Tanaka Mari, Tsujii Tomomi, Komiya Toshiyuki, Iwasaki Yukako, Sugishita Takeshi, Yonemoto Satomi, Tsukamoto Tatsuo, Fukui Satoshi, Takasu Akimasa, Muso Eri
Department of Nephrology, Kitano Hospital, Tazuke Kofukai Medical Research Institute, Osaka, Japan.
Contrib Nephrol. 2007;157:90-3. doi: 10.1159/000102309.
The pathological role of obesity has rarely been studied in primary glomerular diseases. The purpose of this study is to examine the clinicopathological influence of obesity in IgA nephropathy (IgAN). 74 patients with IgA nephropathy in our institution from October 2000 to January 2004 were retrospectively divided into two groups according to body mass index (BMI): the non-obese group (group N) with BMI < 25 kg/m(2), and the obese group (group O) with BMI > or = 25 kg/m(2). There were 50 patients in group N and 24 patients in group O. Clinical analysis showed no significant difference between these two groups in blood pressure, serum cholesterol, creatinine clearances or grade of hematuria. However, urinary protein excretion and serum creatinine were significantly greater in group O than in group N. Although semiquantitative analysis of light-microscopical findings showed no significant differences in the severity of mesangial proliferation, matrix expansion, glomerulosclerosis or crescent formation, image analysis showed that total glomerular area and tuft area were significantly larger in group O. In addition, ultrastructural study revealed significantly higher glomerular basement membrane thickness in group O. 62 patients (46 patients, group N; 16 patients, group O) were followed in our institution for one year. Urinary protein was significantly decreased only in patients who received steroid in both groups. Although administration of ACE inhibitor or ARB tended to decrease urinary protein in group O, the change was not statistically significant. Our findings indicate that obesity may accelerate the increase of proteinuria in IgAN through ultrastructural modification of the glomerular basement membrane.
肥胖在原发性肾小球疾病中的病理作用鲜有研究。本研究旨在探讨肥胖对IgA肾病（IgAN）的临床病理影响。回顾性分析了2000年10月至2004年1月在我院就诊的74例IgA肾病患者，根据体重指数（BMI）将其分为两组：BMI<25kg/m²的非肥胖组（N组）和BMI≥25kg/m²的肥胖组（O组）。N组50例，O组24例。临床分析显示，两组在血压、血清胆固醇、肌酐清除率或血尿分级方面无显著差异。然而，O组的尿蛋白排泄量和血清肌酐显著高于N组。尽管光镜检查结果的半定量分析显示系膜增生、基质扩张、肾小球硬化或新月体形成的严重程度无显著差异，但图像分析显示O组的总肾小球面积和肾小球毛细血管丛面积显著更大。此外，超微结构研究显示O组的肾小球基底膜厚度显著更高。62例患者（N组46例，O组16例）在我院随访1年。仅在两组中接受类固醇治疗的患者中尿蛋白显著降低。尽管在O组中使用血管紧张素转换酶抑制剂（ACE抑制剂）或血管紧张素Ⅱ受体拮抗剂（ARB）倾向于降低尿蛋白，但变化无统计学意义。我们的研究结果表明，肥胖可能通过肾小球基底膜的超微结构改变加速IgAN中蛋白尿的增加。
