Modulation of urinary CR1 in systemic lupus erythematosus

Lupus. 2004;13(4):228-33. doi: 10.1191/0961203303lu1001oa.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Complement C3 / metabolism
  • Erythrocytes / metabolism
  • Fluorescent Antibody Technique
  • Humans
  • Immunoglobulins / metabolism
  • Kidney Function Tests
  • Kidney Glomerulus / metabolism
  • Lupus Erythematosus, Systemic / blood
  • Lupus Erythematosus, Systemic / urine*
  • Nephrosis, Lipoid / blood
  • Nephrosis, Lipoid / urine
  • Receptors, Complement 3b / analysis*
  • Receptors, Complement 3b / blood
  • Urine / chemistry

Substances

  • Complement C3
  • Immunoglobulins
  • Receptors, Complement 3b