Modulation of CR1 expression in glomerulonephritis.
Das, Nibhiritis; Sivasankar, B.; Tiwari, SC; Dinda, AK and Srivastava, LM (2002) Modulation of CR1 expression in glomerulonephritis. International Journal of Immunopharmacology (2). 1386.
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The investigation aimed at studying the modulation of erythrocyte, glomerular, soluble and urinary complement Receptor 1 (ECR1, GCR1, SCR1 and UCR1) in normal controls and patients with glomerulonephritis to understand the overall dynamics of this important protein in health and disease. A total of 35 healthy controls and 53 patients with glomerulonephritis (FSGS n=20, MCD=16, SLE n=17) were included in the study. Levels of ECR1, GCR1, SCR1 and UCR1 were estimated. Cell surface expression was determined by flow cytometry as mean fluorescence value, expression of GCR1 was visualized by histopathology of kidney biopsies, levels of UCR1 and SCR1 were estimated by a sandwich ELISA. We found 35.63%, 51.14%, 56.93% decline in erythrocyte CR1 as compared to control. Soluble CR1 increased by 18.3%, 72.14% and 106.29% in MCD, FSGS and SLE, respectively. Urinary CR1 showed a positive correlation with glomerular CR1 expression. GCR1 was over expressed in MCD with very poor expression in SLE and sclerotic areas of FSGS. However, non-sclerotic areas of FSGS had GCR1 Expression comparable to MCD. Soluble CR1 had no correlation with ECR1 or UCR1 but correlated with disease activity. The pattern of CR1 expression was similar in MCD and FSGS. Hence, we speculate FSGS as a progression of MCD and not a separate disease entity. We also speculate decline in E-CR1 as the primary cause of pathological manifestations and increase in soluble CR1 as a compensatory increase in leukocyte CR1 synthesis induced by prevailing environmental factors. Urinary CR1 was directly correlated with the expression of GCR1 and hence may serve as a marker of glomerular damage or glomerular involvement in secondary nephritis like SLE.
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