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Diabetic nephropathy, the development in addition to hereditary, the high blood sugar also plays a very important role. Numerous studies have shown that strict control of blood glucose can significantly reduce the risk of occurrence of diabetic nephropathy. How is high blood sugar causes diabetic nephropathy, which is not fully understood. But many studies have shown that high blood sugar can activate many of the local renal hormone (or cytokine), the current study found that these substances and is closely related to the development of diabetic nephropathy. Of course, the pathogenesis of diabetic nephropathy include abnormal blood rheology, oxygen-carrying red blood cell disorder, hyperthyroidism bypass sorbitol and other factors, but these factors more or less with local renal hormone (or cytokine) related.
1. Renin-angiotensin system (RAS): study found that in diabetic rats (AT ) levels were significantly increased AT1R expression in renal tissue also increased significantly. Clinical and Experimental Research and Application of ACE inhibitors have proved effective in preventing the occurrence and development of diabetic nephropathy.
2. Kidney local growth factors: The study found a variety of local growth factor in kidney of diabetic nephropathy are, closely related, such as insulin-like growth factor, platelet-derived growth factor and transforming growth factor (TGF- ) and so on, they can stimulate mesangial cell proliferation, increased mesangial depositio


n of extracellular matrix. TGF- 1 of one more, studies have shown, in diabetic rats significantly increased the expression of TGF- 1 is important that after application of ACE inhibitors can be significantly decreased. Thus, in diabetic nephropathy that may play a key role.
3. Endothelin (ET): ET has a strong role in the contraction of blood vessels, of which the strongest ET1. It is known to stimulate mesangial cell proliferation. Experimental study found that diabetic rats and its receptor expression in ET2 was significantly increased, and the application of ET1 receptor antagonist can prevent diabetic nephropathy. In addition, in vitro studies have shown that TGF- 1 can increase expression of renal tubular cells ET 4. Nitric oxide (NO): NO has a strong role in dilation of blood vessels, it is in NO synthase (NOS) L-arginine under the evidence from the synthesis of. NOS has two kinds, structured and inducible NOS NOS (iNOS). Early renal tissue of diabetic rats iNOS expression and NO content increased, that may be related to the early renal blood flow. In the late DM rat renal tissue, iNOS expression was not significantly increased NOS expression and NO-type structure were significantly decreased. L-arginine was the treatment of diabetic rats can prevent the occurrence of diabetic nephropathy, but long term use of NOS inhibitors may accelerate glomerular lesions in diabetic rats, suggesting that NO can prevent the occurrence and development of diabetic nephropathy. The study suggests, NO can protect the glomerular lesions in diabetic rats later. While many studies have shown that renal NO and TGF- 1 AT and adjust between themselves.
Key words Diabetic nephropathy; pathogenesis
Diabetic nephropathy (DN) is a mesangial cell proliferation and extracellular matrix increase, glomerular basement membrane thickening and glomerular sclerosis as the basic pathology of the disease, the mechanism of complex, currently not fully elucidated, including the glomerular blood kinetics, metabolism disorder, blood rheology changes, oxidative stress, cytokines and the interaction of genetic susceptibility and other factors led to the occurrence of DN. Information is at home and abroad, to diabetic nephropathy in recent years (DN) in the pathogenesis of Reis as follows.
1 diabetic nephropathy Mechanisms of Inflammation
In recent years, even though clinical and experimental studies have shown that strict control of blood glucose, angiotensin converting enzyme inhibitors or angiotensin II receptor antagonist of the renin - angiotensin system (Renin-angiotensin system, RAS) is only part of the DN a certain delay effect, recent studies revealed the incidence of DN in metabolic disorders and hemodynamic mechanism based on the inflammatory reaction mechanism is a key factor in its continued development. Intrinsic renal cells in pathological conditions can produce TNF- , IL-1, IL-6, NO and other inflammatory factors, these factors but also by autocrine and paracrine effect of expanding the inflammatory response, causing inflammatory cascade. Recently Katherine [1] proposed that as a diabetic metabolic disorder caused by the inflammatory response disease.
1.1 hyperglycemia and diabetic nephropathy hyperglycemia between the inflammatory response is the basic clinical manifestations of diabetes is also involved in the pathogenesis of diabetic nephropathy the major metabolic disorders.


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