ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2020 and some content may be unavailable. To unlock all content for 2020, please visit the archives.

Abstract: PO1769

Clinico-Pathological Associations with Serum Thrombomodulin Level in Patients with Lupus Nephritis

Session Information

Category: Glomerular Diseases

  • 1202 Glomerular Diseases: Immunology and Inflammation

Authors

  • Chan, Tak Mao Daniel, The University of Hong Kong, Hong Kong, Hong Kong
  • Yu, Kelvin Y. C., The University of Hong Kong, Hong Kong, Hong Kong
  • Yap, Desmond Yat Hin, The University of Hong Kong, Hong Kong, Hong Kong
  • Yung, Susan, The University of Hong Kong, Hong Kong, Hong Kong
Background

Conventional serological markers do not always correlate with clinical activity or histolopathology in lupus nephritis (LN). There is evidence of endothelial activation and injury in LN pathogenesis. Thrombomodulin (TM), a component of endothelial glycocalyx, is shed into the circulation in endothelial cell injury. We investigated clinico-pathological associations of circulating TM level.

Methods

TM level was measured by ELISA in sera collected serially every 3-4 months over >2 years (n=482) from 31 patients with biopsy-proven Class III/IV LN. Patients with non-renal SLE or non-lupus kidney diseases (CKD) and healthy subjects were included as Controls.

Results

Patients with active LN had the highest serum TM level, compared with LN patients in remission, patients with active non-renal SLE, CKD patients, or healthy subjects (P<0.01, for all). Serum TM level correlated with anti-dsDNA antibody titre, proteinuria, serum creatinine, SLEDAI-2K and renal SLEDAI-2K score; and inversely correlated with eGFR and C3 (P<0.05, for all). 8 patients had blood samples collected before disease flare, and 6 showed increased TM level (3.65±2.16 months before clinical flare). All episodes of LN flare were accompanied by elevated TM level, which decreased after treatment. A temporal relationship was noted between TM level and anti-dsDNA titre and C3 levels, proteinuria, SLEDAI-2K and renal SLEDAI-2K scores. TM level also correlated with renal interstitial inflammation score (r=0.54, P=0.0081). ROC analysis showed that serum TM level distinguished active LN from healthy subjects (sensitivity 100.00%, specificity 100.00%), from LN in remission (sensitivity 89.66%, specificity 68.97%), from active non-renal SLE (sensitivity 90.91%, specificity 100.00%), and from CKD (sensitivity 89.66%, specificity 56.52%) (P<0.001, for all).

Conclusion

Determination of serum TM level may facilitate early diagnosis of active LN, and may be useful in monitoring the response to treatment.

Funding

  • Government Support - Non-U.S.