Glomerular lesions in dogs infected with Leishmania organisms

Zatelli, Andrea; Borgarelli, Michele; Santilli, Roberto A.; Bonfanti, Ugo; Nigrisoli, Evandro; Zanatta, Rayssa Ferreira; Tarducci, Alberto; Guarraci, Aurelio

doi:10.2460/ajvr.2003.64.558

Cited by 86 publications

(88 citation statements)

References 10 publications

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“…It occurs by the deposition of immune complexes on the subepithelial surface of the glomerular basement membrane (SERAKIDES, 2010). Although a previous study identified mesangioproliferative glomerulonephritis and focal segmental glomerulonephritis in 21.9% and 19.5% of the dogs with leishmaniosis, respectively, (ZATELLI et al, 2003), these changes were found in only 4.5% and 1.5% of the dogs in this study, respectively.…”

Section: Discussioncontrasting

confidence: 44%

“…Membranoproliferative glomerulonephritis was the most frequently observed and was present in 59% of the dogs, a higher value than the 30% observed by Costa et al (2003) and 18% observed by Rigo et al (2013). Glomerular fibrosis was identified in 45.5% of the dogs and also described by other authors (ZATELLI et al, 2003). Fibrosis is most likely related to a more chronic stage of CKD (NEWMAN et al, 2009), which explains its occurrence mainly in dogs with uremic syndrome (P=0,045, Mann-Whitney test).…”

Section: Discussionmentioning

confidence: 65%

“…Fibrosis is most likely related to a more chronic stage of CKD (NEWMAN et al, 2009), which explains its occurrence mainly in dogs with uremic syndrome (P=0,045, Mann-Whitney test). Membranous glomerulonephritis was present in 34.4% of the dogs and was also described by Zatelli et al (2003) and Rigo et al (2013), but it was not identified in the studies of Costa et al (2003). It occurs by the deposition of immune complexes on the subepithelial surface of the glomerular basement membrane (SERAKIDES, 2010).…”

Section: Discussionmentioning

confidence: 99%

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Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Braga

Leite

Rosa

et al. 2015

Rev. Bras. Parasitol. Vet.

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To evaluate the prevalence of hypertension and its correlation with the severity of renal injury and proteinuria in dogs with leishmaniosis, sixty-six dogs were divided into two groups. Group 1 (G1) was composed of 54 dogs included in stage 1 of chronic kidney disease (CKD), and group 2 (G2) of twelve dogs in stages 2 and 3 of CKD. Prevalence of hypertension was 28.8%, comprising 22.2% of the dogs from G1 and 58.3% from G2 (P=0.011). The mean arterial blood pressure (BP) of dogs from G1 (135.7 ± 20.5) was lower than from G2 (170.0 ± 26.3) (P <0.001). Urine proteincreatinine ratio (UP/C) revealed values above 0.5 in 75.7% of the dogs, with 34% presenting hypertension. All dogs with hypertension had histopathological and laboratory evidence of glomerular disease. Although there was no statistically significant correlation between elevated BP and the severity of glomerular lesions (P=0.408), there was a statistically significant correlation between elevated BP and increased UP/C in the studied population (P=0.002). Thus, dogs with leishmaniosis and renal disease must be screened for the presence of hypertension so that treatment may be instituted as early as possible, in countries where treatment is allowed, to prevent the progression of renal damage.Keywords: Histopathology, kidney, Leishmania infantum chagasi, systolic blood pressure. ResumoPara avaliar a prevalência de hipertensão arterial e sua correlação com a severidade da lesão renal e proteinúria em cães com leishmaniose, 66 cães foram divididos em dois grupos. O grupo 1 (G1), composto por 54 cães em estágio 1 de doença renal crônica (DRC), e o grupo 2 (G2) por 12 cães em estágios 2 e 3 de DRC. A prevalência de hipertensão foi de 28,8%, compreendendo 22,2% dos cães de G1 e 58,3% dos cães de G2 (p = 0,011). A pressão arterial média (PA) de G1 (135,7 ± 20,5) foi inferior a de G2 (170,0 ± 26,3) (P <0,001). A relação proteína creatinina urinária (P/C U) foi maior que 0,5 em 75,7% dos cães, dos quais 34% possuíam hipertensão. Todos os cães com hipertensão apresentavam doença glomerular. Embora não tenha sido observada correlação estatisticamente significativa entre elevação da PA e severidade das lesões glomerulares (P =0,408), houve uma correlação significativa entre PA elevada e aumento da UP/C (P = 0,002). Portanto, cães com leishmaniose e doença renal devem ser pesquisados quanto à presença de hipertensão, para que o tratamento possa ser instituído o mais precocemente possível em países onde ele é permitido, para evitar a progressão da lesão renal.Palavras-chave: Histopatologia, rim, Leishmania infantum chagasi, pressão arterial sistólica.

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Section: Discussioncontrasting

confidence: 44%

Section: Discussionmentioning

confidence: 65%

Section: Discussionmentioning

confidence: 99%

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Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Braga

Leite

Rosa

et al. 2015

Rev. Bras. Parasitol. Vet.

