RenaPGx® Panel
Test Description
The RenaPGx® panel is intended for individuals with kidney disease or those undergoing transplant nephrology management who may benefit from personalized pharmacogenetic-guided therapy. This panel evaluates clinically relevant genetic variants associated with drug metabolism, efficacy, and toxicity risk to support medication selection and dose optimization for therapies commonly used in nephrology and transplant care. Individuals receiving medications such as tacrolimus, thiopurines, anticoagulants, and other therapies with known pharmacogenomic considerations may benefit from testing to reduce the risk of rejection, toxicity, adverse drug reactions, and ineffective treatment while supporting individualized therapeutic management.
Ordering Information
Turnaround Time: 3-7 business days
Preferred specimens: Saliva
Alternate specimens: Buccal Swab
Clinical Description
Renal patients, including those with chronic kidney disease or post-transplant status, are often prescribed medications with narrow therapeutic indices and complex pharmacokinetics. Genetic variability can significantly impact drug metabolism, efficacy, and risk of toxicity. Pharmacogenomic testing can support personalized medication management, improve therapeutic outcomes, and reduce adverse drug events in this high-risk population.
Panel Information
| Medication | Gene | Rationale | References |
| Rosuvastatin | ABCG2 | CPIC Level A; ABCG2 poor function variants increase rosuvastatin exposure ~2-fold, raising myopathy risk; statins are cornerstone therapy in CKD cardiovascular risk management | [1] |
| Clopidogrel, Voriconazole, Pantoprazole | CYP2C19 | Clopidogrel: CYP2C19 poor metabolizers have reduced active metabolite and increased cardiovascular events; Voriconazole: poor metabolizers have 4-fold higher exposure increasing toxicity risk; Pantoprazole: 3rd most prescribed medication post-kidney transplant, CYP2C19 poor metabolizers on PPIs had faster eGFR decline (HR 2.43) | [2-3] |
| Metoprolol, Carvedilol, Tramadol | CYP2D6 | Metoprolol/Carvedilol: CYP2D6 poor metabolizers have increased beta-blocker exposure and bradycardia/hypotension risk; widely used for hypertension and heart failure in CKD; Tramadol: top 5 prescribed medication post-kidney transplant, CPIC Level A pair with CYP2D6 | [2] |
| Warfarin* | CYP2C9, CYP4F2, VKORC1 | CPIC Level A; genetic variants account for ~40% of warfarin dose variability; CKD patients have higher bleeding risk making precise dosing critical; CYP4F2 variants affect vitamin K metabolism and warfarin requirements | [1] |
| Tacrolimus | CYP3A4, CYP3A5 | CPIC Level A; CYP3A5 expressers require ~1.5–2× higher tacrolimus doses to reach target trough; most prescribed immunosuppressant in kidney transplant; narrow therapeutic index with nephrotoxicity risk at supratherapeutic levels | [1-2] |
| Dapsone | G6PD | Second-line PJP prophylaxis when TMP-SMX not tolerated; G6PD deficiency causes hemolytic anemia and methemoglobinemia; G6PD screening recommended before initiation per AST guidelines | [4-6] |
| 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 in CKD-associated gout/hyperuricemia; CKD itself increases SJS/TEN risk | [1] |
| Simvastatin, Atorvastatin | SLCO1B1 | CPIC Level A; SLCO1B1 poor function variants increase statin exposure and myopathy risk (OR ~17 for simvastatin); atorvastatin commonly prescribed in CKD for cardiovascular risk reduction | [1-2] |
| Azathioprine | TPMT, NUDT15 | CPIC Level A (2025 update); TPMT and NUDT15 variants predict myelosuppression; NUDT15 variants carry >12-fold increased hazard for severe myelotoxicity; DPWG classifies NUDT15 testing as “essential” before thiopurine use; azathioprine widely used as maintenance immunosuppression in kidney transplant | [7-10] |
*CPIC guideline pharmacogenetic algorithm https://cpicpgx.org/content/guideline/publication/warfarin/2017/28198005.pdf
Frequency of Cytochrome P450 (CYP2D6) Metabolizer Types in the Population
| Cytochrome | Poor metabolizer | Intermediate metabolizer | Normal metabolizer | Rapid or ultra-rapid metabolizer |
| CYP2D6 | 4-7% | 9-35% | 50-90% | 2-3% |
Tagged Genes
- Fishman JA, Gans H; AST Infectious Diseases Community of Practice. Pneumocystis jiroveci in solid organ transplantation: Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transplant. 2019;33(9).
- U.S. Food and Drug Administration. Dapsone [prescribing information]. Updated February 27, 2026.
- Urbancic KF, Pisasale D, Wight J, Trubiano JA. Dapsone safety in hematology patients: Pathways to optimizing Pneumocystis jirovecii pneumonia prophylaxis in hematology malignancy and transplant recipients. Transpl Infect Dis. 2018;20(6).
- Belfield KD, Tichy EM. Review and drug therapy implications of glucose-6-phosphate dehydrogenase deficiency. Am J Health Syst Pharm. 2018;75(3):97-104.
- Salifu MO, Tedla F, Markell MS. Management of the well renal transplant recipient: Outpatient surveillance and treatment recommendations. Semin Dial. 2006;19(6):516-520.
- Gronich N, Rosh B, Stein N, Saliba W. Medications and acute hemolysis in G6PD-deficient patients: A real-world study. Clin Pharmacol Ther. 2024;115(4):1012-1020.
- Stone RM, Haidar CE, Kornegay NM, et al. Sulfamethoxazole-trimethoprim prophylaxis in pediatric oncology patients with glucose-6-phosphate dehydrogenase deficiency. Pediatr Infect Dis J. 2024;43(5).
- Maillard M, Schwab M, Whirl-Carrillo M, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) guideline for thiopurine dosing based on TPMT and NUDT15 genotypes: 2025 update. Clin Pharmacol Ther. 2026;119(2):345-356.
- Coenen MJH, Nijenhuis M, Soree B, et al. Dutch Pharmacogenetics Working Group (DPWG) guideline for the gene-drug interaction between TPMT/NUDT15 and thiopurines. Eur J Hum Genet. 2025;33(1):22-31.
- Roberts C, Peters J, Sazonvos A, et al. Clinical utility and cost-effectiveness of pretreatment NUDT15 pharmacogenetic testing to prevent thiopurine-induced myelosuppression: A genotype-first reverse phenotyping cohort study within the UK NIHR Inflammatory Bowel Disease Bioresource. Aliment Pharmacol Ther. 2025;61(3):456-468.
