No abstract

Chronic kidney disease, despite being a “silent epidemic” disease, represents one of the main causes of mortality in general population, along with cardiovascular disease, which is the leading cause of poor prognosis for these patients. The specific objective of our study was to characterize the relationship between the inflammatory status, the bone disorders markers, and kidney failure in chronic kidney disease patient stages 2–4, in order to design a novel biomarker panel that improves early disease diagnosis and therapeutic response, thus being further integrated into clinical applications. A panel of proteomic biomarkers, assessed by xMAP array, which includes mediators of inflammation (IL-6, TNF-α) and mineral and bone disorder biomarkers (OPG, OPN, OCN, FGF-23, and Fetuin-A), was found to be more relevant than a single biomarker to detect early CKD stages. The association between inflammatory cytokines and bone disorders markers, IL-6, TNF-α, OPN, OPG, and FGF-23, reflects the severity of vascular changes in CKD and predicts disease progression. Proteomic xMAP analyses shed light on a new approach to clinical evaluation for CKD staging and prognosis.

No abstract

Sepsis is a clinical syndrome defined by the presence of infection and systemic inflammatory response to infection and results from a complex interaction between the host and infectious agents. It is characterized by the activation of multiple inflammatory pathways, with an increased risk of mortality. The incidence of sepsis has been on an ever-increasing pathway in recent years. Sepsis can be induced by several clinical situations that predispose to its occurrence: malignant tumors, organ transplantation, AIDS, radiation therapy, burns, sores, polytrauma, diabetes mellitus, hepatic failure, renal failure, malnutrition, catheters or different invasive devices, and urinary catheters. The microorganisms involved in the pathogenesis of sepsis are Gram-positive cocci ( Staphylococci , Streptococci ) and Gram-negative bacilli ( Klebsiella, Pseudomonas aeruginosa , E. coli ), fungi ( Candida ), parasites, and viruses. Among mechanisms involved in septic shock production, two pathological phenomena appear: the profound decompensation of circulation and metabolic disturbances that evolve towards an irreversible state. The intimate mechanism of shock involves the activation of monocytes, macrophages and neutrophils by lipopolysaccharides of Gram-negative bacteria. The microvascular bed is directly involved in the etiopathogenesis of disorders of acute inflammatory states associated with or without sepsis. A better comprehension of sepsis pathophysiology, especially the molecular mechanisms of septic shock, allows for new therapeutic perspectives.