About

Kathryn Meurs is associated with the College of Veterinary Medicine at NC State University, where she is involved in fostering student engagement and supporting the academic community. Her role includes overseeing student experience initiatives, promoting a collaborative and inclusive culture, and facilitating opportunities for students to grow both personally and professionally. She is dedicated to enhancing the educational environment and ensuring that students have access to extracurricular activities, research projects, and international study opportunities that enrich their veterinary education.

Research topics

• Medicine
• Internal medicine
• Genetics
• Biology
• Endocrinology
• Cardiology
• Gastroenterology
• Pharmacology

Selected publications

• Novel frameshift variant in exon 7 of <i>COL17A1</i> in a domestic shorthair kitten with junctional epidermolysis bullosa

  Journal of Veterinary Diagnostic Investigation · 2026-01-26

  articleOpen access

  Junctional epidermolysis bullosa (JEB) is a congenital blistering skin disorder with clefting within the lamina lucida of the basement membrane zone. We describe the clinical and morphologic features of JEB in a 4-mo-old domestic shorthair kitten and identify the underlying genetic variant. The kitten was presented with blistering lesions affecting friction-prone areas of haired skin, mucocutaneous junctions, and oral mucosa. Histopathology revealed extensive subepidermal cleft formation in affected tissues. Periodic acid–Schiff (PAS) staining showed a thin, PAS-positive line along the dermal side of the cleft, consistent with retention of the lamina densa. Transmission electron microscopy confirmed separation at the level of the lamina lucida with intact basal keratinocytes. Whole genome sequencing identified a homozygous 2-bp deletion in exon 7 of COL17A1 , predicted to result in loss of function and disrupted binding domains. Our findings support a diagnosis of JEB associated with a novel COL17A1 variant.

  PublisherOA PDFDOI

• The T-wave peak-end to QT ratio is prolonged and minimally influenced by RR interval in Doberman Pinschers with subclinical dilated cardiomyopathy

  Journal of the American Veterinary Medical Association · 2025-05-02

  articleOpen access

  Objective: The T-wave peak-end to QT ratio (TpTe:QT) is an ECG marker of myocardial repolarization dispersion that is not influenced by the RR interval. The authors hypothesized that TpTe:QT would be prolonged in Doberman Pinschers with dilated cardiomyopathy (DCM). Methods: This retrospective cross-sectional study included clinically healthy Doberman Pinschers that were pyruvate kinase dehydrogenase 4 and/or titin genotype positive as the controls and dogs diagnosed with subclinical DCM as the DCM+ group. Data were collected between 2019 and 2024. Dogs receiving antiarrhythmic drugs were excluded. The QT interval, corrected QT interval, TpTe, TpTe:QT, and corrected TpTe were measured as repolarization markers with the use of ambulatory ECGs. Interrelationships among RR interval, DCM phenotype, and each marker were determined with a mixed-effects model. Results: 36 dogs were included: 12 in the DCM+ group and 24 in the controls. The TpTe:QT was significantly higher in the DCM+ group compared to controls (risk ratio, 1.23), with negligible to weak correlation identified to RR interval (0.04 in controls; -0.16 in DCM+). The TpTe and corrected TpTe were also elevated in the DCM+ group (risk ratios 1.04 and 1.06, respectively): these values were significantly influenced by RR interval. Conclusions: TpTe:QT is a potential marker for distinguishing Doberman Pinschers with subclinical DCM from those that are normal, yet genetically at risk. Its independence from heart rate variation underscores its potential utility in clinical practice. Clinical Relevance: TpTe:QT is a simple, noninvasive, and readily available test that may predict subclinical, clinically evident DCM in Doberman Pinschers. Larger clinical investigations of this easily obtained variable are warranted.

  PublisherOA PDFDOI

• Familial Narcolepsy in Dogo Argentino Dogs Is Caused by a Tandem Duplication Mutation in HCRTR2

  Journal of Veterinary Internal Medicine · 2025-03-01 · 1 citations

  articleOpen access

  BACKGROUND: Familial narcolepsy in dogs has been associated with mutations in the HCRTR2 gene in Labrador retrievers, dachshunds, and Doberman pinschers, with the causal mutation differing between breeds. OBJECTIVE: To characterize the genetic mutation responsible for familial narcolepsy in Dogo Argentino dogs. ANIMALS: Ten Dogo Argentino dogs, three narcoleptic and seven clinically normal, of which four were related and three were unrelated to the narcoleptic dogs. METHODS: Case control prospective study. DNA was extracted from blood samples of all dogs. Whole-genome sequencing was performed on two affected dogs, and variants were identified using bioinformatic pipelines, with comparisons made to a database of 2766 dogs. Structural variants were validated through PCR and Sanger sequencing. RESULTS: A novel tandem duplication in the HCRTR2 gene was identified. All three affected dogs and the clinically normal parents of one affected dog had this duplication, suggesting an autosomal recessive pattern of inheritance. This duplication was absent in the 2766 dogs in the database, emphasizing its potential relevance in the Dogo Argentino breed. CONCLUSIONS AND CLINICAL IMPORTANCE: This discovery emphasizes the critical role of the HCRTR2 gene in narcolepsy in dogs, and the diversity of mutations that can lead to this condition. Further genetic testing in this breed is warranted to identify carriers and prevent the further spread of this condition.

