The role of monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein (MCP) -1 in subgroups of rapidly progressive glomerulonephritis
To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocytechemoattractant protein (MCP) -1 in the pathogenesis of rapidly progressive glomerulonephritis (RPGN), we determined the urinary levels of MCAF/MCP-1 in 20 healthy subjects, 30 patients showing RPGN with crescents, an...
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| Published in | Nihon Jinzo Gakkai shi Vol. 41; no. 7; pp. 704 - 711 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | Japanese |
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Japan
Japanese Society of Nephrology
01.10.1999
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| Abstract | To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocytechemoattractant protein (MCP) -1 in the pathogenesis of rapidly progressive glomerulonephritis (RPGN), we determined the urinary levels of MCAF/MCP-1 in 20 healthy subjects, 30 patients showing RPGN with crescents, and 39 patients with various types of renal diseases without crescents. We divided RPGN into two subgroups, the acute type and the insidious type, with regard to the declination rate of reciprocals of serum creatinine with time as previously reported. In addition, we divided the patients with RPGN into anti-neutrophil cytoplasmic antibody (ANCA)-related diseases and immune complex (IC)-mediated diseases with regard to etiology. Urinary levels of MCAF/MCP-1 were significantly higher in patientswith RPGN as compared with those of other renal diseases and healthy volunteers (21.8±4.5 vs. 11.6±3.5, 1.0±0.1 pg/ml ⋅ creatinine, respectively, p<0.01, mean±SEM). There was no difference in the urinary levels of MCAF/MCP-1 between the acute and insidious types of RPGN patients. In addition, there was no difference in the urinary levels of MCAF/MCP-1 between the patients with ANCA-related and IC-mediated diseases. Urinary levels of MCAF/MCP-1 in patients with RPGN were correlated well with the percentage of both total crescents and fibrocellular/fibrous crescents and the number of CD68 positive infiltrating cells in the interstitium. Immunohistochemical examinations revealed that MCAF/MCP-1-positive cells were detected in tubular epithelial and endothelial cells and mononuclear infiltrated cells in the interstitium. Moreover, elevated urinary MCAF/MCP-1 levels in patients with RPGN, regardless of subgroups, were dramatically dereased during methylprednisolone pulse therapy induced convalescence. These results suggest that MCAF/MCP-1 may be involved in the pathogenesis of RPGN via macrophage recruitment and activation. |
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| AbstractList | To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein(MCP)-1 in the pathogenesis of rapidly progressive glomerulonephritis (RPGN), we determined the urinary levels of MCAF/MCP-1 in 20 healthy subjects, 30 patients showing RPGN with crescents, and 39 patients with various types of renal diseases without crescents. We divided RPGN into two subgroups, the acute type and the insidious type, with regard to the declination rate of reciprocals of serum creatinine with time as previously reported. In addition, we divided the patients with RPGN into anti-neutrophil cytoplasmic antibody(ANCA)-related diseases and immune complex(IC)-mediated diseases with regard to etiology. Urinary levels of MCAF/MCP-1 were significantly higher in patients with RPGN as compared with those of other renal diseases and healthy volunteers(21.8 +/- 4.5 vs. 11.6 +/- 3.5, 1.0 +/- 0.1 pg/ml creatinine, respectively, p < 0.01, mean +/- SEM). There was no difference in the urinary levels of MCAF/MCP-1 between the acute and insidious types of RPGN patients. In addition, there was no difference in the urinary levels of MCAF/MCP-1 between the patients with ANCA-related and IC-mediated diseases. Urinary levels of MCAF/MCP-1 in patients with