Can the elevated BUN (29 mg/dL) and serum creatinine (1.48 mg/dL) with hyperkalemia (potassium 5.7 mEq/L) be due to a hemolyzed blood specimen in a patient who recently discontinued lisinopril (40 mg)?

Can Hemolysis Explain These Laboratory Abnormalities?

Hemolysis can falsely elevate potassium but cannot explain the elevated BUN and creatinine—these findings represent true acute kidney injury (AKI) likely precipitated by lisinopril in the setting of volume depletion or other contributing factors.

Understanding Hemolysis Effects on Laboratory Values

Hemolysis causes pseudohyperkalemia by releasing intracellular potassium from lysed red blood cells into the serum specimen, but this is an in vitro artifact that does not reflect the patient's true physiologic state 1. However, hemolysis does not cause falsely elevated BUN or creatinine values—these markers remain accurate even in hemolyzed specimens.

Key Laboratory Distinctions:

• Potassium (5.7 mEq/L): Could be artifactually elevated if specimen was hemolyzed, but given the clinical context (lisinopril use, elevated creatinine), this likely represents true hyperkalemia 2, 3
• BUN (29 mg/dL) and Creatinine (1.48 mg/dL): These elevations are real and indicate acute or chronic kidney dysfunction—hemolysis does not affect these measurements 4

Clinical Context: Lisinopril-Induced Changes

The recent discontinuation of lisinopril 40 mg is highly relevant. ACE inhibitors like lisinopril predictably cause rises in both creatinine and potassium, particularly in patients with underlying renal impairment 2, 3.

Expected ACE Inhibitor Effects:

• Creatinine elevation up to 30% above baseline is acceptable and expected when initiating or maintaining ACE inhibitor therapy 2, 4
• Potassium elevation to ≤5.5 mmol/L is considered acceptable during ACE inhibitor therapy 2
• The patient's potassium of 5.7 mEq/L exceeds the acceptable threshold and warrants intervention 2

Risk Factors Present:

• Higher ACE inhibitor dose (lisinopril ≥10 mg daily increases hyperkalemia risk) 3
• Creatinine >1.6 mg/dL progressively increases hyperkalemia risk 2
• The creatinine of 1.48 mg/dL approaches this threshold, especially concerning in elderly patients where this level may represent more severe renal impairment than the number suggests 2

Recommended Diagnostic Approach

To determine if hemolysis contributed to the potassium elevation:

1. Inspect the specimen: Hemolyzed samples appear pink or red-tinged
2. Repeat potassium measurement using a fresh, carefully drawn specimen (avoid prolonged tourniquet time, fist clenching, or traumatic venipuncture) 1
3. Consider whole blood potassium measurement if available, as this may be more accurate in certain clinical scenarios 1

However, regardless of hemolysis, the elevated BUN and creatinine require evaluation for AKI.

Management Algorithm

Immediate Actions:

• Repeat comprehensive metabolic panel with careful specimen handling to confirm potassium level 2
• Assess for volume depletion: Review diuretic use, recent illness, fluid intake 2
• Review all medications for nephrotoxins (NSAIDs, other potassium-retaining agents) 2, 5
• Check baseline creatinine to determine if this represents acute change or chronic kidney disease 4

If True Hyperkalemia Confirmed (K+ >5.5 mEq/L):

According to ESC guidelines, when potassium rises to >5.5 mmol/L, the ACE inhibitor should be stopped and specialist advice sought 2. The lisinopril was appropriately discontinued.

Monitoring After ACE Inhibitor Discontinuation:

• Recheck blood chemistry within 1-2 weeks to ensure potassium and creatinine plateau or improve 2
• Monitor frequently and serially until values stabilize 2
• If values normalize, consider cautious reintroduction at lower dose (e.g., lisinopril 5 mg) with close monitoring, as ACE inhibitors provide significant mortality benefit and discontinuation may lead to clinical deterioration 2

Common Pitfalls to Avoid

Do not assume hemolysis explains all abnormalities—while potassium may be artifactually elevated, the BUN and creatinine elevations are real and require investigation 4, 1.

Do not permanently discontinue ACE inhibitor without specialist consultation if renal function and potassium improve, as these medications provide substantial cardiovascular and renal protection 2, 4. Up to 30% creatinine elevation is acceptable if it stabilizes 2, 4.

Avoid concomitant nephrotoxins: NSAIDs significantly increase risk of both AKI and hyperkalemia with ACE inhibitors and should be discontinued 2, 5.

Consider volume status carefully: Diuretic-induced volume depletion is the most common avoidable cause of creatinine elevation with ACE inhibitors 2, 4.