Student Chonnam National University Gwangju, Kwangju-jikhalsi, Republic of Korea
Abstract: Background CD40-CD40 ligand (CD40L) interaction, one of the inflammatory mechanisms, is known to play a pathological role in heart failure in human medicine. However, its role in dogs with myxomatous mitral valve disease (MMVD) remains unexplored.
Hypothesis CD40-CD40L interaction may play a role in myocardial and renal tubular injury in dogs with MMVD.
Animals Twenty client-owned healthy dogs and forty client-owned dogs with MMVD, categorized into B1, B2, C, and D groups according to the American College of Veterinary Internal Medicine guidelines.
Methods A prospective study with cross-sectional and longitudinal analyses. Serum soluble (s) CD40L, N-terminal pro-B-type natriuretic peptide (NT-proBNP), and urinary neutrophil gelatinase-associated lipocalin/creatinine ratio (uNGALCR) were measured. Longitudinal analysis in MMVD C and D groups compared values at baseline (day 0) and during medical therapy at 6 weeks and 3 weeks, respectively.
Results Serum NT-proBNP (P = .0001), sCD40L (P < .0001), and uNGALCR (P = .0004) were significantly elevated in dogs with MMVD. Medical treatment significantly reduced serum sCD40L levels in the stage C group (P = .0001). Serum sCD40L positively correlated with NT-proBNP (r = .2784, P = .014) and uNGALCR (r = .3025, P = .039).
Conclusions and Clinical Importance Serum sCD40L levels are elevated in dogs with MMVD and positively correlate with biomarkers of cardiac and renal tubular injury. These findings suggest that enhanced CD40–CD40L interactions contribute to the pathogenesis of canine MMVD.
