LAUSR

Hemolytic − uremic syndrome (HUS) is a severe complication of infection by Shiga toxin (STx)‐producing enterohemorrhagic Escherichia coli. Hemolytic − uremic syndrome is defined clinically as a triad of non‐immune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injuries. Neurologic complications such as acute encephalopathy are also observed. In humans, endothelial cells, proximal tubular epithelial cells, mesangial cells, podocytes, intestinal epithelial cells, and monocytes / macrophages are susceptible to STx‐mediated injury. Shiga toxin induces the secretion of inflammatory cytokines and chemokines from susceptible cells, including tumor necrosis factor‐α interleukin (IL)‐1, IL‐6, and IL‐8. These cytokines and chemokines contribute to the pathogenesis of HUS and encephalopathy by enhancing STx‐induced cytotoxicity and inducing inflammatory cell infiltration. Serum cytokine/chemokine levels are therefore useful as indicators of disease activity and predictors of progression from acute kidney injury to chronic kidney disease. Anti‐inflammation therapy combined with apheresis to remove excessive cytokines / chemokines and methylprednisolone pulse therapy to suppress cytokine/chemokine production may be an effective treatment regimen for severe E. coli‐associated HUS. However, this regimen requires careful monitoring of potential side effects, such as infections, thrombus formation, and hypertension.