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Article: Clinico-pathological associations of serum VCAM-1 and ICAM-1 levels in patients with lupus nephritis

TitleClinico-pathological associations of serum VCAM-1 and ICAM-1 levels in patients with lupus nephritis
Authors
KeywordsLupus nephritis
Vascular cell adhesion molecule-1
Intercellular adhesion molecule-1
Issue Date2021
PublisherSage Publications Ltd. The Journal's web site is located at http://lup.sagepub.com
Citation
Lupus, 2021, v. 30 n. 7, p. 1039-1050 How to Cite?
AbstractWe investigated the clinico-pathological associations of serum VCAM-1 and ICAM-1 levels in patients with biopsy-proven Class III/IV±V lupus nephritis (LN). Methods: Serum VCAM-1 and ICAM-1 levels were determined by ELISAs. Sera from patients with non-renal SLE or non-lupus chronic kidney disease (CKD), and healthy subjects served as controls. Results: Seropositivity rate for VCAM-1 and ICAM-1 was 93.10% and 37.93% respectively at the time of nephritic flare, and 44.83% and 13.79% respectively at remission, with both showing higher levels during flare (P < 0.05, for both). VCAM-1 level correlated with proteinuria, serum creatinine, and anti-dsDNA antibodies, and inversely correlated with C3. VCAM-1 level also correlated with leukocyte infiltration and fibrinoid necrosis/karyorrhexis scores in active LN kidney biopsies. ICAM-1 level correlated with proteinuria, but not anti-dsDNA or C3, nor histopathological features. VCAM-1 level increased 4.5 months before renal flare, while ICAM-1 increase coincided with flare, and both decreased after treatment. ROC analysis showed that VCAM-1 distinguished active LN from healthy subjects, LN in remission, active non-renal lupus, and CKD (ROC AUC of 0.98, 0.86, 0.93 and 0.90 respectively). VCAM-1 level in combination with either proteinuria or C3 was superior in distinguishing active LN from remission compared to the measurement of individual markers. Serum ICAM-1 level distinguished active LN from healthy subjects and LN patients in remission (ROC AUC of 0.75 and 0.66 respectively), but did not distinguish between renal versus non-renal lupus. ICAM-1 level in combination with markers of endothelial cell activation (syndecan-1, hyaluronan and thrombomodulin) was superior to proteinuria, anti-dsDNA, or C3 in distinguishing active LN from quiescent disease. Conclusion: Our findings suggest potential utility of serum VCAM-1 and ICAM-1 in clinical management. Monitoring VCAM-1 may facilitate early diagnosis of flare. Combining selected biomarkers may be advantageous in diagnosing active LN. VCAM-1 may have a pathogenic role in renal parenchymal inflammation in active LN. © The Author(s) 2021.
Persistent Identifierhttp://hdl.handle.net/10722/300949
ISSN
2023 Impact Factor: 1.9
2023 SCImago Journal Rankings: 0.812
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYu, KYC-
dc.contributor.authorYung, SY-
dc.contributor.authorChau, MKM-
dc.contributor.authorTang, CSO-
dc.contributor.authorYap, DYH-
dc.contributor.authorTang, AHN-
dc.contributor.authorYing, SKY-
dc.contributor.authorLee, CK-
dc.contributor.authorChan, TM-
dc.date.accessioned2021-07-06T03:12:28Z-
dc.date.available2021-07-06T03:12:28Z-
dc.date.issued2021-
dc.identifier.citationLupus, 2021, v. 30 n. 7, p. 1039-1050-
dc.identifier.issn0961-2033-
dc.identifier.urihttp://hdl.handle.net/10722/300949-
dc.description.abstractWe investigated the clinico-pathological associations of serum VCAM-1 and ICAM-1 levels in patients with biopsy-proven Class III/IV±V lupus nephritis (LN). Methods: Serum VCAM-1 and ICAM-1 levels were determined by ELISAs. Sera from patients with non-renal SLE or non-lupus chronic kidney disease (CKD), and healthy subjects served as controls. Results: Seropositivity rate for VCAM-1 and ICAM-1 was 93.10% and 37.93% respectively at the time of nephritic flare, and 44.83% and 13.79% respectively at remission, with both showing higher levels during flare (P < 0.05, for both). VCAM-1 level correlated with proteinuria, serum creatinine, and anti-dsDNA antibodies, and inversely correlated with C3. VCAM-1 level also correlated with leukocyte infiltration and fibrinoid necrosis/karyorrhexis scores in active LN kidney biopsies. ICAM-1 level correlated with proteinuria, but not anti-dsDNA or C3, nor histopathological features. VCAM-1 level increased 4.5 months before renal flare, while ICAM-1 increase coincided with flare, and both decreased after treatment. ROC analysis showed that VCAM-1 distinguished active LN from healthy subjects, LN in remission, active non-renal lupus, and CKD (ROC AUC of 0.98, 0.86, 0.93 and 0.90 respectively). VCAM-1 level in combination with either proteinuria or C3 was superior in distinguishing active LN from remission compared to the measurement of individual markers. Serum ICAM-1 level distinguished active LN from healthy subjects and LN patients in remission (ROC AUC of 0.75 and 0.66 respectively), but did not distinguish between renal versus non-renal lupus. ICAM-1 level in combination with markers of endothelial cell activation (syndecan-1, hyaluronan and thrombomodulin) was superior to proteinuria, anti-dsDNA, or C3 in distinguishing active LN from quiescent disease. Conclusion: Our findings suggest potential utility of serum VCAM-1 and ICAM-1 in clinical management. Monitoring VCAM-1 may facilitate early diagnosis of flare. Combining selected biomarkers may be advantageous in diagnosing active LN. VCAM-1 may have a pathogenic role in renal parenchymal inflammation in active LN. © The Author(s) 2021.-
dc.languageeng-
dc.publisherSage Publications Ltd. The Journal's web site is located at http://lup.sagepub.com-
dc.relation.ispartofLupus-
dc.rightsAuthor(s), Contribution Title, Journal Title (Journal Volume Number and Issue Number) pp. xx-xx. Copyright © [year] (Copyright Holder). DOI: [DOI number].-
dc.subjectLupus nephritis-
dc.subjectVascular cell adhesion molecule-1-
dc.subjectIntercellular adhesion molecule-1-
dc.titleClinico-pathological associations of serum VCAM-1 and ICAM-1 levels in patients with lupus nephritis-
dc.typeArticle-
dc.identifier.emailYung, SY: ssyyung@hku.hk-
dc.identifier.emailTang, CSO: csotang@hkucc.hku.hk-
dc.identifier.emailYap, DYH: desmondy@hku.hk-
dc.identifier.emailTang, AHN: alextang@pathology.hku.hk-
dc.identifier.emailChan, TM: dtmchan@hku.hk-
dc.identifier.authorityYung, SY=rp00455-
dc.identifier.authorityYap, DYH=rp01607-
dc.identifier.authorityTang, AHN=rp02468-
dc.identifier.authorityChan, TM=rp00394-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1177/09612033211004727-
dc.identifier.pmid33765901-
dc.identifier.scopuseid_2-s2.0-85103183840-
dc.identifier.hkuros323298-
dc.identifier.volume30-
dc.identifier.issue7-
dc.identifier.spage1039-
dc.identifier.epage1050-
dc.identifier.isiWOS:000637121300001-
dc.publisher.placeUnited Kingdom-

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