%0 Journal Article
%T Adalimumab (TNF¦Á Inhibitor) Therapy Exacerbates IgA Glomerulonephritis Acute Renal Injury and Induces Lupus Autoantibodies in a Psoriasis Patient
%A S. S. Wei
%A R. Sinniah
%J Case Reports in Nephrology
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/812781
%X Adalimumab (Humira) is a tumour necrosis factor ¦Á (TNF¦Á) inhibitor that is approved for the treatment of rheumatoid arthritis, psoriasis, psoriatic arthritis, Crohn's disease, ankylosing spondylitis, and juvenile idiopathic arthritis (Sullivan and Preda (2009), Klinkhoff (2004), and Medicare Australia). Use of TNF¦Á inhibitors is associated with the induction of autoimmunity (systemic lupus erythematosus, vasculitis, and sarcoidosis or sarcoid-like granulomas) (Ramos-Casals et al. (2010)). We report a patient with extensive psoriasis presenting with renal failure and seropositive lupus markers without classical lupus nephritis after 18 months treatment with adalimumab. He has renal biopsy proven IgA nephritis instead. Renal biopsy is the key diagnostic tool in patients presenting with adalimumab induced nephritis and renal failure. He made a remarkable recovery after adalimumab cessation and steroid treatment. To our knowledge, this is a unique case of a psoriasis patient presenting with seropositive lupus markers without classical lupus nephritis renal failure and had renal biopsy proven IgA glomerulonephritis after receiving adalimumab. 1. Introduction A 61-year-old man was referred for evaluation of his compromised renal function. He has had chronic extensive plaque psoriasis since 2002 with a psoriasis area and severity index (PASI) score of 27 [1, 2]. For the past few years, he received various treatments including phototherapy, acitretin, methotrexate, cyclosporine, sulphasalazine, and leflunomide without much success until he received adalimumab 18 months prior to his first presentation to the renal clinic in 2011. There was no past history of renal disease and his renal function tests were normal (in 2009, serum creatinine level was 83£¿¦Ìmol/L and urea was 7.2£¿mmol/L). His urine microscopy was normal with no proteinuria detected prior to his adalimumab treatment. He self-injected adalimumab 40£¿mgm fortnightly. He noted transient injection site redness that lasted for a few days after each injection. When routine blood tests showed that he had renal failure with serum creatinine level of 282£¿¦Ìmol/L, urea of 20.3£¿mmol/L, and estimated glomerular filtration rate (eGFR) of 21£¿mL/min/1.73£¿m2 calculated by the abbreviated MDRD equation [3], his attending dermatologist referred him to the renal clinic for further management. On presentation, he did not have any urinary symptoms such as haematuria or dysuria. However, he had a few weeks history of feeling tired with some appetite loss. He had no skin rash, fever, or new joint pain. He developed
%U http://www.hindawi.com/journals/crin/2013/812781/