RPGN were correlated well with the percentage of both total crescents and fibrocellular/fibrous crescents and the number of CD68-positive infiltrating cells in the interstitium. Immunohistochemical examinations revealed that MCAF/MCP-1 positive cells were detected in tubular epithelial and endothelial cells and mononuclear infiltrated cells in the interstitium. Moreover, elevated urinary MCAF/MCP-1 levels in patients with RPGN, regardless of subgroups, were dramatically decreased during methylprednisolone pulse therapy induced convalescence. These results suggest that MCAF/MCP-1 may be involved in the pathogenesis of RPGN via macrophage recruitment and activation. To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein(MCP)-1 in the pathogenesis of rapidly progressive glomerulonephritis (RPGN), we determined the urinary levels of MCAF/MCP-1 in 20 healthy subjects, 30 patients showing RPGN with crescents, and 39 patients with various types of renal diseases without crescents. We divided RPGN into two subgroups, the acute type and the insidious type, with regard to the declination rate of reciprocals of serum creatinine with time as previously reported. In addition, we divided the patients with RPGN into anti-neutrophil cytoplasmic antibody(ANCA)-related diseases and immune complex(IC)-mediated diseases with regard to etiology. Urinary levels of MCAF/MCP-1 were significantly higher in patients with RPGN as compared with those of other renal diseases and healthy volunteers(21.8 +/- 4.5 vs. 11.6 +/- 3.5, 1.0 +/- 0.1 pg/ml creatinine, respectively, p < 0.01, mean +/- SEM). There was no difference in the urinary levels of MCAF/MCP-1 between the acute and insidious types of RPGN patients. In addition, there was no difference in the urinary levels of MCAF/MCP-1 between the patients with ANCA-related and IC-mediated diseases. Urinary levels of MCAF/MCP-1 in patients with RPGN were correlated well with the percentage of both total crescents and fibrocellular/fibrous crescents and the number of CD68-positive infiltrating cells in the interstitium. Immunohistochemical examinations revealed that MCAF/MCP-1 positive cells were detected in tubular epithelial and endothelial cells and mononuclear infiltrated cells in the interstitium. Moreover, elevated urinary MCAF/MCP-1 levels in patients with RPGN, regardless of subgroups, were dramatically decreased during methylprednisolone pulse therapy induced convalescence. These results suggest that MCAF/MCP-1 may be involved in the pathogenesis of RPGN via macrophage recruitment and activation.To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein(MCP)-1 in the pathogenesis of rapidly progressive glomerulonephritis (RPGN), we determined the urinary levels of MCAF/MCP-1 in 20 healthy subjects, 30 patients showing RPGN with crescents, and 39 patients with various types of renal diseases without crescents. We divided RPGN into two subgroups, the acute type and the insidious type, with regard to the declination rate of reciprocals of serum creatinine with time as previously reported. In addition, we divided the patients with RPGN into anti-neutrophil cytoplasmic antibody(ANCA)-related diseases and immune complex(IC)-mediated diseases with regard to etiology. Urinary levels of MCAF/MCP-1 were significantly higher in patients with RPGN as compared with those of other renal diseases and healthy volunteers(21.8 +/- 4.5 vs. 11.6 +/- 3.5, 1.0 +/- 0.1 pg/ml creatinine, respectively, p < 0.01, mean +/- SEM). There was no difference in the urinary levels of MCAF/MCP-1 between the acute and insidious types of RPGN patients. In addition, there was no difference in the urinary levels of MCAF/MCP-1 between the patients with ANCA-related and IC-mediated diseases. Urinary levels of MCAF/MCP-1 in patients with RPGN were correlated well with the percentage of both total crescents and fibrocellular/fibrous crescents and the number of CD68-positive infiltrating cells in the interstitium. Immunohistochemical