Table 1.
Classification of cardiorenal syndrome.
| Definition | Description | Clinical Conditions | Main Pathophysiological Mechanisms of Heart and Kidney Damage |
|---|---|---|---|
| Type 1 CRS (Acute CRS) |
Acute HF resulting in AKI |
AKI in the setting of acute HF or cardiogenic shock |
Venous congestion, Renal hypoperfusion, SNS/RAAS activation, Oxidative stress, Inflammation. |
| Type 2 CRS (Chronic CRS) |
Chronic HF resulting in CKD |
CKD in the setting of chronic HF The diagnosis of CKD is based on the Improving Global Outcomes Kidney Disease Outcomes (KDIGO) Quality Initiative (KDOQI) criteria: - albuminuria and/or glomerular filtration rate (GFR) < 60 mL/in/1.73 m2; - sustained decrease in GFR > 5 mL/min/1.73 m2/year; - decline of GFR > 10 mL/min/1.73 m in 2/5 years; - sustained increase in albuminuria along with suspected diagnosis of congestive HF before the onset or progression of CKD. |
SNS/RAAS activation, Fibrosis, Oxidative stress, Inflammation. |
| Type 3 CRS (Acute renocardiac syndrome) |
AKI resulting in acute HF |
Acute HF in the setting of AKI. Acute HF is linked to acute worsening of renal function with consequent electrolyte imbalance, metabolic acidosis, and volume overload. |
Volume overload, SNS/RAAS activation, Oxidative stress/ mitochondrial dysfunction, Inflammation, Electrolyte disorders and metabolic disorders (due to uremic condition). |
| Type 4 CRS (Chronic renocardiac syndrome) |
CKD resulting in chronic HF |
LVH/dysfunction and chronic HF in the setting of CKD (Uremic Cardiomyopathy) CKD is related to accelerated atherosclerosis, insulin resistance, lipid dysmetabolism, neurohormonal imbalance and consequently to the development of CVD. |
SNS/RAAS activation, Inflammation/fibrosis Hyperphosphatemia, Secondary hyperparathyroidism, Increased levels of circulating erythropoiesis inhibitors, furans, phenols, beta-2-microglobulin, leptin and polyols. |
| Type 5 CRS (Secondary CRS) |
Systemic processes resulting in both HF and kidney damage |
Amyloidosis, Autoimmune Diseases (SLE), Sepsis, COVID-19, Advanced liver diseases, Hepatorenal syndrome, Cirrhosis. |
Inflammatory and prothrombotic states, Secretion of proinflammatory Cytokines, Endothelial dysfunction, Impaired coronary and glomerular autoregulation. |