Review Article
Advances in the Pathogenesis of Cardiorenal Syndrome Type 3
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 |
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