Accumulating evidence suggests that the central locus for the progression of CKD is the
renal proximal tubule. As injured tubular epithelial cells dedifferentiate in attempted repair,
they stimulate inflammation and recruit myofibroblasts. At the same time, tissue loss
stimulates remnant nephron hypertrophy. Increased tubular transport workload eventually
exceeds the energy-generating capacity of the hypertrophied nephrons, leading to anerobic
metabolism, acidosis, hypoxia, endoplasmic reticulum stress, and the induction of additional …