Hydralazine Induced Vasculitis with Pulmonary and Renal Manifestations: Case Report and Review of the Literature

Background:

Hydralazine is a popular and effective antihypertensive and afterload reducing agent. It is frequently used in patients with congestive heart failure and renal insufficiency, or when patients cannot tolerate angiotensin converting enzyme (ACE) inhibitors.. Hydralazine is known to cause a drug induced lupus syndrome, but pulmonary and renal involvement is rarely reported.

Method:

We report a case of a 58 year old gentleman who presented to the emergency department complaining of oliguria, darkened urine, dyspnea on exertion, chills and arthralgias. Past medical history was notable for a congestive heart failure episode one year prior, with subsequent echocardiogram revealing ejection fraction 50%; hypertension, and hyperlipidemia. His current medications included hydralazine 400mg daily; furosemide, carvedilol, valsartan, amitryptyline, and aspirin. Physical examination was significant for a pulse of 105 beats per minute, a 2/6 systolic ejection murmur, and bilateral lower lobe crackles on lung exam. No rash or synovitis was noted. Laboratory evaluation on admission revealed hemoglobin 7.3 g/dl, creatinine 3.3 mg/dl, and urinalysis with 3+ blood and 100 mg/dl protein.

Results:

Empiric therapy for community acquired pneumonia was initiated with ceftriaxone and azithromycin, intravenous fluids were initiated, and furosemide, valsartan, and hydralazine were held. The patient developed worsening hypoxia, bilateral pulmonary infiltrates, and renal insufficiency. Transthoracic echocardiogram showed normal left ventricular function. While initial microscopic urine review did not demonstrate red blood cell casts, subsequent evaluation revealed numerous red cell casts.

Serologies demonstrated a positive ANA, positive anti‐histone antibodies, positive perinuclear antineutrophil cytoplasmic antibodies (p‐ANCA), positive anti‐myeloperoxidase antibodies, positive anti‐single stranded DNA antibodies, and decreased complement factor 4 levels. A renal biopsy demonstrated a pauci‐immune crecentric glomerulonephritis. Hydralazine was withdrawn and the patient was started on daily cyclophosphamide and corticosteroids. The patient's hypoxemia improved, but renal function did not recover, and he currently requires hemodialysis thrice weekly and is being evaluated for renal transplantation.

Conclusion:

Hydralazine induced vasculitis is reported in the literature with diverse manifestations, but lung and kidney involvement are rare and can be associated with significant morbidity and mortality. Prompt discontinuation of hydralazine and early initiation of corticosteroids and immunosuppression are warranted. As more data appear citing the benefits of hydralazine in heart failure, clinicians need to be aware of these potential side effects and act quickly to avoid long term sequelae.

Author Disclosure Block:

Z. McIver, None; M. Newton, None; C.M. Whinney, None.