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Fig. 1 | Critical Care

Fig. 1

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

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

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Critical Care

ISSN: 1364-8535