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ORIGINAL ARTICLE
Year : 2015  |  Volume : 28  |  Issue : 2  |  Page : 540-546

Renal fibrosis


1 Department of Internal Medicine, Faculty of Medicine, Menoufia University, Menoufia, Egypt
2 Hurghada General Hospital, Hurghada, Egypt

Correspondence Address:
Marwa Said Abd Elsaed Foda
El Madares Street, Sakala Square, Hurghada, Red Sea 84511
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-2098.163915

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Objective This mini-review attempted to highlight the recent progress in understanding of the cellular and molecular pathways leading to renal fibrosis and discussed the challenges and opportunities in developing therapeutic strategies. Background Renal fibrosis, characterized by tubulointerstitial fibrosis and glomerulosclerosis, is the final manifestation of chronic kidney disease. Renal fibrosis is characterized by an excessive accumulation and deposition of extracellular matrix components. There are many causes of tubulointerstitial fibrosis 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 proinflammatory mediators as occurs in acute or chronic allograft rejection. Epithelial to mesenchymal transition (EMT) of tubular epithelial cells that are transformed to mesenchymal fibroblasts migrating to adjacent interstitial parenchyma constitutes principal mechanism of renal fibrosis along with local and circulating cells. Proteinuria as well as hypoxia are included among the main mechanisms of EMT stimulation. Transforming growth factor-β1 through the SMAD pathway is considered as the main modulator regulating the EMT molecular mechanism, probably in cooperation with hypoxia-inducible factors. Hepatocyte growth factor and bone morphogenetic factor-7 are inhibitory to EMT molecules, which could prevent at experimental and clinical level the catastrophic process of interstitial fibrosis. Interesting data emerge indicating that hepatocyte growth factor and bone morphogenetic factor-7 administration prevents the peritoneal fibrosis of mesothelial cells. Many promising targets for the treatment of renal fibrosis have been validated in various animal models, and even more new targets have been identified. Angiotensin-converting enzyme inhibitors and angiotensin II receptor type 1 blockers are undisputedly the first-line drugs in combating renal fibrosis. These drugs, however, are not able to halt the progression completely. Methods Data about the patient are collected from different sources that deal with renal fibrosis, including references text books, pictures and presentations, medical journals, and concerned web sites. Conclusion Renal fibrosis characterized as a progressive detrimental connective tissue deposition on the kidney parenchyma appears as a harmful process leading inevitably to renal function deterioration.


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