Urinary activated leukocyte cell adhesion molecule as a novel biomarker of lupus nephritis histology.

ALCAM Activity index Chronicity index Lupus nephritis Renal histopathology Urinary biomarker

Journal

Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438

Informations de publication

Date de publication:
27 05 2020
Historique:
received: 10 03 2020
accepted: 01 05 2020
entrez: 29 5 2020
pubmed: 29 5 2020
medline: 22 6 2021
Statut: epublish

Résumé

Lupus nephritis (LN) is one of the most severe complications of SLE patients. We aim to validate urinary ALCAM as a biomarker in predicting renal disease histpathology in a Chinese lupus cohort. In this cross-sectional study, a total of 256 patients and controls were recruited. Urinary levels of ALCAM were determined by ELISA. Renal histopathology was reviewed by an experienced renal pathologist. Urinary ALCAM levels were significantly increased in active LN patients when compared to active SLE patients without renal involvement (p < 0.001), inactive LN patients (p = 0.023), inactive SLE patients without renal involvement (p < 0.001), and healthy controls (p < 0.001). Correlation analysis revealed a positive correlation between urinary ALCAM and general disease activity-SLEDAI score (r = 0.487, p < 0.001), as well as renal disease activity-rSLEDAI (r = 0.552, p < 0.001) and SLICC RAS (r = 0.584, p < 0.001). Urinary ALCAM also correlated with lab parameters including 24-h urine protein, hemoglobin, and complement 3. Moreover, urinary ALCAM levels were significantly increased in class III and IV (proliferative) LN as compared to those in class V (membranous) LN. It outperformed conventional biomarkers (anti-dsDNA antibody, C3, C4, proteinuria) in discriminating the two groups of LN. On renal histopathology, urinary ALCAM levels correlated positively with activity index (r = 0.405, p < 0.001) but not chronicity index (r = 0.079, p = 0.448). Urinary ALCAM is a potential biomarker for predicting renal pathology activity in LN and may serve as a valuable surrogate marker of renal histopathology.

Sections du résumé

BACKGROUND
Lupus nephritis (LN) is one of the most severe complications of SLE patients. We aim to validate urinary ALCAM as a biomarker in predicting renal disease histpathology in a Chinese lupus cohort.
METHODS
In this cross-sectional study, a total of 256 patients and controls were recruited. Urinary levels of ALCAM were determined by ELISA. Renal histopathology was reviewed by an experienced renal pathologist.
RESULTS
Urinary ALCAM levels were significantly increased in active LN patients when compared to active SLE patients without renal involvement (p < 0.001), inactive LN patients (p = 0.023), inactive SLE patients without renal involvement (p < 0.001), and healthy controls (p < 0.001). Correlation analysis revealed a positive correlation between urinary ALCAM and general disease activity-SLEDAI score (r = 0.487, p < 0.001), as well as renal disease activity-rSLEDAI (r = 0.552, p < 0.001) and SLICC RAS (r = 0.584, p < 0.001). Urinary ALCAM also correlated with lab parameters including 24-h urine protein, hemoglobin, and complement 3. Moreover, urinary ALCAM levels were significantly increased in class III and IV (proliferative) LN as compared to those in class V (membranous) LN. It outperformed conventional biomarkers (anti-dsDNA antibody, C3, C4, proteinuria) in discriminating the two groups of LN. On renal histopathology, urinary ALCAM levels correlated positively with activity index (r = 0.405, p < 0.001) but not chronicity index (r = 0.079, p = 0.448).
CONCLUSION
Urinary ALCAM is a potential biomarker for predicting renal pathology activity in LN and may serve as a valuable surrogate marker of renal histopathology.

Identifiants

pubmed: 32460901
doi: 10.1186/s13075-020-02209-9
pii: 10.1186/s13075-020-02209-9
pmc: PMC7251704
doi:

Substances chimiques

Activated-Leukocyte Cell Adhesion Molecule 0
Biomarkers 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

122

Subventions

Organisme : NIAMS NIH HHS
ID : R01 AR074096
Pays : United States

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Auteurs

Huihua Ding (H)

Department of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shandong (M) Rd, Shanghai, 200001, China.

Cheng Lin (C)

Department of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shandong (M) Rd, Shanghai, 200001, China.

Jingyi Cai (J)

Department of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shandong (M) Rd, Shanghai, 200001, China.

Qiang Guo (Q)

Department of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shandong (M) Rd, Shanghai, 200001, China.

Min Dai (M)

Department of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shandong (M) Rd, Shanghai, 200001, China.

Chandra Mohan (C)

Department of Biomedical Engineering, University of Houston, 3517 Cullen Blvd, Room 2027, Houston, TX, 77204-5060, USA. cmohan@central.uh.edu.

Nan Shen (N)

Department of Rheumatology, Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, 145 Shandong (M) Rd, Shanghai, 200001, China. nanshensibs@gmail.com.
China-Australia Centre for Personalized Immunology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. nanshensibs@gmail.com.
State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, 200032, China. nanshensibs@gmail.com.
Shenzhen Futian Hospital for Rheumatic Diseases, Shenzhen, 518040, China. nanshensibs@gmail.com.
Center for Autoimmune Genomics and Etiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. nanshensibs@gmail.com.
Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH, USA. nanshensibs@gmail.com.

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