Abstract :
Fibrosis in the kidneys arises when there has been damage to the glomeruli or the tubules, resulting in atrophy of normal epithelium and loss of surrounding heparan sulphate proteoglycans. Subsequently, fibroblasts form new extra cellular fibrous tissue expanding the extra cellular space. There are many causes of tubulointerstitial fibrosis (TIF), ranging from the effects of hypertension, glomerulonephritides and pyelonephritis, to conditions causing heavy proteinuria, and any process that incites glomeruli or proximal tubules to produce pro-inflammatory mediators as happens in acute or chronic allograft rejection. Following injury, both interstitial cells and proximal tubular epithelium are activated, and myofibroblasts (MFs) appear. MFs, defined by their expression of a - smooth muscle actin (SMA), generally correlate with the degree of renal impairment and histological damage [1] for they play a key role in development of glomerulosclerosis and interstitial fibrosis. [2] [Table - 1] summarizes the processes that trigger fibrosis. One should be aware that therapeutic corticosteroids synergize with TGFE in causing tissue fibrosis.
