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目的观察胰淀素(amylin)在糖尿病肾病(DN)患者肾组织的沉积和分布特征,探讨肾脏Amylin沉积的致病意义及其影响因素。方法149例经肾活检证实的2型DN患者,免疫组化方法检测肾组织Amylin的沉积,同时行肾组织ApoE检测及电镜观察。竞争性ELISA方法检测血浆Amylin水平,结合患者肾脏病理和临床相关指标进行分析。选择同期经肾活检确诊的肾淀粉样变性、肥胖相关性肾病、轻链沉积病和原发性肾小球肾炎(系膜增生性病变)患者作为相关疾病对照组。结果72例DN患者(48.3%)肾组织Amylin染色阳性,Amylin主要沉积在肾小球系膜基质增多而扩张的系膜区、K-W结节内、增厚的球囊壁和病变的血管壁。肾组织电镜可见无分支、长直线形丝状结构,随意分布于肾小球系膜区、内皮下或基膜内,直径(10.30±1.77)nm。DN患者肾组织Amylin沉积者其肾小球系膜增生,结节病变及肾小球硬化的发生率较无Amylin沉积患者明显增高而小管间质病变程度亦较无Amylin沉积患者重(P<0.05)。肾脏Amylin沉积DN患者24h尿蛋白定量、高血压、肾小管功能受损以及肾功能损伤的程度和贫血均较无Amylin肾组织沉积组更加严重(P<0.05)。DN患者血浆Amylin水平均显著增高(P<0.01),但Amylin肾组织染色阳性和阴性组二者之间并无明显差异(P>0.05)。结论DN患者血浆Amylin水平较正常人明显升高,肾脏可发生Amylin沉积。肾组织Amylin沉积不仅可加重肾组织损伤,而且还与疾病临床表现的严重程度有一定的联系。Amylin在肾脏的沉积参与了DN组织损伤的发生和发展。
Objective To investigate the deposition and distribution of amylin in renal tissue of patients with diabetic nephropathy (DN) and to explore the pathogenic significance of Amylin deposition and its influencing factors. Methods 149 cases of type 2 DN confirmed by renal biopsy were examined for the deposition of Amylin in renal tissue by immunohistochemistry. ApoE and electron microscopy were also performed in renal tissues. The level of Amylin in plasma was detected by competitive ELISA, and the renal pathology and clinically relevant indexes were analyzed. Select the same period by renal biopsy diagnosed renal amyloidosis, obesity-related nephropathy, light chain deposition disease and primary glomerular nephritis (mesangial proliferative lesions) as a related disease control group. Results Amylin staining was found in 72 DN patients (48.3%). Amylin was mainly found in the mesangial area with increased mesangial matrix, K-W nodules, thickened balloon wall and diseased vessel wall. Kidney electron microscopy showed no branch, long linear filamentous structure, randomly distributed in the glomerular mesangial area, subcutaneous or basement membrane, diameter (10.30 ± 1.77) nm. The incidence of glomerular mesangial hyperplasia, sarcoidosis and glomerulosclerosis in DN patients with Amylin deposition was significantly higher than that without Amylin deposition and less in tubulointerstitial lesions than those without Amylin deposition (P <0.05) ). Kidney Amylin sedimentation DN patients with urinary protein in 24h, hypertension, renal tubular damage and renal damage extent and anemia were more severe than those without Amylin renal deposition group (P <0.05). The level of Amylin in DN patients was significantly increased (P <0.01), but there was no significant difference between the Amylin kidney staining positive and negative groups (P> 0.05). Conclusion The plasma Amylin level in patients with DN is significantly higher than that in normal people, and Amylin deposition can occur in the kidney. Amylin deposition in kidney tissue not only aggravates renal tissue damage, but also correlates with the severity of the disease. The deposition of Amylin in the kidney is involved in the occurrence and development of DN tissue damage.