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Association of proteinuria with fasting hypertriglyceridaemia and hyperadrenocorticism in Australian Miniature Schnauzers

Bunn, T.A., Howard, G., Foster, S., Hayward, D., Bruce, M.ORCID: 0000-0003-3176-2094, Rossi, G.ORCID: 0000-0003-4879-9504 and Langner, K. (2021) Association of proteinuria with fasting hypertriglyceridaemia and hyperadrenocorticism in Australian Miniature Schnauzers. Journal of Veterinary Internal Medicine, 35 (6). p. 3111.

Free to read: https://doi.org/10.1111/jvim.16289
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Abstract

Proteinuria has been described in Miniature Schnauzers with primary hypertriglyceridaemia. Hyperadrenocorticism can also cause fasting hypertriglyceridaemia and proteinuria with no overt progression to renal disease. The aim of this study was to investigate the association of proteinuria with primary hypertriglyceridaemia and hyperadrenocorticism in Australian Miniature Schnauzers. Two hundred and fifteen healthy Miniature Schnauzers were recruited into a cross-sectional study. Each dog was assessed with an owner questionnaire and a physical examination. Triglyceride concentrations were measured after a 15-hour fast. If fasting hypertriglyceridaemia was identified, haematology, serum biochemistry, urinalysis including urine protein:creatinine ratio (UPCR), total thyroxine (including thyroid stimulating hormone if total thyroxine was low) and a low-dose dexamethasone suppression test were performed. Dogs with no underlying cause for the fasting hypertriglyceridaemia had an adrenocorticotrophic hormone stimulation test performed. Thirty of the dogs with normal triglyceride concentrations underwent the same testing to act as controls. Proteinuria was defined as UPCR ≥ 0.5. Forty of 215 dogs (18.6%; 95% CI: 14.0%-24.3%) had fasting hypertriglyceridaemia. Thirty-nine hypertriglyceridaemic dogs underwent further testing and 31 (79.4%; 95% CI: 63.5%-90.7%) had hyperadrenocorticism, one (2.5%; 95% CI: 0%-13.4%) had hypothyroidism and seven (17.9%; 95% CI: 7.5%-33.5%) had primary hypertriglyceridaemia. Ten of the 30 control dogs (33.3%; 95% CI: 17.2%-52.8%) were diagnosed with hyperadrenocorticism. No other diseases were identified in the control group. The UPCR was assessed in 39 hypertriglyceridaemic dogs and 29 controls. Proteinuria was associated with hypertriglyceridaemia (P<0.001); an increased UPCR was detected in 18 of 39 hypertriglyceridaemic dogs and 0 of 29 dogs with normal triglycerides. Two dogs with proteinuria had primary hypertriglyceridaemia, 15 had hyperadrenocorticism and one had hypothyroidism. In hypertriglyceridaemic dogs, those with hyperadrenocorticism were 3.5 (95% CI: 1.1-10.9) times as likely to be proteinuric than dogs with hyperadrenocorticism and normal triglycerides. In contrast, there was no evidence of an association between primary hypertriglyceridaemia and proteinuria (P=0.6). The estimated relative risk for proteinuria in hypertriglyceridaemic Australian Miniature Schnauzers diagnosed with hyperadrenocorticism was over 3 times that for dogs with hyperadrenocorticism without hypertriglyceridaemia. Proteinuria only occurred with hyperadrenocorticism when hypertriglyceridaemia was present. As proteinuria was not associated with primary hypertriglyceridaemia, rigorous investigation of hyperadrenocorticism is recommended in hypertriglyceridaemic Miniature Schnauzers with proteinuria.

Item Type: Journal Article
Murdoch Affiliation(s): Veterinary Medicine
Publisher: Wiley-Blackwell
Copyright: © 2021 The Authors.
Other Information: Abstract taken from the Research Communications of the 31st ECVIM-CA Online Congress
URI: http://researchrepository.murdoch.edu.au/id/eprint/63507
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