Table 2.
Direct and indirect mechanisms of cardiorenal syndrome type 3.
| Direct mechanisms | Systemic immune system | Innate |
| Adaptive | ||
| Inflammation, cytokines, and chemokines | TNF-α, IL-1, IL-6, ICAM-1 | |
| Oxidative stress | RNS, ROS | |
| Apoptosis | Cardiac and renal cells | |
| Neutrophil infiltration | ||
| SNS and RAAS | Norepinephrine activity, disturbance in myocardial calcium homeostasis, oxygen demand, cardiac myocite apoptosis | |
|
| ||
| Indirect mechanisms | Fluid overload | Systemic edema, cardiac overload, hypertension, pulmonary edema, myocardial dysfunction |
| Electrolyte imbalances | Hyperkalemia | |
| Hyperphosphatemia | ||
| Hypophosphotemia | ||
| Hypermagnesemia | ||
| Acidemia | Alterations in protein structure and function | |
| Uremic toxins | Myocardial ischemia, pericarditis | |