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 ( > 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.

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