Description

Sepsis is generally characterized as a life-threatening organ dysfunction and dysregulating host reaction to the infection (e.g., bacterial, viral, mycotic (1). Typical pathophysiological processes of sepsis include systemic inflammation, immune suppression, activation of the clotting cascade, and increase of endothelial vascular permeability with subsequent leak of fluids into the interstitial space. One of the most important organ damage due to ongoing sepsis is acute kidney injury (AKI), which is also a predictor of mortality in critically ill patients. The exact pathophysiology of septic AKI remains a challenging and poorly understood mechanism. A decrease of oxygen delivery to the tissues during the septic shock and usually high oxygen consumption of renal tubular cells make them prone to ischemia injury with consequences in tubular cell death. Among potential immune inflammatory response biomarkers in sepsis and septic shock might be promising pentraxin 3 (PTX3), which plays an important role in endothelial dysfunction with several pathogenic pathways' activation. Recently has been shown the positive effect of PTX3 on the inhibition of reactive oxygen species, mitochondrial injury, and apoptosis pathway in AKI (3,4). Another promising urinary or serum biomarker of AKI seems to be uromodulin, which is dynamically regulated in response to sepsis. Serum uromodulin concentrations decrease during septic human AKI development and are associated with increased renal and systemic oxidative damage (5,6,7). MicroRNAs are small non-coding RNAs, that have been reported to be useful biomarkers for AKI development or potential target for AKI treatment. Determination of serum PTX3 and uromodulin concomitantly with specific circulating miRNAs associated with PTX3 and uromodulin-specific signaling pathways in critically ill septic patients could bring new insights to septic AKI pathophysiology and contribute to future development of new preventive or therapeutic options in septic patients.