HISTOLOGICAL EVIDENCE OF NEURAMINIDASE INVOLVEMENT IN ACUTE NEPHRITIS- DESIALIZED LEUKOCYTES INFILTRATE THE KIDNEY IN ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

Serum neuraminidase (NA, sialidase) activity has been demonstrated in acute poststreptococcal glomerulonephritis (APSGN) and implicated in t he pathogenesis of the disease. Recent investigations show that neuram inidase-treated leukocytes accumulate preferentially in kidneys; there fore, we were interested in knowing if desialized cells infiltrate the kidney in APSGN. We first tested the capacity of peanut agglutinin le ctin (PNA) to detect injected NA-treated leukocytes in the kidney of r ats. NA-treated leukocytes were transfused and desialized cells were i dentified with fluorescein-conjugated peanut lectin (FITC-PNA) in rena l tissue. PNA positive cells were identified in rat kidneys 3 hours af ter 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 kidney s (n = 5) were double-stained with FITC-PNA and with monoclonal antibo dy to the CD11b molecule, which is expressed on polymorphonuclear and monocytes the main types of infiltrating cells during APSGN. Desialize d (FITC-PNA positive) cells were found in the glomeruli (2.17 +/- SEM 0.22 cells per glomerular cross section, g.c.s.) and interstitium (0.6 1 +/- 0.15 cells per 0.0625 mm(2), int) in all biopsies of APSGN. Only in 2 of 28 other glomerulonephritis showed desialized cells. More tha n 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 inflammato ry 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.