Twelve Beagle dogs were immunized with aqueous-soluble Dirofilaria immitis
antigens, and subsequent to at least fivefold increases in serum antibody titer, 6 mg of homologous
antigen was infused into the left renal artery. Six dogs were treated once daily starting the day of infusion with 0.75 mg/kg of
1-benzylimidazole (1-BIM) in saline. Six control dogs were given saline only. Light, immunofluorescent, and transmission electron microscopic examinations of renal tissue from control dogs, 10 days after
antigen infusion, showed a mesangioproliferative
glomerulonephritis in the left kidney with polymorphonuclear leukocyte (PMNL) infiltration and
fibrin deposition.
Immunoglobulin (Ig) G, M, C3, and Dirofilaria
antigen deposits were observed in a segmental granular pattern. Mesangial, subendothelial, and intramembranous electron dense deposits were observed, and anti-Dirofilaria
antibodies were demonstrated in kidney eluates from each dog. Administration of 1-BIM had no significant effect on
IgG,
IgM, C3, or
antigen deposits, electron dense deposits, or concentration of antibody in kidney eluates. However, 1-BIM-treated dogs had less glomerular cell proliferation,
periodic acid-Schiff (PAS) positive glomerular staining, PMNL infiltration, and
fibrin deposition. These data suggest that
thromboxane is an important mediator in the development of
immune complex glomerulonephritis, and that in certain circumstances, inhibition of
thromboxane synthesis may be an effective
therapy for
immune complex glomerulonephritis in the dog.