Rapid detection of urinary soluble intercellular adhesion molecule-1 for determination of lupus nephritis activity

Wang, Yanyun; Ye, Tao; Liu, Yi; Zhao, Yi; Song, Chao; Zhou, Bin; Gao, Linbo; Zhang, Lin; Hu, Huaizhong

doi:10.1097/md.0000000000011287

Cited by 15 publications

(13 citation statements)

References 23 publications

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“…There are no studies to date that explore NCAM1 in membranous lupus nephritis. However, increased NCAM1 within urine has been shown in a subset of lupus patients with proliferative lupus nephritis with correlation to disease activity 18 . When lupus sera were reacted against human renal glomerular endothelial cells, NCAM1 expression was significantly reduced.…”

Section: Discussionmentioning

confidence: 99%

Neural cell adhesion molecule 1 is a novel autoantigen in membranous lupus nephritis

Caza

Hassen

Kuperman

et al. 2021

Kidney International

104

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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Section: Discussionmentioning

confidence: 99%

Neural cell adhesion molecule 1 is a novel autoantigen in membranous lupus nephritis

Caza

Hassen

Kuperman

et al. 2021

Kidney International

104

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“…In adults, NCAM1 expression is seen at high levels within the central nervous system, peripheral nerves, thyroid and adrenal gland, heart, stomach, and cells within the immune system including natural killer cells, γΔ T cells, activated CD8+ T cells, and dendritic cells. Interestingly, it could not be detected in podocytes in “normal” kidney biopsiesor biopsies from non-NCAM-1 MN while it was found in urinary exosomes [ 48 ] and its level in the urine was correlated with disease activity in a subset of lupus patients with proliferative lupus nephritis [ 49 ]. This raises the possibility that a soluble form of NCAM-1 might be involved in the pathogenesis of the disease.…”

Section: New Pathophysiological Advances: the Third Antigenic Revomentioning

confidence: 99%

Advances in Membranous Nephropathy

Ronco

Plaisier

Dębiec

2021

JCM

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Membranous nephropathy (MN) is a rare auto-immune disease where the glomerulus is targeted by circulating auto-antibodies mostly against podocyte antigens, which results in the formation of electron-dense immune complexes, activation of complement and massive proteinuria. MN is the most common cause of nephrotic syndrome in adults leading to severe thrombotic complications and kidney failure. This review is focused on the recent therapeutic and pathophysiological advances that occurred in the last two years. For a long time, we were lacking a head-to-head comparison between cyclophosphamide considered as the gold standard therapy and other medications, notably rituximab. Substantial progress has been achieved owing to three randomized controlled trials. MENTOR (Membranous Nephropathy Trial of Rituximab) and STARMEN (Sequential Therapy with Tacrolimus and Rituximab in Primary Membranous Nephropathy) conclusively established that calcineurin inhibitor-based regimens are slower to result in an immunologic response than rituximab or cyclophosphamide, achieve fewer complete clinical remissions, and are less likely to maintainremission. Rituximab Versus Steroids and Cyclophosphamide in the Treatment of Idiopathic Membranous Nephropathy (RI-CYCLO) suggested that competition between cyclophosphamide and rituximab remains open. Given the technological leapcombining laser microdissection of glomeruli and mass spectrometry of solubilized digested proteins, four “new antigens” were discovered including NELL-1 and Semaphorin 3B in so-called primary MN, and exostosins 1 and 2 and NCAM 1 in lupus MN. NELL-1 is associated with about 8% of primary MN and is characterized by segmental immune deposits and frequent association with cancer (30%). Semaphorin 3B-associated MN usually occurs in children, often below the age of two years, where it is the main antigen, representing about 16% of non-lupus MN in childhood. Exostosins 1/2 and NCAM 1 are associated with 30% and 6% of lupus MN, respectively. Exostosins 1/2 (EXT1/2) staining is associated with a low rate of end-stage kidney disease (ESKD) even in mixed classes III/IV+V. These findings already lead to revisiting the diagnostic and therapeutic algorithms toward more personalized medicine.

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“…Adiponectin levels and the adiponectin-to-creatinine ratio are significantly higher in the urine of SLE patients with renal involvement (renal involvement n = 25, no renal involvement n = 25) [ 75 ] and in active LN SLE ( n = 33) compared to active non-LN SLE ( n = 16), or patients with only LN history ( n = 30) [ 76 ]. Similarly, adiponectin urine concentrations are significantly elevated in active LN ( n = 125) compared to inactive LN ( n = 31), SLE without LN ( n = 36), or HC ( n = 55) [ 77 ]. The adiponectin-to-creatinine ratio in patients with LN ( n = 27) was also increased compared to normal controls ( n = 8) [ 66 ].…”

Section: Adiponectin In Systemic Autoimmune Rheumatic Diseasesmentioning

confidence: 99%

Adiponectin Deregulation in Systemic Autoimmune Rheumatic Diseases

Brezovec

Perdan-Pirkmajer

Čučnik

et al. 2021

IJMS

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Deregulation of adiponectin is found in systemic autoimmune rheumatic diseases (SARDs). Its expression is downregulated by various inflammatory mediators, but paradoxically, elevated serum levels are present in SARDs with high inflammatory components, such as rheumatoid arthritis and systemic lupus erythematosus. Circulating adiponectin is positively associated with radiographic progression in rheumatoid arthritis as well as with cardiovascular risks and lupus nephritis in systemic lupus erythematosus. However, in SARDs with less prominent inflammation, such as systemic sclerosis, adiponectin levels are low and correlate negatively with disease activity. Regulators of adiponectin gene expression (PPAR-γ, Id3, ATF3, and SIRT1) and inflammatory cytokines (interleukin 6 and tumor necrosis factor α) are differentially expressed in SARDs and could therefore influence total adiponectin levels. In addition, anti-inflammatory therapy could also have an impact, as tocilizumab treatment is associated with increased serum adiponectin. However, anti-tumor necrosis factor α treatment does not seem to affect its levels. Our review provides an overview of studies on adiponectin levels in the bloodstream and other biological samples from SARD patients and presents some possible explanations why adiponectin is deregulated in the context of therapy and gene regulation.

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Rapid detection of urinary soluble intercellular adhesion molecule-1 for determination of lupus nephritis activity

Abstract: Supplemental Digital Content is available in the text

Cited by 15 publications

References 23 publications

Neural cell adhesion molecule 1 is a novel autoantigen in membranous lupus nephritis

Neural cell adhesion molecule 1 is a novel autoantigen in membranous lupus nephritis

Advances in Membranous Nephropathy

Adiponectin Deregulation in Systemic Autoimmune Rheumatic Diseases

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