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目的观察糖基化终产物(AGEs)在肾脏组织中的沉积及其与肾脏固有细胞表型转化的关系。方法采用免疫组化染色法观察AGEs:羧甲基赖氨酸(CML)、吡咯素、戊糖苷素和细胞骨架蛋白:α-肌动蛋白(-αSMA)、L-收缩平滑肌蛋白(L-CLD)在28例2型糖尿病肾病(DN)患者肾活检组织(疾病组)的沉积,分析二者间及其与肾脏病理改变和临床表现的关系。4例增生硬化型IgA肾病及4例轻微病变型和2例正常肾组织作为对照组。结果(1)四组均可见CML、吡咯素分别沉积在系膜区和肾间质,但对照组明显弱于DN组;戊糖苷素只沉积在DN肾小球基底膜(GBM)。(2)系膜区-αSMA、L-CLD的表达与戊糖苷素呈正相关,吡咯素的沉积与间质L-CLD有关。(3)-αSMA和L-CLD及戊糖苷素的沉积与肾小球硬化指数、间质纤维化百分数及蛋白尿、Scr正相关。结论戊糖苷素在GBM的沉积是糖尿病肾小球硬化的重要原因;AGEs对肾脏的影响部分可能是通过引起肾脏固有细胞的表型转化而起作用的。
Objective To observe the deposition of advanced glycosylation end products (AGEs) in the kidney and its relationship with the phenotype of kidney intrinsic cells. Methods The expressions of AGEs: carboxymethyl lysine (CML), pyrrolo, pentoside and cytoskeletal proteins α-actin (α-SMA), L-CLD ) In 28 cases of type 2 diabetic nephropathy (DN) patients with renal biopsy tissue (disease group) deposition, between the two and its relationship with renal pathological changes and clinical manifestations. 4 cases of proliferative IgA nephropathy and 4 cases of mild lesions and 2 cases of normal kidney tissue as a control group. Results (1) CML was observed in all four groups. Pirarin was deposited in the mesangial area and the renal interstitium, but the control group was significantly weaker than the DN group. Pentoside was only deposited on the DN glomerular basement membrane (GBM). (2) The expression of α-SMA and L-CLD in mesangial area was positively correlated with pentoside, and the deposition of pyrrole was related to interstitial L-CLD. (3) The deposition of -αSMA, L-CLD and pentosidine positively correlated with glomerulosclerosis index, percentage of interstitial fibrosis, proteinuria and Scr. Conclusion The deposition of pentosidine in GBM is an important cause of diabetic glomerulosclerosis. The effect of AGEs on the kidney may partly affect the phenotype of innate cells in the kidney.