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Results Beta 1 integrin expression was significantly up‐regulated on peripheral blood T cells from patients with active SLE, particularly those with the complication of World Health Organization class IV nephritis, whereas CD28 was significantly decreased in patients with active SLE compared with normal individuals. Beta 1 integrin expression closely correlated with serum hypocomplementemia.

Engagement of β1 integrin on T cells from patients with active SLE, but not on those from normal individuals, induced cell proliferation as well as CD40L expression on T cells. Up‐regulation of CD40L expression and T cell proliferation, induced by β1 integrin stimulation, were completely inhibited by transfection of the dominant‐negative truncations of FAK or WT PTEN.

Results APS nephropathy existed in 39.5% of patients with aPL, compared with only 4.3% of patients without aPL. Serial number pinnacle studio 18 ultimate serial. APS nephropathy was associated with both lupus anticoagulant and anticardiolipin antibodies. Among aPL‐positive SLE patients, APS nephropathy was found in two‐thirds of those with APS and in one‐third of those without APS.

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A strong association between APS nephropathy and the presence of arterial thrombosis and livedo reticularis was noted. Patients with APS nephropathy had a higher frequency of hypertension and elevated serum creatinine levels at the time of kidney biopsy but did not have a higher frequency of renal insufficiency, end‐stage renal disease, or death at the end of followup. Serial kidney biopsy specimens were available from 11 patients and showed progression of APS nephropathy lesions.

During followup, manifestations of APS (especially arterial thromboses) developed more frequently in the SLE/non‐APS patients with APS nephropathy than in those without APS nephropathy. Conclusion Among patients with SLE, APS nephropathy occurs almost exclusively in those with aPL, suggesting an important role of aPL in the pathogenesis of APS nephropathy. Patients with APS nephropathy develop hypertension, raised serum creatinine levels, and progression of histologic lesions, all of which are associated with a poor renal outcome. Manifestations of APS also tend to develop in these patients.

APS nephropathy should be included in the APS classification criteria, and the use of appropriate anticoagulant therapy should be tested. The antiphospholipid syndrome (APS) is a multisystem disease characterized by arterial and venous thromboses, pregnancy morbidity, and the presence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL) and lupus anticoagulant (LAC) (, ). APS is classified as primary or classified as secondary when it occurs in the context of other underlying disorders, mainly systemic lupus erythematosus (SLE) ( ). Antiphospholipid antibodies are detected in ∼30–40% of patients with SLE; arterial or venous thrombosis will develop in nearly one‐third of these patients (, ).

Thrombosis may occur at any vascular site and in any organ system. However, the intrarenal vascular involvement in association with APS was poorly recognized until recently. A possible explanation is that kidney biopsies were rarely performed in patients with primary APS, and the majority of studies in SLE focused on immune complex glomerulonephritis rather than renal microangiopathy. The most commonly reported intrarenal vascular lesion in patients with APS (primary or secondary) ( -) and in patients with SLE and aPL ( -) is thrombotic microangiopathy (TMA), which is characterized by the presence of fibrin thrombi in glomeruli and/or arterioles. In a recent multicenter retrospective study, Nochy et al examined kidney biopsy specimens obtained from 16 patients with primary APS ( ). All of the patients had vasoocclusive lesions characterized by acute thromboses (TMA) and chronic vascular lesions such as fibrous intimal hyperplasia (FIH) of interlobular arteries, recanalizing thrombi in arteries and arterioles, fibrous occlusions, or focal cortical atrophy (FCA).