Serum
neuraminidase (NA,
sialidase) activity has been demonstrated in acute poststreptococcal
glomerulonephritis (APSGN) and implicated in the pathogenesis of the disease. Recent investigations show that
neuraminidase-treated leukocytes accumulate preferentially in kidneys; therefore, we were interested in knowing if desialized cells infiltrate the kidney in APSGN. We first tested the capacity of
peanut agglutinin lectin (PNA) to detect injected NA-treated leukocytes in the kidney of rats. NA-treated leukocytes were transfused and desialized cells were identified with
fluorescein-conjugated
peanut lectin (
FITC-PNA) in renal tissue. PNA positive cells were identified in rat kidneys 3 hours after injection (glomeruli: 1.67 +/- 0.19 cells/g.c.s.; interstitium: 0.50 +/- 0.12 cells/int). Sections from available renal biopsy material of APSGN (n = 11), other
glomerulonephritis (n = 28) and normal kidneys (n = 5) were double-stained with
FITC-PNA and with
monoclonal antibody to the CD11b molecule, which is expressed on polymorphonuclear and monocytes the main types of infiltrating cells during APSGN. Desialized (
FITC-PNA positive) cells were found in the glomeruli (2.17 +/- SEM 0.22 cells per glomerular cross section, g.c.s.) and interstitium (0.61 +/- 0.15 cells per 0.0625 mm2, int) in all biopsies of APSGN. Only in 2 of 28 other
glomerulonephritis showed desialized cells. More than 80% of the PNA positive cells in APSGN expressed the CD11b molecule and the infiltration was more intense in early biopsies. In conclusion, desialized leukocytes represent a significant part of the inflammatory infiltrate in APSGN. This finding gives support for a role of NA in the disease and provides clinical validation for a mechanism of renal cellular infiltration suggested by experimental observations.