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シライ ヨウコ
白井 陽子 所属 医学部 医学科（東京女子医科大学病院） 職種 助教 |
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| 論文種別 | 原著 |
| 言語種別 | 英語 |
| 査読の有無 | 査読あり |
| 表題 | Morphologic Analysis of Urinary Podocytes in Focal Segmental Glomerulosclerosis. |
| 掲載誌名 | 正式名：Kidney360 略 称：Kidney360 ISSNコード：26417650/26417650 |
| 掲載区分 | 国外 |
| 巻・号・頁 | 2(3),pp.477-486 |
| 著者・共著者 | Shirai Yoko, Miura Kenichiro, Yokoyama Takashi, Horita Shigeru, Nakayama Hideki, Seino Hiroshi, Ando Taro, Shiratori Atsutoshi, Yabuuchi Tomoo, Kaneko Naoto, Ishiwa Sho, Ishizuka Kiyonobu, Hara Masanori, Hattori Motoshi |
| 担当区分 | 筆頭著者 |
| 発行年月 | 2021/03 |
| 概要 | Background:The development of glomerulosclerosis in FSGS is associated with a reduction in podocyte number in the glomerular capillary tufts. Although it has been reported that the number of urinary podocytes in FSGS exceeds that of minimal-change nephrotic syndrome, the nature of events that promote podocyte detachment in FSGS remains elusive.Methods:In this study, we provide detailed, morphologic analysis of the urinary podocytes found in FSGS by examining the size of the urinary podocytes from patients with FSGS, minimal-change nephrotic syndrome, and GN. In addition, in urinary podocytes from patients with FSGS and minimal-change nephrotic syndrome, we analyzed podocyte hypertrophy and mitotic catastrophe using immunostaining of p21 and phospho-ribosomal protein S6.Results:The size of the urinary podocytes was strikingly larger in samples obtained from patients with FSGS compared with those with minimal-change nephrotic syndrome and GN (P=0.008). Urinary podocytes from patients with FSGS had a higher frequency of positive immunostaining for p21 (P<0.001) and phospho-ribosomal protein S6 (P=0.02) than those from patients with minimal-change nephrotic syndrome. Characteristic features of mitotic catastrophe were more commonly observed in FSGS than in minimal-change nephrotic syndrome urinary samples (P=0.001).Conclusions:We posit that the significant increase in the size of urinary podocytes in FSGS, compared with those in minimal-change nephrotic syndrome, may be explained by hypertrophy and mitotic catastrophe. |
| DOI | 10.34067/KID.0005612020 |
| PMID | 35369007 |