CKM PGx Panel

Test Description

Cardiovascular-kidney-metabolic (CKM) conditions often require complex medication regimens, with patients frequently experiencing variability in drug response. Genetic differences in drug-metabolizing enzymes, transporters, and drug targets can influence treatment outcomes, particularly for cardiovascular therapies commonly used in CKM populations. These medications are also commonly co-prescribed in patients with chronic kidney disease, where altered pharmacokinetics from reduced renal clearance may compound the effects of genetic variation. Pharmacogenomic testing enables personalized prescribing, helping to improve efficacy, reduce adverse drug reactions, and support long-term disease management.

Patient (Consult a Provider)
Patient (Order a Kit)
Provider
Ordering Information

Turnaround Time: 3-7 business days
Preferred specimens: Saliva
Alternate specimens: Buccal Swab

Testing Kit Request Form

Clinical Description

Cardio-kidney-metabolic (CKM) conditions often require complex medication regimens, with patients frequently experiencing variability in drug response. Genetic differences in drug-metabolizing enzymes, transporters, and target pathways can influence treatment outcomes for cardiovascular disease, chronic kidney disease, and metabolic disorders. Pharmacogenomic testing enables more personalized prescribing, helping to improve efficacy, reduce adverse drug reactions, and support better long-term disease management.

Panel Information
MedicationGeneRationaleReferences
RosuvastatinABCG2CPIC Level A; ABCG2 poor function variants increase rosuvastatin exposure ~2-fold, raising myopathy risk; rosuvastatin is a cornerstone of cardiovascular risk reduction in CKM syndrome[1-3]
ClopidogrelCYP2C19 CPIC Level A; CYP2C19 loss-of-function carriers have reduced active metabolite and increased ischemic events; AHA scientific statement supports CYP2C19 testing before P2Y12 inhibitor prescribing in ACS/PCI[4-5]
Carvedilol, Metoprolol  CYP2D6 CPIC Level A; CYP2D6 poor metabolizers have increased beta-blocker exposure with risk of bradycardia and hypotension; metoprolol and carvedilol are guideline-directed therapies for heart failure in CKM Stage 4[6-7]
Warfarin* CYP2C9, CYP4F2, VKORC1CPIC Level A; CYP2C9 and VKORC1 variants account for ~40% of warfarin dose variability; CYP4F2 variants affect vitamin K metabolism and warfarin requirements; CKM patients with atrial fibrillation or thromboembolic disease frequently require anticoagulation[4, 7]
Glipizide CYP2C9CYP2C9*3 carriers have ~80% reduced glipizide clearance and 2-fold higher AUC, significantly increasing hypoglycemia risk; glipizide is commonly prescribed for type 2 diabetes, a core component of CKM syndrome[8-10]
Allopurinol HLA-B*5801 CPIC Level A; HLA-B5801 carriers have markedly increased risk of severe cutaneous adverse reactions (SJS/TEN); allopurinol is first-line urate-lowering therapy for gout/hyperuricemia, common metabolic comorbidities in CKM syndrome[7, 11]
Simvastatin SLCO1B1 CPIC Level A; SLCO1B1 poor function variants increase simvastatin exposure with OR ~17 for myopathy; statins are foundational therapy for dyslipidemia management across all CKM stages[1, 7, 12]
Tagged Genes

Primary panel:

8 genes selected

References
  1. Heidenreich P, Spacek L, Gregor N, et al. Clinical Practice Guideline on Lipid Management for Cardiovascular Disease Risk Reduction. Department of Veterans Affairs; 2026.
  2. González-Iglesias E, Novalbos J, Abad-Santos F. The pharmacogenetics of rosuvastatin and implications for treatment: a systematic review. Pharmacogenomics. 2025.
  3. Lehtisalo M, Taskinen S, Tarkiainen EK, et al. A comprehensive pharmacogenomic study indicates roles for SLCO1B1, ABCG2 and SLCO2B1 in rosuvastatin pharmacokinetics. Br J Clin Pharmacol. 2023.
  4. Pereira NL, Cresci S, Angiolillo DJ, et al. CYP2C19 genetic testing for oral P2Y12 inhibitor therapy: a scientific statement from the American Heart Association. Circulation. 2024.
  5. El Rouby N, Johnson JA. Pharmacogenetic testing—evidence, challenges, and pathways to adoption. NEJM Evidence. 2025.
  6. Ingelman-Sundberg M, Pirmohamed M. Precision medicine in cardiovascular therapeutics: evaluating the role of pharmacogenetic analysis prior to drug treatment. J Intern Med. 2024.
  7. Cavallari LH, Mason DL. Cardiovascular pharmacogenomics—implications for patients with CKD. Adv Chronic Kidney Dis. 2016.
  8. Yang F, Liu L, Chen L, et al. OATP1B3 (699G>A) and CYP2C9*2, *3 significantly influenced the transport and metabolism of glibenclamide and glipizide. Sci Rep. 2018.
  9. Kim NT, Cho CK, Kang P, et al. Effects of CYP2C9*3 and *13 alleles on the pharmacokinetics and pharmacodynamics of glipizide in healthy Korean subjects. Arch Pharm Res. 2022.
  10. Kirchheiner J, Roots I, Goldammer M, Rosenkranz B, Brockmöller J. Effect of genetic polymorphisms in cytochrome P450 (CYP) 2C9 and CYP2C8 on the pharmacokinetics of oral antidiabetic drugs: clinical relevance. Clin Pharmacokinet. 2005.
  11. Alshabeeb MA, Alyabsi M, Aziz MA, Abohelaika S. Pharmacogenes that demonstrate high association evidence according to CPIC, DPWG, and PharmGKB. Front Med (Lausanne). 2022.
  12. Kaufman AL, Spitz J, Jacobs M, et al. Evidence for clinical implementation of pharmacogenomics in cardiac drugs. Mayo Clin Proc. 2015.