Renal microvascular lesions in lupus nephritis

Ding, Ying; Tan, Ying; Qu, Zhen; Feng, Yu

doi:10.1080/0886022x.2019.1702057

Cited by 37 publications

(41 citation statements)

References 70 publications

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“…Five pathological types of renal microvascular lesions have been described in patients with lupus nephritis ( Table 1 ) [ 70 ]. So far, the attention has been mainly focused on glomerular pathology, and renal vascular lesions have been overlooked.…”

Section: Renal Vasculitismentioning

confidence: 99%

Lupus Vasculitis: An Overview

et al. 2021

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Lupus vasculitis (LV) is one of the secondary vasculitides occurring in the setting of systemic lupus erythematosus (SLE) in approximately 50% of patients. It is most commonly associated with small vessels, but medium-sized vessels can also be affected, whereas large vessel involvement is very rare. LV may involve different organ systems and present in a wide variety of clinical manifestations according to the size and site of the vessels involved. LV usually portends a poor prognosis, and a prompt diagnosis is fundamental for a good outcome. The spectrum of involvement ranges from a relatively mild disease affecting small vessels or a single organ to a multiorgan system disease with life-threatening manifestations, such as mesenteric vasculitis, pulmonary hemorrhage, or mononeuritis multiplex. Treatment depends upon the organs involved and the severity of the vasculitis process. In this review, we provide an overview of the different forms of LV, describing their clinical impact and focusing on the available treatment strategies.

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Section: Renal Vasculitismentioning

confidence: 99%

Lupus Vasculitis: An Overview

et al. 2021

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“…Renal microvascular lesions are common in LN and are increasingly being recognized as a marker of LN. Five pathological types of LN renal microvascular lesions have been proposed and they are vascular immune complex deposits (ICD), arteriosclerosis (AS), thrombotic microangiopathy (TMA), non-inflammatory necrotizing vasculopathy (NNV), and true renal vasculitis (TRV) (69). Up to one-third of LN patients have two or more vascular lesions at the same time.…”

Section: Renal Microvascular Lesionsmentioning

confidence: 99%

“…Damaged TECs induce loss of pericytes leading to thinning of capillaries (50,57,58,(62)(63)(64). The activation and dysfunction of vascular ECs, as well as immune system dysfunction, are key mechanisms of LN renal microvascular lesions, especially IC-induced vascular inflammation and antiphospholipid antibody (APL)-related thrombotic events (69). The binding of autoantibodies to vascular ECs and the deposition of CICs on the microvessels lead to changes in the connections between ECs, thus activating complement, increasing the expression of adhesion molecules, inflammatory cytokines and chemokines, and increasing the permeability of ECs.…”

Section: Renal Microvascular Lesionsmentioning

confidence: 99%

IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis

Ding

Ren

2021

Front. Immunol.

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Lupus nephritis (LN) is a common complication of systemic lupus erythematosus (SLE) and a major risk factor for morbidity and mortality. The abundant cell-free nucleic (DNA/RNA) in SLE patients, especially dsDNA, is a key substance in the pathogenesis of SLE and LN. The deposition of DNA/RNA-immune complexes (DNA/RNA-ICs) in the glomerulus causes a series of inflammatory reactions that lead to resident renal cell disturbance and eventually renal fibrosis. Cell-free DNA/RNA is the most effective inducer of type I interferons (IFN-I). Resident renal cells (rather than infiltrating immune cells) are the main source of IFN-I in the kidney. IFN-I in turn damages resident renal cells. Not only are resident renal cells victims, but also participants in this immunity war. However, the mechanism for generation of IFN-I in resident renal cells and the pathological mechanism of IFN-I promoting renal fibrosis have not been fully elucidated. This paper reviews the latest epidemiology of LN and its development process, discusses the mechanism for generation of IFN-I in resident renal cells and the role of IFN-I in the pathogenesis of LN, and may open a new perspective for the treatment of LN.

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“…Охарактеризован субтип ТМА при СКВ и АФС, связанный с аутоантитело-опосредованной активацией системы комплемента [40][41][42][43][44] [45], при котором развитие ТМА ассоциируется с неблагоприятным прогнозом и риском развития обострений на фоне терапии [46]. Наряду с ВН активация комплемента играет фундаментальную роль в развитии АФС и особенно КАФС [15,45,46].…”

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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Renal microvascular lesions in lupus nephritis

Cited by 37 publications

References 70 publications

Lupus Vasculitis: An Overview

Lupus Vasculitis: An Overview

IFN-I Mediates Lupus Nephritis From the Beginning to Renal Fibrosis

Thrombotic microangiopathy in rheumatology: a link between thrombosis and autoimmunity

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