Growing evidence in animal models suggests that AKI is not an isolated event but results in remote organ dysfunction involving the heart, lungs, and brain through an inflammatory mechanism that involves neutrophil migration, cytokine expression, and increased oxidative stress.4 In mice, kidney ischemia reperfusion resulted in increased levels of pro-inflammatory chemokines, which increased expression of glial fibrillary acidic protein in astrocytes in the cortex and corpus callosum.17 Chronic kidney dysfunction might impair growth and influence brain function in the pediatric population.18,19. The gene discussed is GFAP; the disease is acute kidney injury.