Polycystic Kidney Disease (PKD) is an autosomal domiant disorder, whose development is the course of renal fibrosis being formed. As times goes, renal functions will lose along with renal fibrosis deteriorating. Although the genetic pathogenesis of PKD is unknown, scholars have made clear the basic pathogenic factors resulting in renal fibrosis. There are three main causes of Polycystic Kidney Disease.
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| Three Causes of Polycystic Kidney Disease |
The causing genes
With genetic flaw or genic mutation, the body of the patient will secrete some substances, arousing the cysts. Stimulated by those substances, tubular basement membrane turns to be abnormal and secrete epidermal growth factor (EGF), Transforming Growth Factor (TGF-β) and Insulin-like growth factor (IGF), which all are able to boost the proliferation and secretion of epithelial cells of kidney tubules. This is the first step of Polycystic Kidney Disease on exertion.
Kidney tubule epithelial cells’ proliferating and secreting
As renal tubular epithelial cells proliferate unusually, blocking its unobstructed flow passage. The upstream of liquid will be forced to extrude the wall of tubules and form cysts. As the cysts grow, they will squeeze other tissues in kidney and result in the lack of blood and oxygen, which open the course of renal fibrosis.
With fibrosis developing, a lot of nephritoxic factors are released, such as platelet-derived growth factor (PDGF) and Transforming Growth Factor (TGF-β), which will make renal tubular epithelial cells transform into abnormal tissues and Myofibroblast. Those myofibroblast tend to produce and secretes a large quantity of extracellular matrix which is hard to be degraded.
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