2017 ACVIM Forum Research Abstract Program

Hyperinoculation with a market leading FVRCP parenteral vaccine induced both antibody and cell-mediated immune response towards alpha-enolase, increased alpha-enolase expression in both renal tubules and glomeruli, and led to elevations in select inflammatory cytokines and chemokines within this 16-week model. Although there has been no direct link made between parenteral FVRCP vaccines and feline interstitial nephritis to date, results of urinary cytokines and further assessment of alpha-enolase expression within feline kidneys will be used to continue evaluation of this potential IN model. Tamm-Horsfall Protein (THP) is exclusively synthesized by the distal nephron under physiological conditions. Therefore, it is expected larger amounts of this protein in the urine of healthy individuals. In chronic kidney disease (CKD) dogs, a few investigations have reported about the quantities of THP in urine. Lower urinary excretion of THP in CKD dogs might be associated with distal tubular injuries and/or to the loss of renal mass, and then, THP may act as a marker of disease progression. The aim of this study was to assess the role of THP as a marker of CKD progression in dogs. Nine clinically healthy dogs were recruited as control group. Forty CKD dogs were enrolled (IRIS staging, Stage 1, n = 10; Stage 2, n = 10; Stage 3, n = 10; Stage 4, n = 10). Western blotting of THP was performed, and the results of densitometry were expressed in mean AE SEM. Urinary immunodetection of THP was 100.0 AE 7.7% in control dogs, and 117.2 AE 10.8%, 86.0 AE 9.0%, 65.4 AE 8.7% and 46.7 AE 9.0% in CKD dogs in stages 1, 2, 3 and 4, respectively. Differences among all groups were observed, particularly between Stages 1 and 4 (P ≤ 0.0001). It is likely that progressive reduction in urinary excretion of THP may contribute to detect gradual loss of nephrons, and it may act as a marker of disease progression in CKD dogs. Infection with Angiostrongylus vasorum (Av) is an emerging disease in dogs with a wide range of clinical signs. To date, it is not clear whether Av is able to cause glomerular immune complex deposition or other renal damage.