examinations revealed that MCAF/MCP-1 positive cells were detected in tubular epithelial and endothelial cells and mononuclear infiltrated cells in the interstitium. Moreover, elevated urinary MCAF/MCP-1 levels in patients with RPGN, regardless of subgroups, were dramatically decreased during methylprednisolone pulse therapy induced convalescence. These results suggest that MCAF/MCP-1 may be involved in the pathogenesis of RPGN via macrophage recruitment and activation. To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocytechemoattractant protein (MCP) -1 in the pathogenesis of rapidly progressive glomerulonephritis (RPGN), we determined the urinary levels of MCAF/MCP-1 in 20 healthy subjects, 30 patients showing RPGN with crescents, and 39 patients with various types of renal diseases without crescents. We divided RPGN into two subgroups, the acute type and the insidious type, with regard to the declination rate of reciprocals of serum creatinine with time as previously reported. In addition, we divided the patients with RPGN into anti-neutrophil cytoplasmic antibody (ANCA)-related diseases and immune complex (IC)-mediated diseases with regard to etiology. Urinary levels of MCAF/MCP-1 were significantly higher in patientswith RPGN as compared with those of other renal diseases and healthy volunteers (21.8±4.5 vs. 11.6±3.5, 1.0±0.1 pg/ml ⋅ creatinine, respectively, p<0.01, mean±SEM). There was no difference in the urinary levels of MCAF/MCP-1 between the acute and insidious types of RPGN patients. In addition, there was no difference in the urinary levels of MCAF/MCP-1 between the patients with ANCA-related and IC-mediated diseases. Urinary levels of MCAF/MCP-1 in patients with RPGN were correlated well with the percentage of both total crescents and fibrocellular/fibrous crescents and the number of CD68 positive infiltrating cells in the interstitium. Immunohistochemical examinations revealed that MCAF/MCP-1-positive cells were detected in tubular epithelial and endothelial cells and mononuclear infiltrated cells in the interstitium. Moreover, elevated urinary MCAF/MCP-1 levels in patients with RPGN, regardless of subgroups, were dramatically dereased during methylprednisolone pulse therapy induced convalescence. These results suggest that MCAF/MCP-1 may be involved in the pathogenesis of RPGN via macrophage recruitment and activation. |
| Author | YOKOYAMA, Hitoshi FURUICHI, Kengo TAKEDA, Shin-ichi WADA, Takashi SHIMIZU, Kazuaki KIDA, Hiroshi YOSHIMOTO, Kei-ichi MUKAIDA, Naofumi KOBAYASHI, Ken-ichi SAKAI, Norihiko IWATA, Yasunori SHIMIZU, Miho TAKAEDA, Chikako MATSUSHIMA, Kouji |
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| References | 18. Yokoyama H, Takaeda M, Wada T, Ohta S, Hisada Y, Segawa C, Furuichi K, Kobayashi K. Glomerular ICAM-1 expression related to circulating TNF-a in human glomerulonephritis. Nephron 1997 ; 76 : 425-33. 19. Stahl RAK, Thaiss F, Disser M, Helmuchen U, Hora K, Schlondorff D. Increased expression of monocyte chemoattractant protein-1 in anti-thymocyte antibody-induced glomerulonephritis. Kidney Int 1993 ; 44 : 1036-47. 24. Diamond JR, Folts DK, Ding G, Frye JE, Restrepo NC. Macrophages, monocyte chemoattractant peptide 1, and TGF-?A1 in experimental hydronephrosis. Am J Physiol 1994 ; 266 : F926-33. 11. Schlondorff D, Nelson PJ, Luckow B, Banas B. Chemokines and renal disease. Kidney Int 1997 ; 51 : 610-21. 6. Yang N, Isbel NM, Paterson DJN, Li Y, Ye R, Atkins RC, Lan HY. Local macrophage proliferation in human glomer ulonephritis. Kidney Int 1998 ; 54 : 143-51. 20. Tang WW, Feng L, Mathison JC, Wilson CB. Cytokine expression, up regulation of intercellular adhesion molecule-1, and leukocyte infiltration in experimental tubulointerstitial nephritis. Lab Invest 1994 ; 70 : 631-8. 17. Gross WL, Schmitt WH, Csernok E. ANCA and associated diseases : immunodiagnostic and pathogenetic aspects. Clin Exp Immunol 1993 ; 91: 1-12. 13. Yokoyama H, Wada T, