Abstract: PO1515
Hydralazine-Induced ANCA Vasculitis and Lupus Nephritis
Session Information
- Glomerular Diseases: The Excitement of Clinical Cases
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Ashoka, Ankita, Banner University Medical Center Tuscon, Tucson, Arizona, United States
- Vahdani, Golnaz, Banner University Medical Center Tuscon, Tucson, Arizona, United States
- Albasha, Waseem, Banner University Medical Center Tuscon, Tucson, Arizona, United States
- Bracamonte, Erika R., Banner University Medical Center Tuscon, Tucson, Arizona, United States
- Subramanian, Preethi, Banner University Medical Center Tuscon, Tucson, Arizona, United States
- Mansour, Iyad S. M., Banner University Medical Center Tuscon, Tucson, Arizona, United States
- Yau, Amy, Banner University Medical Center Tuscon, Tucson, Arizona, United States
Introduction
Hydralazine is a common antihypertensive drug, but drug induced glomerulonephritis (DI-GN) is observed in 5-10% of the population on hydralazine after three years of therapy. We present a case of rapidly progressive glomerulonephritis due to hydralazine.
Case Description
65-year-old female with a history of hypertension, diabetes mellitus, and chronic kidney disease presented for altered mental status. Her serum creatinine (SCr) three months and two years prior were 2.3 mg/dl and 0.9mg/dl respectively. On presentation, her SCr was 12.7 mg/dL, and she was started on hemodialysis. During her hospitalization, she had persistent hemoptysis with worsening dyspnea, skin rash, and oral ulcers (Fig 1, 2). Work up revealed hematuria, low complement levels, positive histone antibody and ANCA titers, and negative double stranded DNA antibody (Table 1). Skin biopsy showed small and medium vessel vasculitis. Kidney biopsy revealed class 3 and 5 lupus nephritis with full house immunofluorescence staining and active cellular crescents (Fig 3).
Review of her medications included hydralazine 25 mg three times a day for three years, and she was diagnosed with hydralazine induced glomerulonephritis and systemic vasculitis. She was given pulse steroids and cyclophosphamide with improvement in extrarenal manifestations, but no renal recovery.
Discussion
Hydralazine has been known to cause DI-GN since the 1950s, and it can manifest with features of pauci-immune glomerulonephritis and lupus nephritis. Drug induced vasculitis has a high incidence of renal involvement compared to drug induced systemic lupus erythematosus, however both entities have multiple auto-antibodies and ANCA positivity. The use of hydralazine has increased over the years due to trials demonstrating mortality benefit in heart failure. There is no consensus on the treatment, but discontinuing the offending agent, early diagnosis, and immunosuppressant therapy may result in favorable prognosis.
Table 1
Complement 3 Complement 4 Antinuclear antibody immunofluorescence and titer Anti-histone antibody immunofluorescence dsDNA Antibody ANCA immunofluorescence MPO PR3 pANCA titer | 76 mg/dL (90-180) 17 mg/dL (16-47) Positive, titer of 1:320 Positive (8.9 U) Negative Positive Positive Negative 1:640 |