AIM: In recent reports, C-reactive protein (CRP) has emerged as a component that may play important roles in atherogenesis. Based on the analogies set out in a previous report between focal-segmental sclerosis and atherosclerosis, we hypothesized that CRP contributes to the pathogenesis of glomerular diseases. To our knowledge, no immunohistochemical study of CRP localization in the kidneys has been previously reported. PATIENTS AND METHODS: In the present study, we investigated 106 kidney biopsy specimens from children with various types of glomerular diseases and minor glomerular abnormalities. Of the 106 cases, 74 were proliferative diseases, 17 were non-proliferative diseases, and 15 were minimal-change nephrotic syndrome (MCNS). Immunohistochemical staining was performed using monoclonal antibody to CRP. RESULTS: CRP immunoreactivity was found in 48 of 106 (45.3%) specimens. CRP deposition was encountered more often in patients with proliferative diseases (56.8%) than in those with non-proliferative diseases (23.5%) (p < 0.01). CRP deposition, most frequently observed along the capillary walls of glomeruli, was found in 33 of 46 (71.7%) cases with positive expression of CRP. CRP was also located in the peritubular capillary walls and small vessels in the interstitium in 13 of 46 cases (28.3%). CRP deposition was also found in 2 of 15 cases of MCNS. The two MCNS specimens showing positive CRP immunoreactivity were both from patients who had undergone cyclosporin therapy. CRP deposition was not shown in any cases treated with steroids or cyclophosphamide. The cases of patients who had undergone renal biopsies within 6 months after onset revealed a tendency toward positive CRP deposition. The clinical outcomes at the latest follow-up were quite similar between the groups of patients with and without CRP deposition. CONCLUSIONS: We surmise that circulating CRP may deposit at the site of endothelial injury, and may not be relevant to the progression of renal lesions.
AIM: In recent reports, C-reactive protein (CRP) has emerged as a component that may play important roles in atherogenesis. Based on the analogies set out in a previous report between focal-segmental sclerosis and atherosclerosis, we hypothesized that CRP contributes to the pathogenesis of glomerular diseases. To our knowledge, no immunohistochemical study of CRP localization in the kidneys has been previously reported. PATIENTS AND METHODS: In the present study, we investigated 106 kidney biopsy specimens from children with various types of glomerular diseases and minor glomerular abnormalities. Of the 106 cases, 74 were proliferative diseases, 17 were non-proliferative diseases, and 15 were minimal-change nephrotic syndrome (MCNS). Immunohistochemical staining was performed using monoclonal antibody to CRP. RESULTS:CRP immunoreactivity was found in 48 of 106 (45.3%) specimens. CRP deposition was encountered more often in patients with proliferative diseases (56.8%) than in those with non-proliferative diseases (23.5%) (p < 0.01). CRP deposition, most frequently observed along the capillary walls of glomeruli, was found in 33 of 46 (71.7%) cases with positive expression of CRP. CRP was also located in the peritubular capillary walls and small vessels in the interstitium in 13 of 46 cases (28.3%). CRP deposition was also found in 2 of 15 cases of MCNS. The two MCNS specimens showing positive CRP immunoreactivity were both from patients who had undergone cyclosporin therapy. CRP deposition was not shown in any cases treated with steroids or cyclophosphamide. The cases of patients who had undergone renal biopsies within 6 months after onset revealed a tendency toward positive CRP deposition. The clinical outcomes at the latest follow-up were quite similar between the groups of patients with and without CRP deposition. CONCLUSIONS: We surmise that circulating CRP may deposit at the site of endothelial injury, and may not be relevant to the progression of renal lesions.
Authors: Karine Sahakyan; Barbara E K Klein; Kristine E Lee; Michael Y Tsai; Ronald Klein Journal: Eur J Endocrinol Date: 2010-03-23 Impact factor: 6.664