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      Primary Antiphospholipid Antibody Syndrome and Mesangial IgA Glomerulonephritis

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          The antiphospholipid antibody syndrome (APS) is characterized by recurrent thrombosis, fetal loss, multiorgan involvement, and the presence of lupus anticoagulant and/or anticardiolipin antibody. When not associated with systemic lupus erythematosus, other collagen diseases, or ingestion of medications, the condition is called primary APS. The kidney may be involved in the APS syndrome with acute nephritis and renal failure. The cases with renal biopsy studies have shown variable glomerular morphology, ranging from mild mesangial changes to a diffuse endocapillary proliferative glomerulonephritis. The most frequent lesion is thrombotic microangiopathy or features seen in the hemolytic uremic syndrome. Apart from fibrin thrombus deposition, only a few cases have shown focal and segmental deposits of IgG and/or IgM and/or C3. We describe a patient with primary APS who had thrombosis with lower limb amputation and acute renal failure. The renal biopsy specimen showed a focal proliferative glomerulonephritis with endothelial proliferation and damage, with diffuse heavy mesangial deposits of IgA and fibrinogen. This case with diabetes mellitus, but without diabetic nephropathy, represents the occurrence of primary APS and mesangial IgA nephropathy which potentiated the renal injury, leading to acute renal failure. The relationship to the Henoch-Schönlein syndrome is discussed.

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          Most cited references 6

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          Association between antiphospholipid antibodies and cardiac abnormalities in patients with systemic lupus erythematosus.

          Although the antiphospholipid antibodies are well recognized to be associated with thrombosis, recurrent abortion, and thrombocytopenia in patients with systemic lupus erythematosus (SLE), their relationship with cardiac disease is less clear. The purpose of this study was to evaluate the association between anti-phospholipid antibodies and cardiac abnormalities in patients with SLE. A total of 75 consecutive SLE patients and 60 healthy sex- and age-matched control subjects were evaluated in a case-control study. All participants underwent M-mode, two-dimensional, and Doppler echocardiography. Antiphospholipid antibodies levels were assayed in each patient. The prevalence of antiphospholipid antibodies in patients with and without echocardiographic abnormalities was compared. Compared with the control group, SLE patients had significantly more pericardial abnormalities, left ventricular hypertrophy, left atrial enlargement, left ventricular dysfunction and verrucous valvular thickening, global valvular thickening with dysfunction, and mitral and aortic regurgitation. Among these abnormalities, antiphospholipid antibodies were significantly associated with isolated left ventricular (global or segmental) dysfunction (four of five positive; p less than 0.05), verrucous valvular (mitral or aortic) thickening (seven of nine positive; p less than 0.005), global valvular (mitral or aortic) thickening and dysfunction (five of six positive; p less than 0.02), as well as mitral regurgitation (16 of 19 positive; p less than 0.001) and aortic regurgitation (five of six positive; p less than 0.02). Valvular lesions and myocardial dysfunction are associated with elevated antiphospholipid antibodies. This study has important implications for the pathogenic role of anti-phospholipid antibodies in relation to these cardiac abnormalities.
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            The relationship between lupus anticoagulants and antibodies to phospholipid

             D Triplett (1988)
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              Answers to the antiphospholipid-antibody syndrome?

               M Lockshin (1995)

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                April 2001
                07 May 2001
                : 21
                : 2
                : 134-140
                Departments of Pathology and Medicine, National University Hospital, Singapore
                46236 Am J Nephrol 2001;21:134–140
                © 2001 S. Karger AG, Basel

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                Figures: 3, References: 56, Pages: 7
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