Pole, and Contribute to Crescent Formation. Recent Studies

support the second possibility [1–6]. It was reported that chemokines produced by proximal tubular cells promoted the infiltration [3,4]. Proximal tubular epithelial cells activate urinary complement proteins in situ and contribute to the mediation of tubulointerstitial injury [6]. The tubular epithelial cell is the major site of M-CSF production within the injured kidney; macrophage accumulation and local proliferation can occur in the tubulointerstitium in the absence of glomerular inflammation [2]. Proximal tubular cells also promote fibrogenesis by transforming growth factor1-mediated induction of peritubular myofibroblasts [1]. Most important is that recent studies performed on cultured cells and experimental nephropathies suggest the possibility of epithelial–mesenchymal transition of tubular epithelial cells, i.e. transdifferentiation. One study, done on a human renal biopsy, also suggested such a transdifferentiation [7]. Finally, is it possible that proximal tubular cells transdifferentiate and migrate towards the glomerular urinary pole and contribute to crescent formation?