A 3-year follow-up of a patient with acute renal failure caused by thrombotic microangiopathy related to antiphospholipid syndrome: case report

Xj, Zhou; Chen, M; Sx, Wang; Fd, Zhou; Zhao, Ming‐Hui

doi:10.1177/0961203316682098

Cited by 4 publications

(2 citation statements)

References 16 publications

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“…СКВ -системное аутоиммунное ревматическое заболевание неизвестной этиологии, характеризующееся гиперпродукцией органонеспецифических аутоАТ к различным компонентам клеточного ядра и развитием иммуновоспалительного повреждения внутренних органов [22,23]. ТМА при СКВ рассматривается как редкий патогенетически гетерогенный синдром, связанный как с классическими механизмами, которые характерны для ТМА, -дефицит ADAMTS3 [24,25], патология системы комплемента [13,26], так и аутоиммунными нарушениями -синтез антиядерных аутоАТ и антифосфолипидных антител (аФЛ), ассоциирующихся с развитием АФС [26][27][28][29][30][31][32][33][34]. Напомним, что АФС, характеризующийся развитием рецидивирующих тромбозов сосудов различной локализации и калибра, акушерской патологией (рецидивирующие потери плода), условно подразделяется на «вторичный», ассоциирующийся с СКВ, «первичный», не связанный с каким-либо ведущим заболеванием, и катастрофический (КАФС), который клинически наиболее близок к ТМА [35][36][37][38][39].…”

Section: тромботическая микроангиопатия в ревматологииunclassified

Thrombotic microangiopathy in rheumatology: a link between thrombosis and autoimmunity

Насонов¹,

Reshetnyak²,

Alekberova³

2020

Terapevticheskii arkhiv

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Uncontrolled hypercoagulation and inflammation (thromboinflammation), which are both independent and closely related and amplifying each other pathological processes, form the basis for pathogenesis of a wide range of diseases and complications, including immuno-inflammatory (autoimmune) rheumatic diseases, with the development of potentially fatal injuries of internal organs. Thrombotic microangiopathy is one of the most prominent prototypes of thromboinflammatory pathological conditions. The close link between environmental factors, hemostasis genetic defects and the complement system, inflammation and autoimmunity as pathogenetic mechanisms of microthrombosis draws particular attention to studying thrombotic microangiopathy in immuno-inflammatory rheumatic diseases, primarily systemic lupus erythematosus, antiphospholipid syndrome and scleroderma renal crisis. In future, these studies may be important for expanding the idea of the role of autoimmune mechanisms in pathogenesis of critical hemostasis disorders in human diseases, and for developing new approaches to therapy. Recently, special attention has been paid to the treatment of systemic lupus erythematosus and antiphospholipid syndrome with eculizumab, which is humanized monoclonal IgG2/4k antibody that blocks the complement component C5a and the membrane attack complex (C5b-9) formation, and which is registered for the treatment of atypical hemolytic uremic syndrome, paroxysmal nocturnal hemoglobinuria, as well as severe forms of myasthenia gravis and neuromyelitis optica. Further studies in this direction will create prerequisites for improving the prognosis not only in patients with orphan disorders, but also for widespread human diseases.

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Section: тромботическая микроангиопатия в ревматологииunclassified

Thrombotic microangiopathy in rheumatology: a link between thrombosis and autoimmunity

Насонов¹,

Reshetnyak²,

Alekberova³

2020

Terapevticheskii arkhiv

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“…The use of novel oral anticoagulant medications has not been examined in patients with APS nephropathy. Other treatment approaches may include the use of heparin based on its effect on the classical complement activation pathway inhibition or the use of intravenous immunoglobulin and/or plasma exchange given their efficacy on severe/refractory cases and catastrophic APS ( 56 , 57 ). Targeted therapies may also be considered such as B-cell directed therapies, complement inhibition, tissue factor inhibition, or mTOR pathway inhibition, but large prospective multicenter studies are needed to address their role.…”

Section: Treatment Of Aps Nephropathymentioning

confidence: 99%

Antiphospholipid Syndrome Nephropathy: From Pathogenesis to Treatment

Tektonidou

2018

Front. Immunol.

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Kidney damage is a well-recognized complication of the antiphospholipid syndrome (APS), either primary or systemic lupus erythematosus (SLE)-associated APS. Kidney involvement in APS involves a variety of manifestations, such as renal artery thrombosis or stenosis, renal vein thrombosis, allograft loss due to thrombosis after kidney transplantation, and injury to the renal microvasculature, also known as APS nephropathy. Biopsy in patients with APS nephropathy includes acute thrombotic microangiopathy lesions and chronic intrarenal vascular lesions such as interlobular fibrous intimal hyperplasia, arterial and arteriolar recanalizing thrombosis, fibrous arterial occlusion, and focal cortical atrophy. The most frequent clinical features are hypertension, microscopic hematuria, proteinuria (ranging from mild to nephritic levels), and renal insufficiency. It is uncertain whether antiphospholipid antibodies or other factors are implicated in the development of APS nephropathy, and whether it is driven mainly by thrombotic or by inflammatory processes. Experimental models and clinical studies of thrombotic microangiopathy lesions implicate activation of the complement cascade, tissue factor, and the mTORC pathway. Currently, the management of APS nephropathy relies on expert opinion, and consensus is lacking. There is limited evidence about the effect of anticoagulants, and their use remains controversial. Treatment approaches in patients with APS nephropathy lesions may include the use of heparin based on its role on complement activation pathway inhibition or the use of intravenous immunoglobulin and/or plasma exchange. Targeted therapies may also be considered based on potential APS nephropathy pathogenetic mechanisms such as B-cell directed therapies, complement inhibition, tissue factor inhibition, mTOR pathway inhibition, or anti-interferon antibodies, but prospective multicenter studies are needed to address their role.

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Antibodies Against Complement Components: Relevance for the Antiphospholipid Syndrome—Biomarkers of the Disease and Biopharmaceuticals

Bećarevic

2017

Curr Rheumatol Rep

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Antibodies against complement components described in APS patients, so far, are anti-C1q and anti-factor H Abs, although anti-factor B Abs and anti-C5a Abs were described in animal models of APS. Clinical studies in APS patients are limited to a small number of case reports. Studies that would confirm potential role of Abs against complement components (as potential biomarkers of APS) are lacking. Lack of randomized clinical trials (that would provide complete data for confirmation of beneficial effects of biopharmaceuticals in complement inhibition) in APS is alarming.

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A 3-year follow-up of a patient with acute renal failure caused by thrombotic microangiopathy related to antiphospholipid syndrome: case report

Cited by 4 publications

References 16 publications

Thrombotic microangiopathy in rheumatology: a link between thrombosis and autoimmunity

Thrombotic microangiopathy in rheumatology: a link between thrombosis and autoimmunity

Antiphospholipid Syndrome Nephropathy: From Pathogenesis to Treatment

Antibodies Against Complement Components: Relevance for the Antiphospholipid Syndrome—Biomarkers of the Disease and Biopharmaceuticals

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