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P-121 YI Case Report: Minimal Change Nephrotic Syndrome Associated with Adalimumab Therapy in a Pediatric Patient with Crohn's Disease

BACKGROUND:Objective: To report a case of minimal change glomerulonephritis with the use of Adalimumab therapy in a pediatric patient with Crohn's disease. METHODS:Case Summary: Our patient is 16 year old male with Crohn's Disease. Initial treatment with 6-Mercaptopurine was ineffective in controlling gastrointestinal symptoms. He was hospitalized on several occasions for exacerbation of his IBD and was started on Infliximab therapy. Initially he responded well with resolution of his abdominal symptoms. During his fourth Infliximab infusion the patient experienced difficulty breathing, facial flushing and throat tightness. Despite pre-medication with acetaminophen, diphenhydramine and steroids, he once again experienced a similar adverse reaction at his next infusion. At this point, he was switched to Adalimumab. Gastrointestinal symptoms were well controlled and he did well over the course of his next 4 injections. A week following the fourth injection, he presented to the emergency department with complaints of edema of the scrotum, face, legs and feet. He had low albumin at 1.2, creatinine of 1.3 and proteinuria and was found to be hypertensive. Renal biopsy performed was consistent with Minimal Change Nephrotic Syndrome believed to be secondary to the Adalimumab. He was started on prednisone therapy with resolution of his edema over the next several days and his hypoalbuminemia improved over several weeks. RESULTS:Since their introduction in the 1990s, anti-TNF agents have changed the way physicians and their patients control the symptoms of Crohn's Disease and Ulcerative Colitis. Infliximab (Remicade) and Adalimumab (Humira) are monoclonal anti-TNF alpha agents approved for the treatment of moderate to severe Inflammatory Bowel Disease. Infliximab is a chimeric IgG antibody derived from both mice and humans while Adalimumab is a 100% human-derived monoclonal antibody. Both act to block TNF-alpha molecules in the blood and cells of the gastrointestinal tract to achieve clinical remission. Acute side effects of anti-TNF biologics include erythema, pruritus, nausea, vomiting and airway compromise. Delayed side effects include autoimmune diseases, infection, dermatologic, cardiovascular and neurologic diseases as well as malignancies such as lymphoma which can occur weeks to months after therapy begins. There have been few cases of nephrotoxic reactions following commencement of anti-TNF therapy. Only 1 case of nephrotic syndrome has been reported to date in an adult. Gupta et al reported a case of nephrotic syndrome in an adult patient shortly after beginning Adalimumab for treatment of Crohn's Disease. Kaushik et al reported a case of Membranous Glomerulonephritis with the use of Etanercept in treatment of ankylosing spondylitis and Koya et al presented a case of minimal change disease in an adult treated with Etanercept for psoriasis. To our knowledge, there are no prior documented cases in pediatrics of nephrotic syndrome secondary to anti-TNF medications. As our patient was in clinical remission of his Crohn's Disease with PCDAI scores of 0 we feel it is highly unlikely that his nephrotic syndrome presentation is a result of his underlying disease. CONCLUSIONS:Patients on anti-TNF therapy should be monitored for signs of nephrotic syndrome which include edema, hypertension, proteinuria and hypoalbuminemia.