Kidney disease in antiphospholipid antibody syndrome: Risk factors, pathophysiology and management

Scheen, Marc; Adedjouma, A.; Estève, Emmanuel; Buob, David; Abisror, Noémie; Planche, Vincent; Fain, Olivier; Boffa, J.J.; Seigneux, Sophie de; Mékinian, A.; Haidar, Fadi

doi:10.1016/j.autrev.2022.103072

Cited by 20 publications

(19 citation statements)

References 69 publications

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“…The catastrophic form of APS is a rare, life threatening condition involving multiple organ failure with mortality rate near 50% and it may occur in renal transplant recipients as a severe relapse of APS, as a consequences of surgical procedure, trauma, anticoagulation withdrawal/change, infection, rejection and endothelial damage caused by immuno-suppression [ 6 ]. Treatment of CAPS remains a subject of debate, apart from that triple therapy (methylprednisolone, TPE, IVIG), rituximab or eculizumab may be promising but expensive options [ 18 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

“…Acute form is represented by the presence of thrombotic microangiopathy (TMA) in glomerular capillaries with mesangiolysis and/or TMA in arteries and arterioles manifested by thrombotic lesions, intimal mucoid thickening and medial hyperplasia, while the chronic form of APS nephropathy is characterized by fibrous intimal hyperplasia, focal cortical atrophy and focal segmental glomerulosclerosis. Clinical manifestation of APS nephropathy is non-specific with hypertension (from moderate to malignant hypertension), sub-nephrotic range of proteinuria, hematuria, and acute kidney injury in 20–50%, but nephrotic syndrome is relatively rare [ 5 , 6 , 7 ].…”

Section: Introductionmentioning

confidence: 99%

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Antiphospholipid Syndrome in Renal Allograft Recipients—A Long-Term Multicenter Analysis

Furmańczyk-Zawiska

Bułło‐Piontecka

Komorniczak

et al. 2023

JCM

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Antiphospholipid syndrome (APS) is a devastating autoimmune disease and in renal transplant recipients may result in allograft thrombosis or in extra-renal manifestation, mostly venous thromboembolism. There are many non- and immune risk factors affecting renal allograft in recipients with APS. However, renal allograft outcome in recipients with APS without APS nephropathy remains unknown. Aim: The aim of the study was to assess renal allograft function and survival in recipients with APS. Methods: Retrospective, multicenter study included 19 adult renal recipients with definite APS (primary or lupus-related) from three Polish transplant centers. Renal allograft function was assessed using serum creatinine concentration (SCr1) at 3rd month post-transplant and at the end of the observation (SCr2) and glomerular filtration rate (GFR) was estimated based on modification of diet in renal disease (MDRD) formula. General linear model was used to assess 12 month GFR change over time. Kaplan-Meier curves and restricted mean survival time were used for allograft survival. Matched control group consisted of 21 stable renal recipients without history of thrombosis and without anticoagulation/antiplatelet treatment. Results: The study group differs in induction therapy (p = 0.019), high-urgency procedure (p = 0.04), proteinuria (p = 0.0058), primary disease (lupus) (p < 0.0001), re-transplantation in primary APS (p = 0.0046) and shorter time since engraftment to SCr2 (p = 0.016). Primary APS was more often diagnosed post-transplant (p = 0.0005). Allograft biopsy revealed thrombotic microangiopathy (TMA) with acute rejection (AR) or isolated AR vs AR or chronic rejection in controls but did not reach significance (p = 0.054). Renal allograft function was inferior in the study group but did not reach significance: mean SCr2 (mg/dL) was 2.18 ± 1.41 and 1.5 ± 0.68 in controls, respectively, p = 0.27; mean GFR2 (ml/min/1.73m2) was 39.9 ± 20.83 and 51.23 ± 19.03, respectively, p = 0.102. Renal allograft duration was inferior in patients with APS and was (in years) 11.22 ± 1.44 vs. 14.36 ± 0.42, respectively, p = 0.037, in patients with primary APS (p = 0.021), in patients with APS diagnosed post-transplant (p = 0.012) but not in lupus-related APS (p = ns). Fifteen year renal allograft survival was inferior in APS vs. controls (73,86% vs. 90.48%, respectively, p = 0.049). Conclusions: Recipients with APS are at higher risk for allograft loss due to immune and non-immune causes. Renal allograft survival was inferior in recipients with APS and renal function remains impaired but stable.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antiphospholipid Syndrome in Renal Allograft Recipients—A Long-Term Multicenter Analysis

Furmańczyk-Zawiska

Bułło‐Piontecka

Komorniczak

et al. 2023

JCM

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“…have revealed the importance of inherited and acquired disorders of complement in SLE and TMA ( 36 ). These gene mutations, including complement factor H, complement factor I, complement factor B, thrombomodulin, and MCP/CD46, contribute to occurring TMA ( 37 ).The clinical manifestations and treatment regimens caused by various causes are distinct ( 38 , 39 ). KDIGO guidelines recommend PEX, glucocorticoids, rituximab, or caplacizumab in patients with ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type I motif, member 13) activity < 10% ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

Thrombotic microangiopathy mediates poor prognosis among lupus nephritis via complement lectin and alternative pathway activation

Zhang

Xing

2022

Front. Immunol.