  PublisherOA PDFDOI

• The role of vector-borne pathogens and cardiac Striatin genotype on survival in boxer dogs with arrhythmogenic right ventricular cardiomyopathy

  Journal of Veterinary Cardiology · 2024-09-19

  article
  PublisherDOI

• An imminent need for veterinary medical educators: are we facing a crisis?

  Journal of the American Veterinary Medical Association · 2024-05-29 · 5 citations

  articleSenior author

  A potential emerging shortage of veterinary medical educators requires the profession to acknowledge and understand the factors leading to this outcome. Expanding class sizes within existing schools and colleges of veterinary medicine and the expected expansion of new programs seeking AVMA-Council of Education accreditation have heightened the need to address an impending shortage of veterinary medical educators. A solution-oriented approach that accurately projects educator workforce needs and identifies factors contributing to the shortage requires effective collaboration across various partnering organizations to develop innovations in pedagogy and educational delivery methods. The veterinary profession must also identify and reduce disincentives that deter students and post-DVM trainees from pursuing careers in education. Finally, efforts at the state and federal level are critical to advocate for financial support and incentives for expansion of the veterinary medical educator workforce. Through these collective approaches and partnerships, the veterinary medical educator workforce can be strengthened to overcome obstacles for educating the next generation of veterinarians to meet societal needs.

  PublisherDOI

• Acquired dysfunction of CFTR underlies cystic fibrosis-like disease of the canine gallbladder

  American Journal of Physiology-Gastrointestinal and Liver Physiology · 2024-07-23 · 5 citations

  articleSenior author

  Cystic fibrosis transmembrane conductance regulatory protein (CFTR) genomic variants and expression of mRNA, protein, and electrogenic anion secretory activity of CFTR were characterized in dog gallbladder. Acquired inhibition of CFTR expression by gallbladder epithelium was identified as underpinning a naturally occurring muco-obstructive disease of the dog gallbladder that bears striking pathological similarity to animal models of cystic fibrosis.

  PublisherDOI

• Evaluation of Renin–Angiotensin–Aldosterone System Components and Enzymes in Systemically Hypertensive Cats Receiving Amlodipine

  Animals · 2023-11-10 · 7 citations

  articleOpen accessSenior author

  Background: Chronic renin–angiotensin–aldosterone system (RAAS) activation is harmful. Amlodipine activates RAAS in humans and dogs, but contradictory data exist for systemically hypertensive (SHT) cats. Hypothesis: Cats with SHT and chronic kidney disease treated with amlodipine (SHT/CKD-A) are RAAS activated. Animals: Client-owned cats: unmedicated normotensive (NT) cats (n = 9); SHT/CKD-A cats (n = 5) with median systolic blood pressure of 170 mmHg (vs. 195 mmHg, pre-treatment), chronic kidney disease, and receiving no RAAS-suppressive therapy. Methods: Serum was frozen (−80 °C) until RAAS analysis via equilibrium analysis. The RAAS variables (reported as median (minimum–maximum)) were compared between groups, using Mann–Whitney U test. Results: Angiotensin 1, angiotensin 1,7, angiotensin III, and angiotensin 1,5, and angiotensin-converting enzyme (ACE)-2 activity were higher in SHT/CKD-A cats compared to NT cats, while ACE activity was lower in SHT/CKD-A cats compared to NT cats (p &lt; 0.05 all). A marker for alternative RAAS influence (ALT-S) was significantly higher (69; 58–73 pmol/pmol) in SHT/CKD-A cats compared to NT cats (35; 14–63 pmol/pmol; p = 0.001). Aldosterone concentrations were significantly higher (393; 137–564 pmol/L) in SHT/CKD-A cats compared to NT cats (129; 28–206 pmol/L; p = 0.007). Conclusion and Clinical Importance: Circulating RAAS is activated in systemically hypertensive cats receiving amlodipine. Although this study did not parse out the individual contributions of SHT, chronic kidney disease, and amlodipine, the findings suggest that the use of concurrent RAAS-suppressant therapy, specifically aldosterone antagonism, in amlodipine-treated SHT cats with chronic kidney disease might be indicated.

