The effect of noncardiac disease on plasma brain natriuretic peptide concentration in dogs


  • Presented as an abstract at the 23rd Annual Meeting of the American College of Veterinary Internal Medicine, Baltimore, MD in June 2005.

  • Supported in part by resident grants from the Matthew J. Ryan Veterinary Hospital at the University of Pennsylvania.

  • This work was completed at the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania, Philadelphia, PA in 2003.

  • Authors declare no conflicts of interest.

Address correspondence and reprint requests to
Mark Rishniw, Department of Clinical Sciences, College of Veterinary Medicine, C2-015 VMC, Cornell University, Tower Road, Ithaca, NY 14853, USA.
Email: Submitted August 10, 2009; Accepted November 22, 2010.


Objective – To evaluate the effects of noncardiac disease on c-terminal brain natriuretic peptide (cBNP) concentrations in dogs.

Design – Prospective observational study.

Setting – Urban university veterinary hospital.

Animals – Thirty-eight apparently healthy dogs, 28 dogs with cardiac disease (14 CHF, 14 non-CHF), and 81 dogs with primary noncardiac diseases.

Interventions – none.

Materials and Methods – Plasma was collected from each dog and analyzed for active (cBNP) B-type natriuretic peptide using an assay that is being investigated for commercial use (Biosite).

Measurements and Main Results – Dogs with CHF had significantly higher plasma cBNP concentrations than dogs with subclinical cardiac disease, apparently healthy dogs, or dogs with primary noncardiac disease. However, 21% (28/133) of dogs without CHF (including healthy dogs, dogs with primary noncardiac disease, and dogs with subclinical cardiac disease) had cBNP concentrations above previously identified diagnostic thresholds for CHF, reiterating the importance of reestablishing new diagnostic cutoffs when considering comorbidities affecting B-type natriuretic peptide levels.

Conclusions – A clinically relevant proportion of nondyspneic dogs with primary noncardiac diseases have increased cBNP concentrations that exceed previously identified diagnostic thresholds, potentially limiting the ability of this test to identify CHF when noncardiac comorbidities exist. Interpretation of increased cBNP concentrations in such cases must be appropriately interpreted with further diagnostic investigation.