The Journal of the Korean Rheumatism Association 2009; 16(3): 248-252
Published online September 30, 2009
© Korean College of Rheumatology
강동구1ㆍ김봉수2ㆍ장은희1ㆍ신상엽1ㆍ김진석1
제주대학교 의과대학 내과학교실1, 영상의학교실2
Correspondence to : Jinseok Kim
Systemic lupus erythematosus (SLE) is a multisystemic inflammatory autoimmune disease caused by various autoantibodies and immune complexes. SLE and antiphospholipid antibodies are associated with thrombotic manifestations. However, renal artery thrombosis which causes renal artery occlusion is uncommon even in SLE patients with antiphospholipid antibodies. A 27-year-old woman with SLE suddenly developed left flank pain and generalized edema. From the laboratory workup, the woman was negative for antiphospholipid antibody and nephrotic- range proteinuria was detected. Computed tomography revealed renal artery thromboembolism and multiple renal infarctions with parenchymal perfusion defects in the left kidney. Renal biopsy showed WHO classification III and V lupus nephritis. Left flank pain, generalized edema and proteinuria were resolved and the thromboembolism resolved itself after a high dose of steroid and anticoagulation therapy. In SLE patients, sudden onset of unexplained flank pain is considered as a possible symptom of renal vessel thromboembolism even if the antiphospholipid antibody is negative.
Keywords Systemic lupus erythematosus, Antiphospholipid antibodies, Renal infarction
The Journal of the Korean Rheumatism Association 2009; 16(3): 248-252
Published online September 30, 2009
Copyright © Korean College of Rheumatology.
강동구1ㆍ김봉수2ㆍ장은희1ㆍ신상엽1ㆍ김진석1
제주대학교 의과대학 내과학교실1, 영상의학교실2
Dong Gu Kang1, Bong Soo Kim2, Eun Hee Jang1, Sang Yop Shin1, Jinseok Kim1
Departments of Internal Medicine1 and Radiology2, College of Medicine, Jeju National University, Jeju, Korea
Correspondence to:Jinseok Kim
Systemic lupus erythematosus (SLE) is a multisystemic inflammatory autoimmune disease caused by various autoantibodies and immune complexes. SLE and antiphospholipid antibodies are associated with thrombotic manifestations. However, renal artery thrombosis which causes renal artery occlusion is uncommon even in SLE patients with antiphospholipid antibodies. A 27-year-old woman with SLE suddenly developed left flank pain and generalized edema. From the laboratory workup, the woman was negative for antiphospholipid antibody and nephrotic- range proteinuria was detected. Computed tomography revealed renal artery thromboembolism and multiple renal infarctions with parenchymal perfusion defects in the left kidney. Renal biopsy showed WHO classification III and V lupus nephritis. Left flank pain, generalized edema and proteinuria were resolved and the thromboembolism resolved itself after a high dose of steroid and anticoagulation therapy. In SLE patients, sudden onset of unexplained flank pain is considered as a possible symptom of renal vessel thromboembolism even if the antiphospholipid antibody is negative.
Keywords: Systemic lupus erythematosus, Antiphospholipid antibodies, Renal infarction
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