Chronic kidney disease may be stimulated by many different etiologies, but its progression involves a common, yet complex, series of events that lead to the replacement of normal tissue with scar. These events include altered physiology within the kidney leading to abnormal hemodynamics, chronic hypoxia, inflammation, cellular dysfunction, and activation of fibrogenic biochemical pathways. The end result is the replacement of normal structures with extracellular matrix. Treatments presently are focused on delaying or preventing such progression, and are largely nonspecific. In pediatrics, such therapy is complicated further by pathophysiological issues that render children a unique population.