title: Anti-tumor necrosis factor therapy in patients with difficult-to-treat lupus nephritis: a prospective series of nine patients.
abstract: OBJECTIVE
  To clarify the efficacy and safety of anti-TNF-alpha therapy for intractable lupus nephritis.
  
  
  METHODS
  In nine patients with systemic erythematosus who presented with lupus nephritis resistant to steroids and immunosuppressants, 200 mg/body of infliximab was drip-infused three times. No changes were made to other treatments for three months after the start of anti-TNF-alpha therapy, and urinary findings, renal function, serum complement, anti-DNA antibody, SLE activity, and adverse events were examined for six months after the start of anti-TNF-alpha therapy.
  
  
  RESULTS
  One of the nine patients developed pyelonephritis after the first infliximab injection and received no further injections. The remaining eight patients received 3 infliximab injections. Of the eight patients, urinary protein decreased after anti-TNF-alpha therapy in six patients, and the SLEDAI improved in five patients. Urinary findings and/or SLE activity improved in six patients. Of the patients whose urinary protein levels decreased after anti-TNF-alpha therapy, proteinuria recurred six months after anti-TNF-alpha therapy in one patient. After anti-TNF-alpha therapy, proteinuria and the SLEDAI improved significantly. With respect to adverse events, therapy was discontinued in one patient who developed pyelonephritis, and one patient developed decreased blood pressure due to infusion reactions. In one patient in whom the steroid dosage was increased due to poor response to anti-TNF-alpha therapy, brainstem infarction occurred four months later. In one patient, anti-DNA antibody levels increased after therapy, but none of the patients had decreased serum complement levels or increased SLE activity.
  
  
  CONCLUSIONS
  In intractable lupus nephritis, anti-TNF-alpha therapy improved urinary protein levels and SLE activity. Although adverse events must be monitored cautiously, it may be possible to use anti-TNF-alpha therapy as a third-line treatment.
authors: Department of Rheumatology, Allergy and Clinical Immunology of Clinical Research Center, Chiba-East National Hospital, Chiba 260-8712, Japan. ryu-ma@ka2.so-net.ne.jp
authors: R
authors: R
authors: Matsumura
authors: K
authors: K
authors: Umemiya
authors: T
authors: T
authors: Sugiyama
authors: M
authors: M
authors: Sueishi
authors: T
authors: T
authors: Umibe
authors: K
authors: K
authors: Ichikawa
authors: M
authors: M
authors: Yoshimura
mesh_terms: D000328:Adult; D000888:Antibodies, Anti-Idiotypic / Q000097:blood; D000911:Antibodies, Monoclonal / Q000009:adverse effects / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D004247:DNA / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D000069285:Infliximab; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000150:complications / Q000503:physiopathology; D008181:Lupus Nephritis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011507:Proteinuria / Q000209:etiology / Q000517:prevention & control; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D004247:DNA; D000069285:Infliximab