Darcy Adin is a clinical professor of cardiology at the College of Veterinary Medicine. Darcy has held positions in both academic and private specialty practice and her clinical research focuses on the investigation of diuretic treatments and neurohormonal modulation of congestive heart failure. Darcy is also active in investigations of diet-associated dilated cardiomyopathy. Darcy's goals in clinical research are to enhance the lives of dogs with heart disease so they can live their best life possible.
Areas of Expertise (5)
Canine and Feline Congestive Heart Failure
Degenerative Mitral Valve Disease
Metabolomic profiling in dogs with dilated cardiomyopathy eating non-traditional or traditional diets and in healthy controlsScientific Reports
Caren E. Smith, et. al
Dilated cardiomyopathy (DCM), caused by genetic and environmental factors, usually progresses to heart failure, a major cause of death in elderly people. A diet-associated form of DCM was recently identified in pet dogs eating non-traditional (NT) diets. To identify potential dietary causes, we analyzed metabolomic signatures and gene set/pathway enrichment in all dogs based on disease, diet and their interactions and dogs with DCM based on diet.
Influence of sex on renin-angiotensin-aldosterone system metabolites and enzymes in Doberman PinschersJournal of Veterinary Internal Medicine
Darcy B. Adin and Jorge A. Hernandez
The renin-angiotensin-aldosterone system (RAAS) is a complex neurohormonal cascade that regulates blood pressure, fluid balance, electrolyte balance and inflammation. The terminal metabolite of the cascade, angiotensin II, mediates classical pathway effects of vasoconstriction, sodium retention, aldosterone synthesis and inflammation.
Toward quantification of loop diuretic responsiveness for congestive heart failureJournal of Veterinary Internal Medicine
Mark A. Oyama and Darcy Adin
Diuretics, such as furosemide, are routinely administered to dogs with congestive heart failure (CHF). Traditionally, dose and determination of efficacy primarily are based on clinical signs rather than quantitative measures of drug action. Treatment of human CHF patients increasingly is guided by quantification of urine sodium concentration (uNa) and urine volume after diuretic administration.