Macrophage subclasses and proliferation in childhood IgA glomerulonephritis.
We immunohistologically compared the number of intraglomerular infiltrating cells in 14 children with poststreptococcal acute glomerulonephritis (PSAGN) and 20 children with immunoglobulin A glomerulonephritis (IgAGN) with histological characteristics similar to those of PSAGN to explain the difference in clinicopathological characteristics between these two diseases. Immunohistological study was performed in kidney tissues from these patients by using monoclonal antibodies of T-cell marker (CD3 and CD45RO), B-cell marker (CD20), neutrophil marker (CD15), macrophage marker (CD68), four subclasses of macrophages (early-stage, acute-stage, chronic-stage, and mature inflammatory macrophage marker), and proliferating cell nuclear antigen (PCNA). The 34 patients were classified into three stages according to the time from the detection of urinary abnormalities to biopsy. Intraglomerular immunopositive cells were expressed as the number of cells per glomerulus. There were more intraglomerular positive cells of CD15, CD68, and the four macrophage subclasses in PSAGN than IgAGN. The number of intraglomerular infiltrating macrophages decreased with time in PSAGN, whereas the number of macrophages in IgAGN remained constant at all stages. Intraglomerular infiltration of acute-stage inflammatory macrophages alone was evident in IgAGN. Both the number of intraglomerular proliferating macrophages (PCNA-positive plus CD68-positive cells) and proportion of proliferating macrophages/total macrophages were greater in IgAGN than PSAGN. Normal urinalysis results were evident in all patients with PSAGN during follow-up, and urinary abnormalities persisted in 18 patients with IgAGN. In conclusion, differences in the maturity of infiltrating macrophages and number of proliferating macrophages are associated with the different clinicopathological characteristics in children with PSAGN and IgAGN.
Second Department of Pathology, School of Medicine, Fukuoka University, Fukuoka, Japan.
S
S
Hisano
Y
Y
Sasatomi
Y
Y
Kiyoshi
S
S
Takebayashi
D000208:Acute Disease; D000293:Adolescent; D015703:Antigens, CD / Q000276:immunology; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology; D015415:Biomarkers; D002455:Cell Division / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D005260:Female; D005922:Glomerulonephritis, IGA / Q000097:blood / Q000175:diagnosis* / Q000276:immunology; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology; D007150:Immunohistochemistry / Q000706:statistics & numerical data; D007678:Kidney Glomerulus / Q000276:immunology; D008264:Macrophages / Q000145:classification* / Q000276:immunology; D008297:Male; D018809:Proliferating Cell Nuclear Antigen / Q000276:immunology; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015415:Biomarkers; D007070:Immunoglobulin A; D018809:Proliferating Cell Nuclear Antigen; C067980:CD68 antigen, human; D000097382:CD68 Molecule