Canine visceral leishmaniasis frequently causes renal damage that leads to chronic kidney disease. Fifteen dogs seropositive for Leishmania were selected and biopsied before (T0) and 60 days later after (T1) treatment with a specific anti-Leishmania pharmacological agent. Various parameters were selected for evaluating the glomerular and tubulointerstitial damage. At T0, mesangioproliferative and membranoproliferative glomerulonephritis were observed in 6 dogs, chronic glomerulosclerosis in 5, and end-stage kidney in 3; renal tissue from 1 dog was within normal histologic limits. The most frequently observed ultrastructural changes were foot-process effacement, thickening of the basement membranes, and immune deposits. One dog had mesangial immune deposits at T1 that had not been present at T0, so the diagnosis was changed to mesangioproliferative glomerulonephritis. In dogs with end-stage kidney, the number of obsolescent glomeruli and cystic atrophied glomeruli was increased at T1. However, progression of the glomerular lesions was minimal in most dogs. Worsening of tubulointerstitial scores was evident in the dogs with the most severe lesions at the first biopsy. Progression of the tubulointerstitial damage was minimal in the mildly affected dogs, and the interstitial inflammation was abated. In conclusion, renal lesions can progress over a 60-day period in canine leishmaniasis. A longer period between the renal biopsies would be necessary to demonstrate more severe changes. In addition a specific anti-Leishmania treatment could have a significant effect in the early stages of the disease.

Light and Electron Microscopic Analysis of Consecutive Renal Biopsy Specimens from Leishmania-Seropositive Dogs

ARESU, LUCA;BENALI, SILVIA LUCIA;FERRO, SILVIA;GALLO, ENRICO;CASTAGNARO, MASSIMO
2013

Abstract

Canine visceral leishmaniasis frequently causes renal damage that leads to chronic kidney disease. Fifteen dogs seropositive for Leishmania were selected and biopsied before (T0) and 60 days later after (T1) treatment with a specific anti-Leishmania pharmacological agent. Various parameters were selected for evaluating the glomerular and tubulointerstitial damage. At T0, mesangioproliferative and membranoproliferative glomerulonephritis were observed in 6 dogs, chronic glomerulosclerosis in 5, and end-stage kidney in 3; renal tissue from 1 dog was within normal histologic limits. The most frequently observed ultrastructural changes were foot-process effacement, thickening of the basement membranes, and immune deposits. One dog had mesangial immune deposits at T1 that had not been present at T0, so the diagnosis was changed to mesangioproliferative glomerulonephritis. In dogs with end-stage kidney, the number of obsolescent glomeruli and cystic atrophied glomeruli was increased at T1. However, progression of the glomerular lesions was minimal in most dogs. Worsening of tubulointerstitial scores was evident in the dogs with the most severe lesions at the first biopsy. Progression of the tubulointerstitial damage was minimal in the mildly affected dogs, and the interstitial inflammation was abated. In conclusion, renal lesions can progress over a 60-day period in canine leishmaniasis. A longer period between the renal biopsies would be necessary to demonstrate more severe changes. In addition a specific anti-Leishmania treatment could have a significant effect in the early stages of the disease.
2013
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/2523876
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