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Page 30

N o v e m b e r 2 1 - 2 2 , 2 0 1 8 | M a d r i d , S p a i n

OF EXCELLENCE

IN INTERNATIONAL

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YEARS

Nephrology 2018

Journal of Clinical Nephrology and Therapeutics

|

Volume 2

NEPHROLOGY AND UROLOGY

International Conference on

J Clin Nephrol Ther 2018, Volume 2

SUBCLINICAL EHRLICHIOSIS: MAY CAUSE KIDNEY ALTERATIONS?

Leandro Z Crivellenti

Universidade de Franca, Brazil

W

e hypothesized that renal glomerulopathy is a common finding in dogs with subclinical ehrlichiosis and pro-inflammatory

cytokines may be associated to renal injury. The aim of this study was to evaluate renal cortex biopsies in 15 dogs with sub-

clinical ehrlichiosis diagnosed by PCR and enzyme-linked immunosorbent assay (ELISA) and in 17 healthy dogs as a control group.

Dogs with presence of clinical signs, comorbidities and/or azotemia were excluded. Biopsy material was examined by light micros-

copy (LM). Sections were stained with hematoxylin and eosin, periodic acid Schiff, Jones methenamine silver, Masson´s trichrome,

and Congo Red. Cytokine quantification of tumor necrosis factor alpha (TNF-α), interferon gamma (INF-γ) and interleukin 6 were

assessed through ELISA using commercial kits specific to dogs (Milliplex), according to the manufacturer’s instructions. LM abnor-

malities were identified in 14 dogs (93.3%) from the ehrlichiosis group, but most findings were subtle. Mesangial cell proliferation

(40.0%), synechiae (40.0%), globally sclerotic glomeruli (33.3%), ischemic glomeruli (33.3%), focal segmental glomerulosclerosis

(FSGS) (33.3%), focal thickening of the glomerular basement membranes (26.7%), hydropic degeneration (26.7%) and interstitial

fibrosis and tubular atrophy (IFTA) (20.0%) were frequent. Cytokines was increased in subclinical phase on levels of TNF-α, INF- γ,

and IL-6 in comparison to control. These results suggest that TNF-α, INF- γ and -IL-6 may be involved in the pathogenesis of tu-

bule-glomeruli injury and subclinical ehrlichiosis may lead in chronic kidney disease (acknowledgement to FAPESP for financial

support - #2014/21506-2).