Detrimental cross-talk between sepsis and acute kidney injury: new pathogenic mechanisms, early biomarkers and targeted therapies

Sergio Dellepiane, Marita Marengo, Vincenzo Cantaluppi, Sergio Dellepiane, Marita Marengo, Vincenzo Cantaluppi

Abstract

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency medicine 2016. Other selected articles can be found online at http://www.biomedcentral.com/collections/annualupdate2016. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.

Figures

Fig. 1
Fig. 1
Pathogenetic mechanisms of sepsis‐associated acute kidney injury (AKI). Systemic inflammation coupled with multi‐organ failure induces renal injury through several mechanisms: renal hemodynamic changes, activation of immune cells, massive release of inflammatory molecules and endocrine dysregulation. All contribute to glomerular and tubular cell injury. NO: nitric oxide; NE: norepinephrine; RAAS: renin‐angiotensin‐aldosterone system; GFR: glomerular filtration rate; PAMP: pathogen‐associated molecular pattern; TEC: tubular epithelial cells; : decreased
Fig. 2
Fig. 2
Interplay between tubular epithelial cells and systemic inflammation. Tubular epithelial cells are directly targeted by inflammation through specific membrane receptors able to modulate cytokines, activated immune cells and bacterial products. In response to these deleterious stimuli, tubular cells dedifferentiate and release a plethora of paracrine factors as an ultimate effort to induce tissue regeneration. On the other hand, tubular cells directly contribute to systemic inflammation by carrying out immune functions, such as cytokine release and leukocyte recruitment and activation

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Source: PubMed

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