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Abstract: FR-PO0851

Identification of Apolipoprotein C-III (ApoC3) as a Novel Serum Biomarker in Patients with Lupus Nephritis

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Scott, Liam Patrick Connor, University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Shoctor, Nicholas A., University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Cummins, Timothy, University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Samuelson, David J., University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Nagane, Siyona S., University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Rane, Madhavi J., University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Powell, David W., University of Louisville School of Medicine, Louisville, Kentucky, United States
  • Caster, Dawn J., University of Louisville School of Medicine, Louisville, Kentucky, United States
Background

Lupus nephritis (LN) remains a challenging problem for physicians and patients. Diagnosis and treatment decisions are based on the results of kidney biopsies that are limited by sampling error and the inability to repeat at frequent intervals and proteinuria is a less reliable predictor of disease activity and response to therapy. Treatment continues to rely on toxic, non-specific immunosuppressive medications with a response rate of 50% or less and high rates of side effect. Thus, there is a critical need for new approaches to diagnosis, disease monitoring, and therapy based on an understanding of cellular events responsible for the heterogeneous LN clinical course and response to therapy. Our recent proteomic findings showed that ApoC3 levels were higher in inflammatory serum from LN patients with active disease versus in remission. Elevated ApoC3 levels are shown to trigger release of pro-inflammatory cytokines causing vascular damage in diabetic nephropathy. Thus, the aim of this study was to test a hypothesis that ApoC3 is a serum marker of activity in LN patients.

Methods

Serum ApoC3 was measured by ELISA from 13 paired proliferative LN patients during active LN and remission (UPCR > or < 500 mg/g, respectively), as well as 10 healthy controls. Correlation analyses were performed between serum ApoC3 and clinical parameters (UPCR, dsDNA antibody titer, eGFR, C3, C4, and serum creatinine).

Results

Serum ApoC3 was significantly higher (p=0.0266) in LN patients during active disease compared to remission. Serum ApoC3 was positively correlated with UPCR (p=0.0164, r2= 0.3468).

Conclusion

Our findings suggest that enhanced serum ApoC3 concentration is an indicator of kidney inflammation and injury in proliferative LN patients and useful in monitoring response to treatment. Future studies will investigate association of ApoC3 levels with serum lipid profiles, potential cardiovascular risk, and activation of immune cells in proliferative LN.

Funding

  • NIDDK Support