CCL-2 and CXCL-8: Potential Prognostic Biomarkers of Acute Kidney Injury after a Bothrops atrox Snakebite

Figure 6

Probable pathogenic mechanism for the development of acute kidney injury after a B. atrox snakebite. Acute kidney injury initially results from the direct damage by the venom to the renal vascular endothelium. After activation of the endothelium, renal epithelial cells, tubular cells, and others produce chemotactic molecules, such as CCL-2 and CXCL-8, and synergistically increase the expression of p-selectins and cell adhesion molecule 1 (ICAM-1). Neutrophils and monocytes adhere to endothelial cells and migrate through the interstitium, causing changes in vascular permeability and compromising the cell integrity of the endothelium and renal tubules. A capillary plug is formed with the infiltration of neutrophils, monocytes, platelets, and red blood cells. Infiltrated neutrophils and monocytes release proinflammatory chemokines and cytokines, exacerbating the immune response, followed by alterations such as NTA and cell apoptosis that lead to decreased renal function with accumulation of metabolites and electrolytes in the body, resulting in acute renal failure in these patients. It is noteworthy that the cells represented in the figure were not evaluated in the present study.