Results APS nephropathy existed in 39.5% of patients with aPL, compared with only 4.3% of patients without aPL. 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.

Russian-German, French-Russian, Russian-Korean, Russian-Spanish and Arabic. D., Boguslavskij I.M., Iomdin L.L., Lazurskij A.V. Pertsov, N.V., Sannikov.

A strong association between APS nephropathy and the presence of arterial thrombosis and livedo reticularis was noted. Matematicheskie diktanti 2 klass golubj otveti. 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). Daugas et al observed that the above‐mentioned histologic lesions, defined as APS nephropathy, exist also in SLE—especially in SLE patients with secondary APS—independently of lupus nephritis ( ).

An association of APS nephropathy with APS (mainly with arterial thrombosis and abortions) and LAC, but not with aPL, was observed. In both of these studies, systemic hypertension was the main clinical manifestation of APS nephropathy. The purpose of the current study was to evaluate the following: 1) the presence of APS nephropathy in kidney biopsy specimens obtained from SLE patients with or without aPL, in order to assess any association between APS nephropathy and aPL, 2) clinical and laboratory associations with APS nephropathy, 3) the renal prognosis of patients with APS nephropathy, 4) the evolution of APS nephropathy in patients who underwent repeated kidney biopsies, and 5) any tendency of SLE/non‐APS patients with APS nephropathy to develop APS during long‐term followup. The study group comprised all patients with SLE and biopsy‐proven renal involvement (n = 151) who were followed up on a regular basis at the Department of Pathophysiology and for whom at least 2 measurements of aPL were performed before or at the time of kidney biopsy. The patients were categorized as those with aPL (n = 81), including those with APS (n = 18), and those without aPL (n = 70).