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Pathogenesis of chronic renal failure

Study on the pathogenesis of chronic renal failure in 1 about the mechanisms of CRF progression, scholars have put forward some theories, effects of some cytokines and growth factors in the progression of CRF in recent years, also have a new understanding.
(1) high filtration of renal units: it is suggested that the presence of high perfusion and high filtration state of residual renal glomerulus in CRF is one of the important reasons leading to glomerular sclerosis and further loss of nephron. Due to the high filtration, can promote the proliferation of mesangial cells and matrix increased, resulting in the formation of micro aneurysms, endothelial cell damage and platelet aggregation increased, inflammatory cell infiltration, mesangial cell apoptosis, thus the development of glomerular sclerosis.
(2) the high metabolism of renal unit: the residual renal tubular metabolism in CRF, which is one of the important causes of renal tubular atrophy, interstitial fibrosis and progressive renal damage. The high metabolism caused by tubular oxygen consumption increased and increased oxygen free radical, liquid Fe2+ tubule formation and metabolic acidosis caused by the alternative pathway of complement activation and membrane attack complex (C5b 9) formation, which can cause tubulointerstitial injury.
(3) the role of renal tissue transformation of epithelial cell phenotype: recent studies indicate that in some growth factors (such as TGF8) or induced by inflammatory factors, renal tubular epithelial cells, glomerular epithelial cells (e.g. Bauman epithelial cells or podocytes), renal interstitial fibroblast can change fibroblast muscle, play an important role in renal interstitial fibrosis, focal segmental or global glomerulosclerosis in the process.
(4) some cytokines a growth factor: recent studies indicate that CRF animal in renal tissue of some growth factors (such as TGF beta, interleukin 1, mononuclear cell chemoattractant protein 1, angiotensin II, endothelin 1, etc.) are involved in the process of glomerular and tubular injury interstitial, and in promoting the extracellular matrix plays an important role in increasing. For example, CRF animal kidney tissue angiotensin II increased significantly, not only increasing in the glomerular pressure, to play an important role in the process of filtration, and can promote the extracellular matrix of mesangial and renal interstitial (ECM). Some degradation of extracellular matrix proteases such as matrix metalloproteinase (MMP) expression, tissue inhibitors of metalloproteinases and plasminogen activator inhibitor (PAI - I) and expression, also has its important role in glomerulosclerosis and renal interstitial fibrosis.
(5): there are a few other studies found that in a variety of animal models of chronic kidney disease, were found in renal cells apoptosis and glomerulosclerosis, tubular atrophy and interstitial fibrosis are closely related, suggesting that apoptosis may play a role in the progression of CRF. In addition, in recent years, it has been found that aldosterone is also involved in the process of glomerulosclerosis and interstitial fibrosis.

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