute HF, arrhythmia, or ischemia)	Acute volume overload, hyperkalemia, acidosis
Type IV	Chronic renocardiac syndrome CKD (e.g., chronic glomerular disease) resulting in decreased heart function (e.g., HF, cardiac hypertrophy, or increased risk of adverse CV events)	Chronic pressure and volume overload, uremic cardiomyopathy, metabolic/micronutrient abnormalities
Type V	Secondary CRS Systemic condition (e.g., amyloidosis, sepsis, cirrhosis, or diabetes mellitus) resulting in loss of both heart and kidney function	Cytokine storm, danger-associated molecular abnormalities

ACS, acute coronary syndrome; AKI, acute kidney injury; CKD, chronic kidney disease; CRS, cardiorenal syndrome; CV, cardiovascular; HF, heart failure.