Table 1.
Hyperactivation of RAAS |
Sympathetic over-reactivity |
Insufficient pressure-natriuresis (with consequent volume overload, arterial hypertension, venous congestion and heart failure) |
CKD-related mineral and bone disorders( CKD-MBD): ↑ P, ↑ FGF23,↓ Kloto, ↑ PTH, ↑ propensity for vascular calcifications, Vitamin D deficiency |
Endothelial dysfunction and nitric oxide inhibition |
Atherosclerosis, intima media thickness, arterial stiffness |
Inflammation (↑ CRP,↑ TNF-α, ↑ fibrinogen, ↑ Cytokines) and malnutrition |
Accumulation of uremic toxins (ADMA, p-cresyl sulfate, indoxyl-sulfate, indole-3 acetic acid, trimethylamine N-oxide, etc.) |
Hyperhomocysteinemia |
Anemia (↓ EPO, iron depletion) |
↑ Uric acid levels |
Low or extremely high bicarbonate levels |
Uremic dyslipidemia |
ADMA asymetric dimethylarginine, CRP C-reactive protein, FGF23 fibroblast growth factor 23, EPO erythropoietin, PTH parathyroid hormone, RAAS renin–angiotensin–aldosterone system, TNF-α tumor necrosis factor-α