Animal studies using mice found that AKI may subsequently result in increased vascular permeability, disruption in the blood-brain barrier, increased cerebral proinflammatory cytokines (IL-6, IL-1β, IL-12, keratinocyte-derived chemokine, granulocyte-colony stimulating factor, and glial fibrillary acidic protein), and increased neuronal pyknosis and microgliosis (up-regulation of brain macrophages) [21, 23]. The gene discussed is IL6; the disease is acute kidney injury.