Pathological influence of obesity on renal structural changes in chronic kidney disease
Pathological influence of obesity on renal structural changes in chronic kidney disease
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DOI：
10.1007/s10157-009-0169-3
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发表时间：
2009-08-01
影响因子：
2.3
通讯作者：
Taguchi, Takashi
中科院分区：
文献类型：
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作者：
Kato, Shigeko;Nazneen, Arifa;Taguchi, Takashi
本研究旨在探讨肥胖对慢性肾脏疾病(CKD)患者肾脏结构的病理影响。研究对象为肥胖(体重指数，BMI/1000ppm 25 kg/m(2))非肾小球肾炎(n=26)、IgA肾病(n=19)、良性肾病(BNS，n=15)和薄基底膜病(TMD，n=6)患者和65例非肥胖对照组(n=20、20、10和15)。评估患者的肾小球病变(系膜增生和局灶性节段性/全局性肾小球硬化)、肾小球大小和肾小球基底膜(GBM)厚度。肥胖的非GN、IgAN和BNS组的尿蛋白高于各自的对照组。所有肥胖组均出现局灶性节段性肾小球硬化(FSGS)病变。肥胖组和非肥胖组的肾小球体积均大于非肥胖组。非肥胖TMD和BNS患者的肾小球体积明显大于非肥胖非GN患者。无论肾小球疾病的类型如何，肥胖患者的肾小球基底膜厚度均高于非肥胖者，但仅在非肾小球肾炎和BNS组中显著增加。在非肾小球肾炎、IgAN和BNS患者中，肥胖会加重蛋白尿，并与结构变化相关，如肾小球增大和基底膜增厚，类似于肥胖相关肾病的变化。肥胖似乎会加重慢性肾脏病的肾脏病理状态。
Role of obesity in renal pathological and structural changes remains poorly investigated, and this study was designed to examine the pathological effects of obesity on renal structural components in patients with chronic kidney diseases (CKD).The study subjects were obese (body mass index, BMI a parts per thousand yen 25 kg/m(2)) patients with nonglomerulonephritis (non-GN, n = 26), IgA nephropathy (IgAN, n = 19), benign nephrosclerosis (BNS, n = 15), and thin basement membrane disease (TMD, n = 6), and 65 nonobese controls (n = 20, 20, 10, and 15, respectively). Patients were evaluated for glomerular lesions (mesangial proliferation and focal segmental/global glomerulosclerosis), glomerular size, and thickness of glomerular basement membrane (GBM).Urinary protein was higher in obese non-GN, IgAN, and BNS groups than in the respective controls. Focal segmental glomerulosclerosis (FSGS) lesions were noted in all obesity groups. The glomeruli were larger in size in obese than in nonobese patients of the non-GN and IgAN groups. The glomeruli of nonobese TMD and BNS patients were significantly larger in size than those of nonobese non-GN patients. GBM were thicker in obese than in nonobese patients irrespective of types of glomerular diseases, but only significantly so in non-GN and BNS groups.In non-GN, IgAN, and BNS, obesity worsens proteinuria and is associated with structural changes such as glomerulomegaly and GBM thickening, similar to changes observed in obesity-related nephropathy. Obesity seems to worsen the renopathological state in CKD.