The authors declare no conflicts of interest.
Predicting the risk of hyperkalemia in patients with chronic kidney disease starting lisinopril†
Version of Record online: 29 JAN 2010
Copyright © 2010 John Wiley & Sons, Ltd.
Pharmacoepidemiology and Drug Safety
Volume 19, Issue 3, pages 266–272, March 2010
How to Cite
Johnson, E. S., Weinstein, J. R., Thorp, M. L., Platt, R. W., Petrik, A. F., Yang, X., Anderson, S. and Smith, D. H. (2010), Predicting the risk of hyperkalemia in patients with chronic kidney disease starting lisinopril. Pharmacoepidem. Drug Safe., 19: 266–272. doi: 10.1002/pds.1923
- Issue online: 24 FEB 2010
- Version of Record online: 29 JAN 2010
- Manuscript Accepted: 15 DEC 2009
- Manuscript Revised: 24 NOV 2009
- Manuscript Received: 1 JUL 2009
- chronic kidney disease;
- risk score;
- cohort study;
- adverse effects
Angiotensin-converting enzyme (ACE) inhibitors are recommended for patients with chronic kidney disease (CKD) because they slow disease progression. But physicians' concerns about the risk of hyperkalemia (elevated serum potassium level), a potentially fatal adverse effect, may limit optimal management with ACE-inhibitors. We synthesized known predictors of hyperkalemia into a prognostic risk score to predict the risk of hyperkalemia.
We assembled a retrospective cohort of adult patients with possible CKD (at least one estimated glomerular filtration rate (eGFR) value less than 60 ml/min/1.73 m2) who started an ACE-inhibitor (i.e., incident users) between 1998 and 2006 at a health maintenance organization. We followed patients for hyperkalemia: (1) potassium value >5.5 mmol/L; or (2) diagnosis code for hyperkalemia. Cox regression synthesized a priori predictors recorded in the electronic medical record into a risk score.
We followed 5171 patients and 145 experienced hyperkalemia, a 90-day risk of 2.8%. Predictors included: age, eGFR, diabetes, heart failure, potassium supplements, potassium-sparing diuretics, and a high dose for the ACE-inhibitor (lisinopril). The risk score separated high-risk patients (top quintile, observed risk of 6.9%) from low-risk patients (bottom quintile, observed risk of 0.7%). Predicted and observed risks agreed within 1% for each quintile. The risk increased gradually in relation to declining eGFR with no apparent threshold for contraindicating ACE-inhibitors.
The risk score separated high-risk patients (who may need more intensive laboratory monitoring) from low-risk patients. The risk score should be validated in other populations before it is ready for use in clinical practice. Copyright © 2010 John Wiley & Sons, Ltd.