Renal lesions in dogs naturally infected with Leishmania infantum

Abstract

ABSTRACT:We analyzed serum urea and creatinine levels and the renal histology of dogs with canine visceral leishmaniasis, and conducted a urinalysis to evaluate their renal damage. Urine, blood, and kidney samples were obtained from 43 dogs. The dogs were divided into 3 groups according to their clinical presentation: asymptomatic (n= 9), oligosymptomatic (n= 17), and symptomatic (n=17). We detected increased creatinine and urea levels in 7/43 and 8/43 of the dogs, respectively. In the urinalysis, nephritis was found in 22/43 seropositive dogs. Histopathologic alterations included tubulointerstitial alterations (39/43) and glomerulonephritis (25/43). Membranoproliferative glomerulonephritis (11/43) was the most common glomerular alteration, followed bymembranous glomerulonephritis (6/43), proliferative glomerulonephritis (7/43), and glomerular sclerosis (1/43). Our data indicate that alterations in the urinalysis and renal histopathology in dogs with leishmaniasis can appear before increases in serum urea and creatinine levels can be detected, even when clinical symptoms of the disease are absent. A diagnosis of leishmaniasis should be considered in dogs with renal damage, and renal function should be evaluated in dogs with leishmaniasis.

Métodos De Diagnóstico Da Leishmaniose Canina: Revisão De Literatura

“…Cães com leishmaniose visceral quase sempre apresentam alterações renais, porém a concentração de creatinina e ureia sérica são úteis para avaliar a lesão renal somente quando mais de 75% da função renal já se encontra comprometida. É válido dizer que com o comprometimento renal há a possibilidade do paciente ter em seu exame de urina presença de proteinúria e hematúria (ARAÚJO E SOUZA, 2013; WILSON et al, 2017;JUNIOR et al, 2016).…”

Doenças infecciosas e parasitárias no contexto brasileiro

“…Dentre os sinais clínicos dos animais sintomáticos incluem: lesões cutâneas, tais como alopecia, inflamação, descamação e úlceras e em estágios mais avançadas da doença, frequentemente observa-se onicogrifose, esplenomegalia, linfoadenopatia, hepatomegalia e hiperqueratose, sendo as lesões renais consideradas a principal causa de óbito da LVC (Figura 2) (NISHIDA & DELMASCHIO, 2017). As lesões renais são relatadas associadas a alterações tubulares incialmente, evoluindo para alterações glomerulares com o agravamento da doença, intimamente relacionados aos animais que apresentam síndrome urêmica (WILSON et al, 2017). A alteração glomerular mais frequente é a glomerulonefrite membranoproliferativa, onde ocorre o espessamento da membrana basal dos glomérulos, pela proliferação de células endoteliais e mesangiais.…”

Canine leishmaniosis and kidney disease: Q&A for an overall management in clinical practice

“…2015, Wilson et al . 2017). The major cause of glomerular pathology in CanL is thought to be deposition of preformed circulating immune complexes at different levels of the glomerular unit; this is determined by the size and charge (cationic) of the complex.…”

“…The kidney lesions associated with CanL are described in more detail below, but include chronic interstitial inflammation (associated with local infection) and GN (leading to proteinuria or nephrotic syndrome). A range of glomerular and secondary tubular lesions are recognised, including membranoproliferative GN (MPGN), membranous GN and mesangioproliferative GN, progressing to interstitial fibrosis, glomerulosclerosis and end-stage renal disease (Costa et al 2003, Aresu et al 2013, dos Santos et al 2013, Esch et al 2015, Wilson et al 2017. The major cause of glomerular pathology in CanL is thought to be deposition of preformed circulating immune complexes at different levels of the glomerular unit; this is determined by the size and charge (cationic) of the complex.…”

“…In membranous GN, immune complex deposition occurs on the epithelial side of the GBM, resulting in basement membrane thickening without cellular proliferation or inflammation. In mesangioproliferative GN, larger immune complexes deposit within the mesangium, leading to cellular proliferation and accumulation of mesangial matrix (Costa et al 2003, Aresu et al 2013, dos Santos et al 2013, Wilson et al 2017.…”