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genetic susceptibility of diabetic nephropathy familial

2017-01-14 16:53

Pathogenesis

1. genetic susceptibility of diabetic nephropathy familial aggregation phenomena, whether it was 1-DM or 2-DM patients, if syndrome cases complicated with DN, after their brothers and sisters DM DN incidence increased significantly. Even poor glycemic control in patients with 1-DM and only eventually develop end-stage 35% DN. Even the strict control of blood sugar close to normal, has been shown to significantly improve or prevent DN, but cannot prevent the occurrence and development of DN. So at present there are cues DN has a genetic susceptibility.

Such susceptibility model has 3 species:

(1) major gene effect: due to a major gene polymorphisms (or mutations) DN interactions occur with poor glycemic control.

(2) the average gene effect: due to several genetic polymorphisms (or mutations), DN interactions occur with poor glycemic control. These types of disease alleles act independently, and the additive effect. These alleles roles generated by the overall effect depends on their frequency in the population if similar to the frequency of the crowd, then each of them than the average of the if high frequency a gene, allele produces the major gene effect, and several other alleles produce minor gene effects.

Most of the studies of angiotensin ⅱ type 1 receptor gene polymorphism (or mutations) frequency was significantly higher in patients with DN no patients with DN, arguing that it could play a major gene effect. As regards the angiotensinogen gene and angiotensin-converting enzyme gene polymorphism (or mutations) with DN's relationship has not reached the same conclusion. In addition, AGT, ACE, and stress peptide and atrial natriuretic peptide gene polymorphism of aldose reductase (or mutations) relationship between frequency and DN has not come to the same conclusion.

2. the occurrence and development of hyperglycemia in diabetic nephropathy in addition to genetic, but also plays a very important role in high blood sugar. Tight control of blood glucose can significantly reduce the risk of DN. High blood sugar and how did they lead to DN, this has not yet been fully elucidated. High blood sugar can activate many local kidney endocrine hormones, which are closely connected with development of DN. Of course mechanism of DN hemorheology anomalies, dysfunction of red blood cells with oxygen, sorbitol bypass factors such as hyperthyroidism, but these factors more or less local endocrine hormones of kidney-related.

(1) the Renin-angiotensin system: the study found levels were significantly increased in renal tissues of rats with DM, ATlR Express has been a significant increase in renal tissues and clinical and experimental studies certificate application of ACE inhibitors can prevent diabetic nephropathy and development.

(2) local growth factor in kidney: the study found that many local growth factor in kidney were closely associated with development of DN, such as insulin-like growth factor, platelet-derived growth factor and transforming growth factor-b (transforming growth factor-beta, TGF-β), which stimulates Glomerular mesangial cell proliferation, increased mesangial matrix deposition. TGF-β 1 research, studies have shown FGF-Beta 1 expression in renal tissues of rats with DM increased significantly, after important application of ACE inhibitors can be decreased significantly.

(3) et: ET has strongly constricts blood vessels, of which ETI were most intense. Known it stimulates Glomerular mesangial cell proliferation. Experiment shows that the ETI and its receptor expression in renal tissues of rats with DM were significantly increased, and ETI receptor antagonists can control DN. In addition, in vitro studies have shown that TGF-β 1 increases the ETI expression in renal tubular cells.

(4) the nitric oxide: NO strong dilation of blood vessels, it is under NO synthase by the synthesis of l-arginine as a donor.


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