Abstract: PO1433
The Significance of Glomerular Galactose-Deficient IgA1 in Patients with Systemic Lupus Erythematosus (SLE)
Session Information
- Glomerular Diseases: Immunology and Inflammation in Vasculitis and Lupus Nephritis
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1202 Glomerular Diseases: Immunology and Inflammation
Authors
- Bu, Lihong, University of Minnesota Medical School Twin Cities, Minneapolis, Minnesota, United States
- Garay, Bayardo I., University of Minnesota Medical School Twin Cities, Minneapolis, Minnesota, United States
- Kim, Youngki, University of Minnesota Medical School Twin Cities, Minneapolis, Minnesota, United States
- Lai, Fm, The Chinese University of Hong Kong Faculty of Medicine, Hong Kong, China
- Zhou, Xin J., Pathologists Bio-Medical Laboratories, Dallas, Texas, United States
- Nachman, Patrick H., University of Minnesota Medical School Twin Cities, Minneapolis, Minnesota, United States
- Nast, Cynthia C., Cedars-Sinai Medical Center, Los Angeles, California, United States
Background
Approximately 0.3% of end stage kidney disease in SLE patients is due to non-lupus nephritis. IgA nephropathy (IgAN) is rarely reported in SLE patients. As galactose-deficient IgA1 (Gd-IgA1) plays a key role in the pathogenesis of IgAN but not SLE, the aim was to investigate whether KM55, a Gd-IgA1 specific monoclonal antibody, might identify IgAN in patients with SLE.
Methods
Immunofluorescence (IF) staining of KM55 was performed on 77 native kidney biopsies from 25 non-SLE (IgAN or IgA vasculitis (IgAV)) and 52 SLE patients, the latter including lupus nephritis (LN) with IgG dominant full house staining (LN; n=20), IgAN without features of LN (IgAN; n=11), concurrent LN class V and IgAN (n=2), and LN with dominant/co-dominant IgA (IgG-IgA-LN; n=19). In SLE patients, principal component analysis was carried out on LN, IgAN, and IgG-IgA-LN cases.
Results
KM55 staining intensity >0.5 (trace) on a scale of 0-4 discriminates IgAN/IgAV from LN with a sensitivity of 1.00 [0.86-1.00] and specificity of 1.00 [0.82-1.00] (p<0.0001) (Fig 1). KM55 staining with mean 2+ intensity was detected in all SLE patients with lgAN and no features of LN. IgAN had no difference in KM55 intensity or distribution in non-SLE vs SLE patients. Mesangial KM55 staining was detected in cases with dual LN class V and IgAN. Of 19 IgG-IgA-LN biopsies, 9 (47%) showed positive KM55 staining in the same distribution as IgA.
Conclusion
Our results demonstrate that IF staining of KM55 is valuable in distinguishing IgAN from LN. In SLE patients, negative KM55 staining argues against the presence of IgAN while >0.5 (trace) KM55 staining with dominant/co-dominant IgA staining is suggestive of IgAN as the sole lesion or a co-occurring component of dual glomerulonephritis.
A) KM55 staining intensity in LN and IgAN/IgAV. B) Principal component analysis shows LN with dominant/co-dominant IgA (IgG-IgA-LN; pink) with overlapping features with LN (grey) and/or IgAN (blue).
Funding
- Other NIH Support