Acute kidney injury in sepsis

Acute kidney injury in sepsis (septic AKI) is the most frequently occurring form of AKI in intensive care accounting for more than 50% of all cases. At least initially, functional failure prevails with normal or increased renal blood flow, vascular endothelial damage, microvascular shunting and renal tubular cell stress. This is mediated by proinflammatory substances filtered by the glomeruli, namely pathogen-associated molecular pattern (PAMP) and damage-associated molecular pattern (DAMP). Shock-induced ischemia and nephrotoxin-mediated damage can exacerbate the effect. The diagnosis of septic AKI is still based on serum creatinine and urine output, representing the intersection of the corresponding consensus definitions according to the third international consensus definitions for sepsis and septic shock (Sepsis-3) and Kidney disease: improving global outcomes (KDIGO). A specific treatment for AKI does not currently exist. Therefore, early risk stratification and prevention are of special importance. In manifest septic AKI a carefully thought out fluid management in combination with vasopressors are the mainstays of treatment. Besides the well-established use of noradrenalin currently vasopressin and angiotensin II are clinically investigated. Renal replacement procedures are used in advanced forms of organ failure. Hospital survivors of septic AKI have an increased risk of developing chronic kidney disease and mortality. This is particularly true for patients who have undergone a renal replacement procedure. A nephrological aftercare of these patients is recommended.