  PublisherOA PDFDOI

• No impact of polymorphism in the phosphodiesterase 5A gene in Cavalier King Charles Spaniels on pimobendan-induced inhibition of platelet aggregation response

  Journal of Veterinary Internal Medicine · 2023-09-25 · 2 citations

  articleOpen access

  BACKGROUND: A variant in the canine phosphodiesterase (PDE) 5A gene (PDE5A:E90K) is associated with decreased concentrations of circulating cyclic guanosine monophosphate (cGMP) and response to PDE5 inhibitor treatment. Pimobendan is a PDE inhibitor recommended for medical treatment of certain stages of myxomatous mitral valve disease (MMVD) in dogs. HYPOTHESIS: PDE5A:E90K polymorphism attenuates the inhibitory effect of pimobendan on in vitro platelet aggregation and increases basal platelet aggregation in Cavalier King Charles Spaniels (CKCS). Selected clinical variables (MMVD severity, sex, age, hematocrit, platelet count in platelet-rich plasma [PRP], and echocardiographic left ventricular fractional shortening [LV FS]) will not show an association with results. ANIMALS: Fifty-two privately owned CKCS with no or preclinical MMVD. METHODS: Using blood samples, we prospectively assessed PDE5A genotype using Sanger sequencing and adenosine diphosphate-induced platelet aggregation response (area under the curve [AUC], maximal aggregation [MaxA], and velocity [Vel]) with and without pimobendan using light transmission aggregometry. Dogs also underwent echocardiography. RESULTS: Pimobendan inhibited platelet function as measured by AUC, MaxA, and Vel at a concentration of 10 μM (P < .0001) and Vel at 0.03 μM (P < .001). PDE5A:E90K polymorphism did not influence the inhibitory effect of pimobendan or basal platelet aggregation response. CONCLUSIONS AND CLINICAL IMPORTANCE: The PDE5A:E90K polymorphism did not influence in vitro basal platelet aggregation response or the inhibitory effect of pimobendan on platelet aggregation in CKCS. Dogs with the PDE5A:E90K polymorphism did not appear to have altered platelet function or response to pimobendan treatment.

  PublisherOA PDFDOI

• Clinical outcome of idiopathic juvenile ventricular arrhythmias in 25 dogs

  Journal of Veterinary Cardiology · 2023-12-15 · 2 citations

  articleSenior author
  PublisherDOI

• Pharmacokinetics of pimobendan after oral administration to dogs with myxomatous mitral valve disease

  Journal of Veterinary Internal Medicine · 2023-09-30 · 8 citations

  articleOpen access

  BACKGROUND: Pimobendan is an important therapy for dogs with myxomatous mitral valve disease (MMVD). The pharmacokinetics are reported in healthy dogs but not in dogs with heart disease. HYPOTHESIS/OBJECTIVES: To determine if dog characteristics such as age, breed, body condition score, ACVIM stage of heart disease or biochemical laboratory value alter the pharmacokinetics of orally administered pimobendan and its metabolite in a cohort of dogs with naturally occurring MMVD. ANIMALS: Fifty-seven client-owned dogs with MMVD ACVIM Stage B2, C, or D and administered pimobendan to steady state blood concentrations. METHODS: Prospective, observational study. Samples were collected using a sparse-sampling protocol at specific intervals after administration of pimobendan. Plasma pimobendan and the active metabolite (O-desmethyl-pimobendan, ODMP) concentrations were determined via high-pressure liquid chromatography and fluorescence detection. Data was analyzed via a population pharmacokinetic approach and nonlinear mixed effects modeling (NLME). Numerous covariates were examined in the NLME model. RESULTS: ) were approximately 1.4 and 1 hour for pimobendan and 1.4 and 1.3 hours for ODMP, respectively. Pharmacokinetic parameters were highly variable, especially the values for pimobendan absorption and elimination rate, and absorption rate of ODMP with coefficients of variation of 147.84%, 64.51% and 64.49%, respectively. No covariate evaluated was a significant source of variability. CONCLUSIONS AND CLINICAL IMPORTANCE: The pharmacokinetic parameters were highly variable among this group of dogs with MMVD. The variability was not associated with the dog's age, body weight or condition score, stage of heart disease, dose, serum creatinine, or alkaline phosphatase.

  PublisherOA PDFDOI

Recent grants

• NIH Grant K08HL003236

  NIH · $453k · 2001

Frequent coauthors

• Bruce W. Keene

  North Carolina State University

  75 shared

• Alan W. Spier

  75 shared

• Philip R. Fox

  The Schwarzman Animal Medical Center

  61 shared

• Matthew W. Miller

  Auburn University

  58 shared

• Joshua A. Stern

  North Carolina State University

  48 shared

• Teresa C. DeFrancesco

  North Carolina State University

  47 shared

• Jeffrey A. Towbin

  Le Bonheur Children's Hospital

  46 shared

• Linda B. Lehmkuhl

  40 shared

Labs

• CVM: Research Area of Emphasis: GeneticsPI

Awards & honors

• Diplomate of the American College of Veterinary Internal Med…