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ObjectiveThe pathogenesis of thrombotic microangiopathy (TMA) in lupus nephritis (LN) remains complicated. This study aimed to detect the deposition of complement lectin pathway (LP) and alternative pathway (AP) components in renal tissues, then evaluate the clinicopathological characteristics and risk factors for renal survival between patients with or without TMA in LN cohorts.MethodsWe included 79 patients with biopsy-proven LN-associated TMA and matched the same number of LN patients without TMA as the control group. The deposition of mannose binding lectin (MBL), MBL-associated serine proteases 1/3 (MASP1/3), complement factor B (CFB), complement factor D (CFD), C4d, and von Willebrand factor (VWF) in renal tissue was assessed by immunohistochemistry and immunofluorescence. Besides, co-localization of C5b-9 and CD34 was detected by confocal microscopy.ResultsIn our retrospective cohort, the incidence of acute kidney injury (30% vs. 14%, p = 0.013), acute hemodialysis (35% vs. 5%, p < 0.001), and interstitial fibrosis (43% vs. 13%, p < 0.001) is higher in the TMA, compared with the control group. Despite aggressive steroids pulse, plasma exchange, and immunosuppressive therapy among TMA group, they still had significantly inferior 3-year renal survival rates (68% vs. 89%, p = 0.002) than those in the non-TMA group. COX regression analysis identified that TMA (HR 4.807, 95% CI [2.052, 11.263], p < 0.001) is a risk factor in LN. MBL, MASP1/3, CFB, CFD, C4d, and VWF deposited along the glomerulus among LN, while TMA had stronger staining intensity and deposition. The co-localized expression of CD34 and C5b-9 in the endothelial cells was also observed in the renal tissues.ConclusionsTMA is an independent risk factor for renal survival in LN patients. Moreover, LP and AP activation are involved in the pathogenesis of LN-associated TMA.

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“…Наиболее тяжелый вариант этого состояния -катастрофический АФС, который характеризуется поражением не только почек, но и других органов с развитием полиорганной недостаточности. Необходимо учитывать, что при АФС встречаются и другие варианты поражения почек, в частности односторонний или двусторонний стеноз или тромбоз почечных артерий, сопровождающийся реноваскулярной артериальной гипертонией и ишемической нефропатией, тромбоз почечных вен, редко гломерулонефрит [27]. Течение ТМА может быть не только острым, но и хроническим.…”

Section: тромботическая микроангиопатияunclassified

“…Течение ТМА может быть не только острым, но и хроническим. В последнем случае при биопсии почки выявляют реканализированные тромбы в артериолах, артериосклероз, гиперплазию интимы почечных артериол и их фибропластическую окклюзию, атрофию канальцев, в то время как характерным гистологическим признаком острой ТМА является наличие микротромбов в почечных артериолах и/или клубочках при отсутствии признаков воспаления и иммунных депозитов при иммунофлюоресцентом исследовании [27].…”

Section: тромботическая микроангиопатияunclassified

Autoimmunity, autoinflammation and kidney

Moiseev¹,

Bulanov²

2022

CPT

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Systemic autoimmune and autoinflammatory disease are associated with all types of diffuse kidney disease, that is, glomerulonephritis (including rapidly progressive), thrombotic microangiopathy, tubulointerstitial nephritis, and AA-amyloidosis. However, the occurrence and types of nephropathies differ significantly in patients with various systemic immunemediated inflammatory diseases. For example, glomerulonephritis is one of the leading manifestation of systemic lupus erythematosus and small-vessels vasculitis, thrombotic angiopathy occurs frequently in patients with both primary and secondary antiphosholipid syndrome, tubulointerstitial nephritis is frequently found in patients with Sjogren syndrome and IgG4-associated disease, whereas AA-amyloidosis can complicate rheumatoid arthritis, ankylosing spondilytis, psoriatic arthritis, familial Meditarranean fever, and certain other monogenic autoinflammatory diseases. Over last decades, renal survival in patients with autoimmune and autoinflammatory diseases improved significantly due to earlier diagnosis and development of effective immunosuppressive and anti-inflammatory treatments. However, a proportion of patients still present with progressive impairment of kidney function that can be unrelated to activity of underlying diseases.

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Kidney disease in antiphospholipid antibody syndrome: Risk factors, pathophysiology and management

Cited by 20 publications

References 69 publications

Antiphospholipid Syndrome in Renal Allograft Recipients—A Long-Term Multicenter Analysis

Antiphospholipid Syndrome in Renal Allograft Recipients—A Long-Term Multicenter Analysis

Thrombotic microangiopathy mediates poor prognosis among lupus nephritis via complement lectin and alternative pathway activation

Autoimmunity, autoinflammation and kidney

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