Table 2.
Pathophysiological mechanisms along with biomarkers in cardiorenal crosstalk.
| Pathophysiological Mechanism | Biomarkers | |
|---|---|---|
| Hemodynamic pathways | Cardiac output | BNP, copeptin, cardiac troponin-I |
| Arterial pressure | CRP, TNF alpha, ox-LDL, | |
| Extracellular fluid volume | NT-proBNP, cardiac troponin-I, copeptin | |
| Elevated renal venous pressure | Creatinine | |
| Non hemodynamic pathways | Fibrosis | Gal-3, NGAL, sST-2, cardiotrophin-1 |
| Oxidative stress | MMP, Ox-HDL, MR-proADM, 8-epi-isoprostanes | |
| Obesity | Aldosteron | |
| Endothelial dysfunction | sFLT-1, VEGF, PDGF soluble thrombomodulin, angiopoietin-2, anti-endothelial cell antibodies | |
| Chronic Inflammation | C-reactive protein, procalcitonin, NGAL, IL-6, IL-18, TNF-alpha | |
| Epigenetics | microRNAs, miR-21 |
BNP: B-type natriuretic peptide; NT-proBNP: N-terminal pro-brain natriuretic peptide; CRP: C-reactive protein; Gal-3: Galectin-3; sST-2: soluble suppression of tumourigenicity 2; MMP: matrix metalloproteinase; Ox-HDL: oxidized high-density lipoprotein; sFlt-1: soluble vascular endothelial growth factor receptors-1; VEGF: vascular endothelial growth factor; PDGF: platelet-derived growth factor; IL-18: interleukin-18; IL-6: interleukin-6; MR-proADM: midregional proadrenomedullin; NGAL: neutrophil gelatinase-associated lipocalin; miR-21: microRNA 21; TNF-alpha: tumor necrosis factor-alpha.