A. Kashem et al., GLOMERULAR FC-ALPHA-R EXPRESSION AND DISEASE-ACTIVITY IN IGA NEPHROPATHY, American journal of kidney diseases, 30(3), 1997, pp. 389-396
In this study, we examined the receptors for the Fc portion of immunog
lobulin A (IgA) (Fc alpha R) in the glomeruli as well as circulating p
olymorphonuclear leukocytes and monocytes at the mRNA level by reverse
transcription-polymerase chain reaction (RT-PCR) assay and at the pro
tein level by an immunohistochemistry/flow cytometry technique using a
specific anti-Fc alpha R monoclonal antibody (My 43), Glomeruli were
isolated from biopsy specimens of renal tissues from IgA nephropathy (
IgAN; 20 cases) and non-IgA mesangial proliferative glomerulonephritis
(PGN; 13 cases) patients, and from normal renal tissue specimens obta
ined from kidneys removed because of malignancies (five cases) applyin
g the microdissection method, There was a relative increase in Fc alph
a R in the circulating phagocytes from IgAN patients compared with tho
se from PGN and healthy controls, Fc alpha R expression was present in
approximately 40% of glomeruli samples from IgAN patients at the mess
age levels, Fc alpha R-positive specimens were also strongly positive
for expression of tumor necrosis factor-alpha, interleukin-1, and inte
rleukin-6 mRNA, Specimens from PGN patients and healthy controls did n
ot show any detectable Fc alpha R message, Serum IgA levels and severi
ty of hematuria were significantly higher in patients with positive Fc
alpha R expression, A message for Fc alpha R was detected in the tiss
ues that were more damaged histologically, Our data suggest that there
is some in vivo induction of glomerular Fc alpha R expression, possib
ly mediated by a synergistic stimulus from IgA and inflammatory cytoki
nes, and the expressed receptor is likely to be involved in the diseas
e process of IgAN, (C) 1997 by the National Kidney Foundation, Inc.