Missed Primary Aldosteronism with HydrANCAzine Consequences

Introduction: Primary aldosteronism (PA) is responsible for up to 25% of treatment resistant hypertension (TRH). However, less than 4% of eligible patients undergo screening. This leads to escalating antihypertensive regimens subjecting patients to otherwise circumventable side effects. We hereby present 3 cases of missed PA sub-optimally managed with hydralazine complicated by drug induced ANCA associated vasculitis (AAV). Case Description: These are 3 cases of p-ANCA/MPO positive biopsy proven hydralazine induced pauci-immune glomerulonephritis sharing striking similarities (Table 1). All 3 had a diagnosis of TRH on 6 blood pressure medications on average. Notably, none were on mineralocorticoid receptor antagonists. Despite multiple providers spanning many specialties and suggestive biochemical profiles PA testing was not done. In addition to discontinuing hydralazine, significant immunomodulatory therapy was employed to achieve disease remission. PA was diagnosed thereafter, and blood pressure control achieved with only 2-3 medications (including an MRA). Patient #3 also underwent adrenalectomy for unilateral disease. Discussion: Autonomous hyperaldosteronism has well documented deleterious end-organ effects. Underrecognized PA can lead to unwarranted side effects in attempts to control blood pressure with non-targeted and suboptimal treatments. These cases describe a potentially life-threatening idiosyncratic hydralazine side effect. More importantly they highlight the persistent poor rates of PA screening, underutilization of MRAs, and overreliance on agents relegated to the bottom of our antihypertensive arsenal. Realizing that PA can even have a milder phenotype without overtly obvious biochemical profiles, expanded screening to achieve an accurate diagnosis is instrumental in choosing the right therapy and circumventing significant adverse events such as hydrANCAzine.Table 1 - Patient Characteristics