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Updated: Aug 9, 2026
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Glomerular macrophage proliferation in experimental immune complex nephritis
K Y Ren1, J Brentjens, Y X Chen
1Department of Microbiology, School of Medicine, State University of New York, Buffalo 14214.
Insights
In immune complex nephritis, macrophages within the glomerulus actively divide. This proliferation significantly contributes to glomerular hypercellularity and kidney damage during disease.
Area of Science:
- Nephrology
- Immunopathology
- Cell Biology
Background:
- Immune complex nephritis causes glomerular hypercellularity due to intrinsic cell proliferation and mononuclear cell infiltration, mainly macrophages.
- The role of macrophage proliferation within the glomerular tuft during nephritis remains incompletely understood.
Purpose of the Study:
- To investigate whether macrophages undergo mitosis within the glomerular tuft in immune complex nephritis.
- To quantify the contribution of glomerular macrophage proliferation to hypercellularity in a rat model of nephritis.
Main Methods:
- Utilized an immunohistochemical double-labeling technique with ED1 antibody (macrophage marker) and bromodeoxyuridine (S-phase marker).
- Studied chronic serum sickness in LEW rats, a well-characterized model of immune complex nephritis.
- Assessed glomerular macrophage proliferation in vivo and in short-term culture in vitro.
Main Results:
- In normal glomeruli, resident mesangial macrophages constituted a significant portion (≥1/3) of mitotic activity.
- During immune complex glomerulonephritis, glomerular macrophage proliferation increased sharply at proteinuria onset and remained elevated.
- Macrophages from nephritic rats exhibited more vigorous proliferation in vitro and expressed abnormal surface markers.
Conclusions:
- Mesangial macrophage proliferation is a key component of normal glomerular cell turnover.
- In immune complex nephritis, enhanced glomerular macrophage proliferation significantly amplifies their contribution to glomerular damage.
- Targeting macrophage proliferation may offer a therapeutic strategy for immune-mediated kidney diseases.
Abstract:
In immune complex nephritis, glomerular hypercellularity is known to result from the proliferation of intrinsic cells and from the infiltration of mononuclear cells, primarily macrophages. An immunohistochemical double-labeling procedure was used to determine whether macrophages were among the cells which may undergo mitosis within the glomerular tuft. The monoclonal antibody ED1 served as a macrophage marker; cells in the S-phase of mitosis were recognized by uptake of bromodeoxyuridine. Glomerular proliferation was studied in chronic serum sickness of LEW rats, an animal model of immune complex nephritis for which the relationship between immunopathology and pathophysiology has been well described. In normal glomeruli, resident mesangial macrophages accounted for an unexpectedly large proportion (greater than or equal to one-third) of the total mitotic activity. In immune complex glomerulonephritis, the rate of glomerular macrophage proliferation increased rapidly just at the onset of proteinuria and remained high throughout the remaining course of disease. Glomerular macrophages from rats with proliferative nephritis also divided more vigorously than normal in short term culture in vitro, while persistently expressing abnormal surface marker phenotypes. The proliferation of mesangial macrophages appears to be a prominent feature of the normal process of glomerular cell renewal. In hypercellular glomeruli, vigorous local proliferation could greatly amplify the potential of macrophages to cause damage.
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