Abstract: SA-PO0729
Not All Angioedema on an ACE Inhibitor Is ACE Inhibitor Angioedema
Session Information
- Glomerular Diseases: Complement-Mediated Glomerulopathies and Infection-Related GN
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Kaushal, Amit, West Virginia University, Morgantown, West Virginia, United States
- Wu, Hongyan, West Virginia University, Morgantown, West Virginia, United States
- Tomar, Ojaswi Singh, West Virginia University, Morgantown, West Virginia, United States
- Shahzad, Sheikh Raza, West Virginia University, Morgantown, West Virginia, United States
Introduction
Acute angioedema can be bradykinin-mediated, mast cell-mediated, or complement-driven, and the initial workup is aimed at telling these apart. Initial investigation typically includes tryptase, histamine, C1 inhibitor (C1-INH), C3, C4, and C1q. We describe a woman with severe lisinopril-attributed angioedema and multi-organ injury whose panel did not fit ACEi angioedema alone.
Case Description
A 47-year-old woman on lisinopril for hypertension presented with acute angioedema. Failed intubation required emergent cricothyroidotomy. She developed distributive shock with multi-organ injury: oliguric dialysis-requiring AKI with new-onset proteinuria, hematuria, and granular casts; ischemic hepatitis; DIC requiring cryoprecipitate; and acute myocardial injury. Complement on prior testing had been normal. The angioedema panel showed normal tryptase, histamine, C1-INH, C3, and C4, but C1q was profoundly low (<3.6 mg/dL). She received CRRT for 48 hours followed by intermittent hemodialysis. Lisinopril was stopped, ACEi and ARB classes avoided, and amlodipine started. Creatinine improved from a peak of 8.3 to 3.88 mg/dL, and dialysis was discontinued before discharge.
Discussion
The clinical setup pointed toward ACEi angioedema, but the panel did not match. Every test was normal except C1q, which was profoundly low. Normal tryptase and histamine ruled out anaphylaxis; normal C1-INH with preserved C3 and C4 excluded C1-INH deficiency and immune complex disease. ACEi angioedema does not affect C1q. The differential narrowed to acquired complement-mediated disease — hypocomplementemic urticarial vasculitis syndrome (HUVS), anti-C1q vasculitis, and lupus — and her previously normal complement made this acquired. Among the three, HUVS fit best. Glomerulonephritis is a recognized feature, and her new proteinuria, hematuria, and AKI fit a developing GN. The alternative — ischemic injury from shock and DIC — does not match the complement profile, since shock-driven consumption lowers C3 and C4 together, not C1q in isolation. To distinguish HUVS, anti-C1q vasculitis, and lupus, anti-C1q antibody, lupus serologies, and anti-C1-INH antibody are needed; the low C1q with anti-C1q antibody is the hallmark of HUVS.
Conclusion. A patient on lisinopril with angioedema is not always lisinopril angioedema. When there is multi-organ injury or an unexpected lab value such as isolated low C1q, the panel is more informative than the medication list.