What are the implications of UGT2B15 poor metabolism on a patient taking lisinopril (Angiotensin-Converting Enzyme (ACE) inhibitor)?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 2, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

UGT2B15 Poor Metabolism and Lisinopril: No Clinical Interaction

UGT2B15 poor metabolism has no clinically relevant impact on lisinopril therapy, as lisinopril is not metabolized by UGT enzymes or any hepatic pathway—it is excreted unchanged exclusively by the kidneys.

Lisinopril Metabolism and Elimination

Lisinopril does not undergo hepatic metabolism of any kind:

  • Lisinopril is absorbed in its active form and excreted completely unchanged in the urine, with no measurable metabolism occurring in the body 1, 2, 3
  • Approximately 25-29% oral bioavailability, with renal excretion as the sole elimination pathway 1, 2
  • The elimination half-life is 12.6 hours in patients with normal renal function 2

Why UGT2B15 Status is Irrelevant

UGT2B15 is a phase II conjugation enzyme involved in glucuronidation of certain drugs and endogenous compounds. Since lisinopril:

  • Requires no hepatic activation or metabolism 1, 2
  • Is not a substrate for any cytochrome P450 enzymes
  • Is not conjugated by UGT enzymes
  • Undergoes zero biotransformation before renal excretion 3

Poor, intermediate, or extensive UGT2B15 metabolizer status has absolutely no bearing on lisinopril pharmacokinetics, efficacy, or safety.

What Actually Matters for Lisinopril Dosing

Renal Function is the Critical Factor

  • Significant drug accumulation occurs only when creatinine clearance falls below 30 mL/min 1, 4
  • Initial dosing should be 2.5 mg daily when GFR <30 mL/min, and 5 mg daily for GFR 30-60 mL/min 4, 5
  • Steady state is achieved in 2-3 days with normal renal function, but accumulation occurs with severe renal impairment 1

Standard Monitoring Parameters

The American College of Cardiology and American Heart Association recommend:

  • Check serum creatinine and potassium within 2-4 weeks of initiation or dose increase 6, 7
  • Accept up to 10-20% increase in serum creatinine as expected pharmacodynamic effect 6, 8
  • Monitor for hyperkalemia, particularly in patients with baseline renal impairment 9, 5

Evidence-Based Dosing Strategy

For cardiovascular indications with proven mortality benefit:

  • Start lisinopril at 2.5-5 mg once daily and titrate to target dose of 20-40 mg once daily 7, 8
  • High-dose lisinopril (32.5-35 mg/day) demonstrated significantly lower mortality compared to low-dose (2.5-5 mg/day) in the ATLAS trial 9, 7
  • Titrate doses every 1-2 weeks based on blood pressure response and tolerance 7, 8

Clinical Bottom Line

No dose adjustment, special monitoring, or therapeutic concern exists for patients with UGT2B15 poor metabolism taking lisinopril. Focus clinical attention on renal function monitoring, potassium levels, and blood pressure response—these are the only factors that influence lisinopril therapy 6, 1, 4.

References

Research

The clinical pharmacology of lisinopril.

Journal of cardiovascular pharmacology, 1987

Guideline

Off-Label Uses for Lisinopril

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

ACE Inhibitor Selection and Management in Cardiovascular Disease

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

ACE Inhibitor Selection for Heart Failure and Diabetes

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.