Morioka T, Sugano H, Matsui K, Kagami S, Shimizu F, Oite T
Department of Immunology, Niigata University School of Medicine, Japan.
Nephron. 1988;50(2):116-20. doi: 10.1159/000185140.
Urinary protein excreted in active in situ immune complex glomerulonephritis (ICGN) was qualitatively analyzed by the comparison of sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) patterns of urinary proteins from rats with Masugi GN, active Heymann GN (AHGN), and chronic serum sickness GN (CSSGN). In the SDS-PAGE analysis of urinary protein excreted in the active in situ ICGN and Masugi GN models, 200- and 145-kD macromolecules and low molecular weight components around 12 kD were excreted in large quantities at the full development stage (greater than 100 mg/24 h urinary protein). These findings, however, were obscure or lacking in CSS-GN and AHGN at the peak of proteinuria. Electrophoretic patterns of urinary proteins including lower molecular weight proteins could be divided into two groups: either active in situ ICGN and Masugi GN or AHGN and CSSGN. These two groups corresponded to the differences of morphologic expression such as proliferative changes rather than degree of proteinuria. The location of immune complex formation and deposition, probably different among the experimental models, may play an important role for determining the mediation and nature of glomerular injury.
通过比较Masugi肾小球肾炎（GN）、活动性海曼肾炎（AHGN）和慢性血清病性肾炎（CSSGN）大鼠尿蛋白的十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE）图谱，对原位免疫复合物性肾小球肾炎（ICGN）活动期排泄的尿蛋白进行了定性分析。在对原位ICGN活动期和Masugi GN模型中排泄的尿蛋白进行SDS-PAGE分析时，在疾病充分发展阶段（尿蛋白大于100 mg/24 h）大量排泄出200 kD和145 kD的大分子以及12 kD左右的低分子量成分。然而，在蛋白尿高峰期，CSS-GN和AHGN的这些结果并不明显或未出现。包括低分子量蛋白在内的尿蛋白电泳图谱可分为两组：原位ICGN活动期和Masugi GN组，以及AHGN和CSSGN组。这两组对应于增殖性改变等形态学表现的差异，而非蛋白尿程度的差异。免疫复合物形成和沉积的位置在不同实验模型中可能有所不同，这可能对确定肾小球损伤的介导作用和性质起着重要作用。
