Abstract
An ancillary paradigm that has evolved recently in the pathogenesis of diabetic nephropathy includes subclinical microinflammation with influx of macrophages and consequent generation of myriad proinflammatory cytokines and ensuing kidney damage. Among various proinflammatory cytokines, tumor necrosis factor-α (TNF-α) has attracted the most attention, since it amplifies the inflammatory network of cytokines, leading to worsening of the progression of diabetic nephropathy. The article by Awad et al. examines the role of TNF-α in the pathogenesis of experimental diabetic nephropathy.