Immune complex glomerulonephritis in experimental kala‐azar

Abstract

In the present work we demonstrate that hamsters infected with L. donovani eliminate large quantities of immunoglobulins in the urine. This alteration is clearly a consequence of a conspicuous immune complex glomerulonephritis readily detectable 7 days after the beginning of infection. L. donovani antigens and hamsters immunoglobulins (Igs) were revealed as granular deposits in the mesangial areas and contiguous loops of the glomeruli. Histopathological alterations such as focal mesangial proliferation with progression to diffuse proliferation were observed in the first 3 weeks of infection. From day 35 onwards, all diseased animals presented large deposits of amyloid material of predominantly glomerular localization. In consonance with these alterations, Igs were detected in the urine by day 21 of infection and their concentration increased substantially with the progression of disease. In contrast, serum Igs increased until day 21, when their concentration dropped steadily.

Renal involvement in canine leishmaniasis: a morphological and immunohistochemical study

“…These results suggest that the glomerulonephritis responsible for abnormal filtration would be initiated or induced by a type III hyper sensibility. The lesions were more pronounced from three to four weeks (Sartori et al, 1987). In the present study, the deposit of IgG and IgM in kidneys was assessed by immunohistochemical technique.…”

“…These mechanisms involve many processes that have in common the deposition of humoral immune response elements, mainly immunoglobulins and components of the complement system, on glomerular walls and/or mesangial matrix (Zatz and Fujihara, 1999).…”

Immunoactivation and immunopathogeny during active visceral leishmaniasis

“…Dogs and hamsters with visceral leishmaniasis presenting lesions similar to those in humans are used as models to understand human pathology 16,57 . Until recently, studies of glomerular alterations in visceral leishmaniasis pathogenesis have only found immune complex deposition 19,53,58 .…”

Amiloidosis en Didelphis marsupialis infectado experimentalmente con Leishmania chagasi.

“…No obstante, este depósito de amiloide no ha sido antes observado en Didelphis infectados naturalmente con diversos agentes animales que han sido estudiados en el Laboratorio de Patología del INS. Por otra parte, otros animales experimentales como el hámster, desarrollan amiloidosis secundaria sistémica con la leishmaniosis experimental (12,13). En los humanos deben transcurrir varios años con la infección crónica para que se deposite el amiloide (9); lo mismo ocurre con los caballos inoculados repetidamente para producir sueros antirrábicos o antiofídicos, los cuales desarrollan amiloidosis secundaria sistémica después de varios años de ser inoculados con los inmunógenos correspondientes (Laboratorio de Patología, INS, observaciones sin publicar).…”

“…La amiloidosis secundaria ocurre con regularidad en modelos experimentales de animales que reciben inyecciones reiteradas de antígenos, como en los hámsteres (12,13), ratones (14) y perros con leishmaniosis visceral (15); los depósitos se ven en el hígado, el bazo, las glándulas suprarrenales, el riñón y los testículos (16,17).…”