Clinico-pathological and renal morphological findings in dogs naturally infected with Dirofilaria repens.

BACKGROUND: Dirofilaria repens is a mosquito-borne filarial nematode that causes subcutaneous dirofilariasis in dogs and is closely related to Dirofilaria immitis. Infection with D. immitis can lead to immune-mediated glomerulonephritis characterized by immune complex deposition along the glomerular basement membrane, resulting in proteinuria and renal dysfunction. Reported histopathological changes include membranous glomerulonephritis with potential chronic progression to chronic interstitial nephritis, glomerulosclerosis, and amyloidosis. Despite the close relationship between these two Dirofilaria species, renal clinicopathological changes associated with D. repens infection have been only rarely investigated, and renal ultrastructural and immunofluorescence findings have not been described in naturally infected dogs. The objective of this study was to collect clinicopathological data and evaluate kidneys from dogs naturally infected with D. repens for structural abnormalities using light microscopy (LM), immunofluorescence (IF), and transmission electron microscopy (TEM). RESULTS: Seventy-two shelter dogs from the university neutering program were screened for D. repens infection. Six infected dogs were identified, and renal biopsies were obtained during neutering. Serum urea, creatinine, and SDMA concentrations were measured, and comprehensive urinalysis was performed, including urinary protein-to-creatinine and albumin-to-creatinine ratios. None of the dogs had increased serum creatinine or SDMA; two of six dogs had mildly increased urea. Mean urine specific gravity was 1.029 ± 0.011, and urine sediment was unremarkable in all dogs. Two dogs were borderline proteinuric and one was proteinuric; the mean urine protein-to-creatinine ratio was 0.29 ± 0.15. Microalbuminuria was detected in one case (median: 0.001). Histopathology predominantly demonstrated podocyte injury with variable podocyte foot process effacement, without evidence supporting an immune complex-mediated glomerulopathy. Two dogs had mild focal and segmental glomerulosclerosis (FSGS). IF was available for two dogs and did not support immune complex-mediated disease, in agreement with TEM findings. CONCLUSIONS: In this cohort, dogs naturally infected with D. repens showed predominantly mild renal lesions characterized mainly by podocyte injury and, less frequently, focal segmental glomerulosclerosis. These findings differ from the immune-complex-dominant renal pathology commonly described in D. immitis infection and highlight the value of ultrastructural and immunofluorescence assessment for characterizing renal changes associated with D. repens infection.