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Archive » 1999 » 2 » | Archive » Medical field » Fields » Infectious Diseases » Archive » Medical field » Fields » Pathology »

Histomorphology and immunohistology of postinfectious glomerulonephritis in relation to the duration of the disease and type of infection


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In addition to the classical picture of endocapillary proliferative and exudative glomerulonephritis, patients with acute postinfectious glomerulonephritis may manifest a broad spectrum of various histomorphological and immunohistological changes which may reflect the stage of the disease, their responsivness to the disease and/or the specific type of infection. The data on the correlation between histomorphological changes and immune deposits are still sparse. The purpose of this study was to evaluate these, most probably key relationships in the pathogenesis related to the duration of the disease and type of infection. This retrospective study involved 113 kidney biopsies from 91 men and 22 women with the diagnosis of postinfectious glomerulonephritis. The tissue samples were examined by standard light and immunofluorescent microscopy techniques. Mesangial, endocapillary and mesangiocapillary proliferation, exudation, tubulo-interstitial changes,
vascular lesions and glomerular immune deposits were evaluated semiquantitatively using the generally recognized nephropatological methods. Extracapillary proliferation and global and segment glomerulosclerosis were evaluated as a percentage of the affected glomeruli. Immune deposits demonstrated the following three immunofluorescent patterns: garland, starry sky and mesangial. Streptococcus was confirmed to be causally related to postinfectious glomerulonephritis in 54% of cases. Staphylococcus was found in 6% of cases and both, streptococcus and staphylococcus in 5%. In 35% of cases no causative agent was demonstrated. IgG and complement component C3 deposits with a starry sky pattern were confirmed to be significantly associated with with glomerular endocapillary proliferation and exudation characteristic of the in the first month of the disease course. A mesangial, often less intensive, pattern of C3 deposits associated with mesangial proliferation predominated in the second and third month. A higher percentage of sclerosed glomeruli and increased intensity of vascular lesions during the course of the disease were not statistically significant. In more than half the patients tubulo-interstitial changes were found independently of the duration of glomerulonephritis, but mostly to a limited extent. A garland pattern accompanied by a very intensive endocapillary and mesangiocapillary proliferation and exudation was observed in 8 (7%) patients exclusively in the first two months of the disease. Extracapillary crescents were found in 27 (24%) patients, but they were located only focally and involved a maximum of 38% of glomeruli. They were noticed almost exclusively in the first two months of the disease. There were some unusual samples demonstrating endocapillary proliferation (4/14), exudative reaction (5/14) and glomerular capillary starry sky deposits (5/14), which persisted after three months of the course of glomerulonephritis. In some cases, the intensity of inflammatory changes did not correlate with the pattern and intensity of immune deposits. Our study confirmed a significant association of starry sky and garland pattern with endocapillary proliferation and exudation in the first, and partly, the second month of acute postinfectious glomerulonephritis. The mesangial patern of the C3 deposits and mesangial proliferation are characteristic of the later phases of the disease. All deviations seem to be attributable to individual differences in responsiveness as we failed to prove the obvious differences depending on the type of infection. Only slightly more frequent extracapillary crescents and IgA were found in immune deposits in patients with glomerulonephritis mediated by staphylococcal and undefined infectious agents.

Hermann Dejan

glomerulonephritis – pathology – immunology, streptococcal infections, fluorescent antibody technique direct

Cite as:
Med Razgl. 1999; 38: 339–65.

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