A 65-year-old man comes to the clinic for a follow-up evaluation. Two weeks ago, he was diagnosed with heart failure with reduced ejection fraction (left ventricular ejection fraction of ). At that time, lisinopril was added to his medication regimen, which also includes metoprolol succinate and furosemide. The patient reports feeling well, with significant improvement in his exertional dyspnea. He denies orthopnea, paroxysmal nocturnal dyspnea, or dizziness. Blood pressure is 122/78 mmHg and pulse is 68/min. Physical examination shows no jugular venous distention and clear lungs bilaterally.
Laboratory results two weeks ago (prior to lisinopril initiation):
| Test | Result |
|---|---|
| Blood urea nitrogen | 16 mg/dL |
| Serum creatinine | 1.1 mg/dL |
| Serum potassium | 4.2 mEq/L |
Laboratory results today:
| Test | Result |
|---|---|
| Blood urea nitrogen | 22 mg/dL |
| Serum creatinine | 1.4 mg/dL |
| Serum potassium | 4.8 mEq/L |
Which of the following is the most appropriate next step in the management of this patient's pharmacotherapy?
- Continue the current regimen without dose adjustmentCevap
- BDecrease the lisinopril dose by half
- CDiscontinue lisinopril and initiate diltiazem
- DAdmit the patient to the hospital for intravenous hydration
- ESchedule a renal ultrasound with Doppler
Cevap
Continue the current regimen without dose adjustment
The correct approach is to continue the current regimen without dose adjustment. ACE inhibitors (such as lisinopril) block the production of angiotensin II, leading to vasodilation of the efferent arteriole in the kidney. This decreases intraglomerular hydrostatic pressure and effectively lowers the glomerular filtration rate (GFR), which clinically manifests as an initial rise in serum creatinine. Guidelines establish that an increase in serum creatinine of up to 30% from baseline within the first few weeks of starting an ACE inhibitor or angiotensin receptor blocker (ARB) is an expected, physiologic response that stabilizes over time. In this patient, the creatinine increased from mg/dL to mg/dL, which is an approximately increase and falls within the acceptable threshold. Furthermore, his serum potassium is mEq/L, which is safely below the typical intervention threshold of to mEq/L. Because the patient is clinically stable and these laboratory changes are within safe limits, lisinopril should be continued to maintain its long-term mortality benefits in heart failure with reduced ejection fraction (HFrEF).
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Anahtar Kavram
Initiation of ACE inhibitors can cause a benign, physiologic increase in serum creatinine of up to 30% from baseline due to efferent arteriolar vasodilation. If the increase is ≤30% and hyperkalemia is absent, the medication should be continued without dose adjustment.