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“…8,29,72,116,118 Tubulointerstitial lesions appear secondarily to glomerular pathology as well as to immune complex-mediated inflammation and the fibrosis of renal interstitium. 8,29,116,153 This proteinuric nephropathy progressively leads to excretory dysfunction or sometimes to decreased or increased glomerular filtration rate and to systemic hypertension that can establish a vicious cycle, thus amplifying the underlying glomerular pathology. 25,26 Ocular disease is quite common in CanL and can be the only or the main clinical manifestation in 3.7% to 16% of the affected dogs.…”

Section: General Pathomechanismsmentioning

confidence: 99%

Pathologic Mechanisms Underlying the Clinical Findings in Canine Leishmaniosis due to Leishmaniainfantum/chagasi

Koutinas¹,

2014

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In dogs with symptomatic or asymptomatic leishmaniosis, Leishmania infantum appears to induce a mixed Th1/Th2 immune response that in the sick dog may eventually result in tissue damage via different pathomechanisms, notably granulomatous inflammation (eg, nodular dermatitis, osteomyelitis), immune complex deposition (eg, glomerulonephritis), and/or autoantibody production (eg, polymyositis). This is a compensatory but detrimental mechanism generated mainly because of the insufficient killing capacity of macrophages against the parasite in the susceptible dog. Clinical disease is typically exemplified as exfoliative and/or ulcerative dermatitis, with or without nasodigital hyperkeratosis and onychogryphosis, glomerulonephritis, atrophic myositis of masticatory muscles, anterior uveitis, keratoconjunctivitis sicca, epistaxis, and/or polyarthritis, appearing alone or in various combinations. The pathogenesis of these clinical conditions has recently been highlighted, to a greater or lesser extent. The usually subclinical conditions expressed as chronic colitis, chronic hepatitis, vasculitis, myocarditis, osteomyelitis, orchiepididymitis, and meningoencephalomyelitis, though uncommon, are of pathologic importance from a differential point of view. The leading cause of death among canine leishmaniosis patients is chronic proteinuric nephritis that may progress to end-stage kidney disease, nephrotic syndrome, and/or systemic hypertension. However, even the asymptomatic proteinuria, when profuse, may be a serious problem because it predisposes to arterial thromboembolism and eventually contributes to the deterioration of the body condition.

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“…Bernese Mountain Dogs, [75][76][77][78] found to be more likely Lyme-seropositive than other breeds with the same lifestyle, were originally thought to have a predisposition for Lyme nephritis, however their Lyme-seropositive status is not associated with proteinuria or lameness and their membranoproliferative glomerulonephritis is familial with an autosomal recessive mode of inheritance possibly with an X-linked modifier gene, affecting mostly females (female:male =4). Other breeds at risk for ICGN because of a higher risk for associated infectious diseases or drug sensitivity are American Foxhounds (Leishmaniasis), [79][80][81][82] Basenjis (IBD/PLE), 83 Doberman Pinschers (sulfonamides), [84][85][86] German Shepherds (Ehrlichia canis), [87][88][89][90] and SCWT (IBD/PLE). [46][47][48][49][50][51][52][53][54][55][56][57][58][59][60] A colony of Brittany Spaniel dogs was found to have type 1 membranoproliferative glomerulonephritis secondary to complement C3 deficiency, due to a deletion mutation in the gene encoding C3.…”

Section: Immune-complex Depositionmentioning

confidence: 99%

Emerging perspectives on hereditary glomerulopathies in canines

Littman¹

2015

AGG

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Familial glomerulopathies have been described in more than two dozen dog breeds. These canine spontaneous cases of glomerular disease are good models for their human counterparts. The dogs present clinically with protein-losing nephropathy and variable signs of hypertension, thromboembolic events, edema/effusions/nephrotic syndrome, or eventually with signs of renal disease such as anorexia, vomiting, weight loss, and/or polyuria/polydipsia. Laboratory changes include proteinuria, hypoalbuminemia, hypercholesterolemia, and eventually azotemia, hyperphosphatemia, anemia, and isosthenuria. Renal biopsies examined with transmission electron microscopy, immunofluorescence, and thin section light microscopy may show ultrastructural glomerular basement membrane abnormalities, glomerulosclerosis, amyloidosis, non-amyloid fibrillary deposition, or breed-associated predispositions for immunecomplex glomerulonephritis. Genome-wide association studies and fine sequencing of candidate genes have led to the discovery of variant alleles associated with disease in some breeds; eg, 1) glomerular basement membrane ultrastructural abnormalities due to defective collagen type IV, caused by different premature stop codons in each of four breeds; ie, in COL4A5 in Samoyeds and Navasota mix breed dogs (X-linked), and in COL4A4 in English Cocker Spaniels and English Springer Spaniels (autosomal recessive); and 2) glomerulosclerosis-related podocytopathy with slit diaphragm protein anomalies of both nephrin and Neph3/filtrin due to nonsynonymous single nucleotide polymorphisms in conserved regions of their encoding genes, NPHS1 and KIRREL2, in Soft Coated Wheaten Terriers and Airedale Terriers, with a complex mode of inheritance. Age at onset and progression to end-stage renal disease vary depending on the model. Genetic counseling using DNA testing is available for several breeds but many more inherited canine models of glomerulopathy still need to be characterized. Dog breeds, with their long haplotypes and linkage disequilibrium, represent excellent models to study the underlying molecular basis for protein-losing nephropathy, glomerular function, genetic manipulations, possible environmental triggers, and treatments. Results of studies of genetic canine diseases will help dogs and other species, including man.

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Glomerular lesions in dogs infected with Leishmania organisms

Cited by 86 publications

References 10 publications

Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Hypertension and its correlation with renal lesions in dogs with leishmaniosis

Pathologic Mechanisms Underlying the Clinical Findings in Canine Leishmaniosis due to Leishmaniainfantum/chagasi

Emerging perspectives on hereditary glomerulopathies in canines

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