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Modulation of urinary CR1 in systemic lupus erythematosus
B Sivasankar1, A K Dinda, S C Tiwari
1Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India.
Insights
Urinary CR1 (uCR1) levels significantly decline in lupus patients, reflecting reduced glomerular CR1 (GCR1). This suggests uCR1 may serve as a novel biomarker for lupus kidney disease.
Area of Science:
- Nephrology
- Immunology
- Biochemistry
Background:
- Decreased erythrocyte complement receptor 1 (ECR1) is a known feature of systemic lupus erythematosus (SLE).
- Proteolytic shedding is the suspected cause of reduced ECR1 in SLE.
- Glomerular CR1 (GCR1) also declines in SLE patients.
Purpose of the Study:
- To investigate the relationship between urinary CR1 (uCR1), ECR1, and GCR1 in SLE.
- To determine the correlation of these markers with SLE disease activity.
- To evaluate uCR1 as a potential biomarker for lupus nephritis.
Main Methods:
- Quantification of uCR1, ECR1, and GCR1 levels in SLE patients, minimal change disease (MCD) patients, and healthy controls.
- Immunofluorescence staining for GCR1.
- Bivariate scatter analysis to assess correlations.
Main Results:
- SLE patients exhibited significantly lower levels of both uCR1 and GCR1 compared to controls.
- MCD patients did not show a decline in uCR1; levels were comparable to or higher than controls.
- A strong positive correlation was found between uCR1 and GCR1 levels.
- No significant correlation was observed between ECR1, uCR1, and kidney function tests.
Conclusions:
- Urinary CR1 (uCR1) levels accurately reflect glomerular CR1 (GCR1) expression.
- The drastic decline in GCR1 in SLE patients is mirrored by decreased uCR1.
- uCR1 shows promise as a non-invasive biomarker for detecting glomerular involvement in SLE.
Abstract:
The decline in the levels of erythrocyte complement receptor 1 (ECR1) in systemic lupus erythematosus (SLE) has been widely reported. The most probable cause for this decline is excessive proteolytic shedding of CR1 from the cell surface. Similarly a decline in glomerular CR1 (GCR1) has also been reported in SLE. Because CR1 is excreted in urine it is imperative to study the relationship of urinary CR1 (uCR1) with ECR1 and GCR1, and their overall correlation with disease activity. We have determined the levels of uCR1, ECR1 and GCR1 in SLE patients and compared them with normal controls and minimal change disease (MCD) patients. We found a significant decline in both uCR1 and GCR1 in SLE but not in MCD; levels of uCR1 in MCD were either comparable to those of controls or higher. Immunofluorescence for GCR1 was very high in MCD. We did not find any correlation between ECR1, uCR1 and kidney function tests on divariate scatter analyses. The correlation coefficient for uCR1 and GCR1 was highly significant and positive. Our findings thus suggest that uCR1 reflects the levels of GCR1 expression, which decline drastically in SLE. Therefore we envisage uCR1 as a potential marker for glomerular involvement in SLE.