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Abstract: FR-PO628

Hydralazine-Induced Antinuclear Antibody (ANA) Negative "Lupus-Like Nephritis" With Normal Complements

Session Information

Category: Glomerular Diseases

  • 1302 Glomerular Diseases: Immunology and Inflammation


  • Balina, Hema, Temple University Hospital, Philadelphia, Pennsylvania, United States
  • Noel, Edva, Temple University Hospital, Philadelphia, Pennsylvania, United States
  • Rabbani, Rizwan, Temple University Hospital, Philadelphia, Pennsylvania, United States
  • Lee, Iris J., Temple University Hospital, Philadelphia, Pennsylvania, United States
  • Bastl, Christine P., Temple University Hospital, Philadelphia, Pennsylvania, United States

Isolated severe lupus nephritis from hydralazine without systemic manifestations of vasculitis is rare. Hydralazine can trigger autoimmune disease, and most of these cases have positive ANA and anti-histone antibodies. This case describes the presentation of ANA negative isolated lupus-like nephritis from hydralazine with normal complements, but positive anti-histone and anti-phospholipase A2 antibodies (Anti-PLA2R).

Case Description

A 65-year-old female with hypertension, and diabetes who was on hydralazine for two years presented with acute kidney injury and edema. Labs include Creatinine 5.38mg/dl, BUN 42 mg/dl. WBC 8.2K/mm3, Hemoglobin 7.5g/dl, Platelets 284K/mm3. The urine protein creatinine ratio was 16 grams. ANA, Anti-ds DNA, ANCA, Rheumatoid factor, hepatitis panel, kappa lambda ratio, serum electrophoresis, urine electrophoresis, and immunofixation were negative. Anti-histone antibodies and anti-PLA2R were positive. Renal biopsy showed membranoproliferative glomerulonephritis with the crescent formation, membranous glomerulopathy, and "full-house" staining on immunofluorescence. A diagnosis of hydralazine-induced lupus-like nephritis was made based on her medication history, positive anti-histone antibody, lack of criteria fulfilling SLE, and findings of lupus nephritis on biopsy. Treatment with mycophenolate mofetil and prednisone led to improvement in proteinuria and renal function.


The incidence of hydralazine-induced lupus is approximately around 5-8%. The diagnosis is made based on the temporal relationship between drug exposure and at least one clinical characteristic of SLE. Hydralazine-induced lupus usually presents with arthralgias, myalgias, fever, rash, and/or serositis. In severe cases, vasculitis, glomerulonephritis, or respiratory failure can be seen. The main serological findings in drug-induced lupus include a positive ANA (In 90-95% cases), anti-histone antibodies (90-95%), anemia, leukopenia, and positive Coombs test. Hypocomplementemia can be seen in 50% of the cases. Our patient had a unique presentation of hydralazine-induced lupus-like nephritis with no other systemic manifestations, normal complements, and a negative ANA. In addition, our patient had anti-PLA2R antibodies which are usually associated with primary membranous and rarely seen in membranous disease due to lupus.