The symmetric dimetyl-arginine (SDMA) is produced by protein metabolism and eliminated by renal clearance. In the recent years, it has been used as a marker of kidney disease as it correlates with the glomerular filtration rate. In humans, SDMA is increased in patients with cardiovascular disease and has a negative prognostic value. The aim of the study is to assess the SDMA in dogs with myxomatous mitral valve disease (MMVD) at various disease stages, to evaluate the effect of pulmonary hypertension (PH) and the possible influence of cardiovascular therapies.

Dogs visited between May-2014 and September-2016 were retrospectively recruited if they had a diagnosis of MMVD after complete cardiovascular assessment (physical examination, thoracic radiogram, ECG, trans-thoracic echocardiography), CBC, biochemistry profile, and a sample of serum stored at -20°C (n=45). A control group of healthy dogs was also included (n=8). Dogs with MMVD were divided according to the ACVIM guidelines in stage B1 (n=9), B2 (n=11), C+D (n=17). Dogs in the ACVIM-groups were further subdivided into treated (n=0, 3, and 14,) and non-treated (n=9, 8, 3) for groups B1, B2, and C+D respectively. Dogs were considered affected by PH if they had tricuspid regurgitation with peak velocity >3 m/s and no right ventricle outflow tract obstruction (n=11). SDMA was determined by a referring laboratory using a routinely available immunoassay. Selected echocardiographic, CBC, biochemical parameters, and SDMA were compared among ACVIM-groups using Kruskal-Wallis test; the same test was used to assess the combined effect of therapies and ACVIM-group on serum urea nitrogen (BUN), creatinine, and SDMA. Correlations between SDMA and echocardiographic, CBC, and biochemical variables were assessed using Pearson's test. Man-Whitney test was used to assess differences of SDMA between PH-groups.

SDMA was increased in ACVIM-group C+D compared to group B1 (p=0.035) and B2 (p=0.021); BUN was increased in group C+D compared to healthy (p=0.01), B1 (p=0.007), and B2 (p=0.009), while creatinine was not significantly different among groups. SDMA was positively and significantly correlated with BUN (r=0.55; p<0.001), creatinine (r=0.529; p<0.001), sodium (r=0.448; p=0.003), left-atrium to aorta ratio (r=0.335; p<0.025) and mitral valve e-wave velocity (r=0.334, p=0.27). Treatment did not significantly affect SDMA, BUN, or creatinine in any ACVIM-group. No significant difference of SDMA was observed between PH-groups.

Increased SDMA is observed in the advanced stages of canine MMVD and likely reflects reduced renal function better than BUN and creatinine. Therapies and PH do not seem to affect SDMA in dogs with MMVD.

Disclosures

Disclosures to report.

SDMA was determined by IDEXX Laboratories and the cost of the analysis was partially reduced.