Stenosis in Antiphospholipid Syndrome: A New Finding with Clinical Implications

Ben-Ami, Dana; Bar-Meir, Eran; Shoenfeld, Yehuda

doi:10.1191/0961203306lu2335oa

Cited by 15 publications

(16 citation statements)

References 31 publications

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“…In a multivariate analysis, RAS in APS\APL correlated only with elevated C-reactive protein (CRP) but not with traditional atherosclerotic risk factors [31]. In addition to these large cohorts, various cases of APS and RAS were described in the literature [7,32].…”

Section: Discussionmentioning

confidence: 99%

Renal artery stenosis with significant proteinuria may be reversed after nephrectomy or revascularization in patients with the antiphospholipid antibody syndrome: a case series and review of the literature

et al. 2010

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Renal artery stenosis (RAS) is a disease which might present as hypertension, renal insufficiency or proteinuria and even as nephrotic syndrome. While 90% of cases are secondary to atherosclerosis, the rest of the cases are usually related to fibromuscular dysplasia. Recently, RAS has also been documented in patients with the antiphospholipid syndrome (APS). Although cases of nephrotic syndrome induced by RAS have been published, cases of patients with APS and nephrotic syndrome attributed to RAS were not reported in the literature. In this paper, three young male patients with APS, hypertension and significant proteinuria secondary to RAS are presented. The patients were treated with nephrectomy or revascularization in addition to prior treatment with warfarin, with improvement of the hypertension and the proteinuria. The relationship between renal artery stenosis, nephrotic range proteinuria and APS is reviewed. We suggest that renal artery stenosis should be included in the differential diagnosis of the nephrotic syndrome and that APS should be included in the differential diagnosis of renal artery stenosis especially in young male patients with proteinuria.

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Section: Discussionmentioning

confidence: 99%

Renal artery stenosis with significant proteinuria may be reversed after nephrectomy or revascularization in patients with the antiphospholipid antibody syndrome: a case series and review of the literature

et al. 2010

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“…Large-vessel thrombosis can also involve arteries as a consequence of thromboembolism (e.g., from thrombi on the mitral or aortic valve in those with Libman-Sacks, "paradoxical embolism" through an atrial-septal defect) (6). Arterial thrombosis can also occur in situ, apparently as successive layers of clot accumulate until the lumen is stenosed or completely occluded (7).…”

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confidence: 99%

D-Dimer Level and the Risk for Thrombosis in Systemic Lupus Erythematosus

Birmingham

Rovin

et al. 2008

Clinical Journal of the American Society of Nephrology

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Background and objectives: Patients who have systemic lupus erythematosus (SLE) and manifest antiphospholipid antibodies (APA) are at increased risk for thrombosis; however, it is difficult to predict who will clot. This study tested the hypothesis that peak D-dimer level measured routinely during follow-up identifies whether a hypercoagulable state is developing and, therefore, the patient is at increased risk for thrombosis.Design, setting, participants, & measurements: One hundred consecutive patients who had SLE with recurrent activity (71% renal SLE) and were evaluated for or enrolled in the Ohio SLE Study were studied. D-dimer testing was done annually and usually at SLE flare or other serious illness. When D-dimer was elevated, evaluation for thrombosis (large vessel, small vessel, or Libman-Sacks) was undertaken. Mean follow-up was 37.5 ؎ 15 SD months.Results: Of those with peak D-dimer <0.5 g/ml (n ‫؍‬ 46), 0% thrombosed, 33% had APA. Of those with peak D-dimer 0.5 to 2.0 g/ml (n ‫؍‬ 19), 6% thrombosed, 44% had APA. Of those with peak D-dimer >2.0 g/ml (n ‫؍‬ 36), 42% thrombosed, 76% had APA. The most common causes of elevated D-dimer in the absence of demonstrable thrombosis were SLE flare and systemic infection. D-dimer levels were usually elevated for several months before thrombosis.Conclusions: Patients with SLE and normal D-dimer levels are at low risk for thrombosis, irrespective of APA status. Those with persistent unexplained elevated D-dimer levels, particularly when >2.0 g/ml, are at high risk for thrombosis.

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“…Because the last paper was published in 2003 [1], two additional systems of involvement were published, entailing increased fractures [3] and stenosis of vessels [4].…”

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confidence: 99%

“…Currently, there are no specific guidelines for the management of APS patients with arterial stenosis. The exact mechanism of arterial stenosis in APS patients remains unclear [4].…”

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confidence: 99%