Development of Crescentic Immunoglobulin A Nephritis and Multiple Autoantibodies in a Patient during Adalimumab Treatment for Rheumatoid Arthritis

Correspondence To the Editor: Tumor necrosis factor‑α (TNF‑α) is a pro‑inflammatory cytokine that plays a crucial role in the pathogenesis of rheumatoid arthritis (RA), while the advent of anti‑TNF‑α agents brings better control and low side effects in RA. The most frequent side effects are infectious disease and drug‑induced lupus. Herein, we present a case of Chinese man with a 10‑year history of RA developing crescentic immunoglobulin A (IgA) nephritis and multiple autoantibodies during adalimumab treatment. A 62‑year‑old Chinese man was admitted for new occurrence of hematuria and proteinuria for 20 days. He had a 10‑year history of RA diagnosed according to the American College of Rheumatology Criteria. Thereafter, a low dose of prednisone, oral methotrexate (15 mg/week) and intermittent administration of nonsteroidal anti‑inflammatory drugs (NSAIDs) were initiated. Because of tenderness of multiple joints and new occurrence of rheumatoid nodules on the left knee on 16 February 2014, and erythrocyte sedimentation rate (ESR) increased to 70 mm/h and C‑reactive protein (CRP) 16.3 mg/L, with a high disease activity score for 28 joints (DAS28) scored 5.44, adalimumab (40 mg subcutaneous every other week) was initiated. Antinuclear antibody (ANA) and antineutrophil cytoplasmic antibody (ANCA) were not detected, and renal parameters were normal before adalimumab treatment. After four doses of adalimumab therapy (2 months later), rheumatoid nodules resolved and ESR decreased to 13 mm/h, CRP was 1.7 mg/L, and DAS28 scored 2.0 suggestive of clinical remission; however, he presented with hematuria, proteinuria and oliguria. On admission, bilateral pitting edema was found in the lower extremities. His hands showed deformities. Laboratory findings showed elevated white blood cell count, 15.72 × 10 9 /L (normal range: 100–300 × 10 9 /L); serum urea nitrogen, 31.84 mmol/L (normal range: 1.07–7.14 mmol/L); serum creatinine (Cr), 249 μmol/L (normal range: 45–84 μmol/L); urinary protein excretion was 5.41 g/24 h, and calculated eGFR was 23 ml·min −1 ·1.73 m −2. On serologic examination, ESR was 38 mm/h (normal range: 0–20 mm/h); CRP, 16.21 mg/L (normal range: 0–3 mg/L), ANA was 1:80 positive (homogeneous pattern); anticardiolipin (ACL) antibody, 24 pLIgG U/ml (normal range: 0–12 U/ml); perinuclear‑ANCA, 1:80 positive; while myeloperoxidase‑ANCA and proteinase 3‑ANCA were negative. Anti‑double‑stranded DNA, anti‑extractable nuclear antigen antibody, anti‑glomerular basement membrane antibody and cryoglobulin were not detected. Rheumatoid factor (RF) was 95.8 U/ml (normal range: 0–20 U/ml); IgA, 6.13 g/L (normal range: 0.7–4.0 g/L); C3 complement fraction, 0.585 g/L (normal range: 0.7–1.4 g/L); IgG, IgM and C4 …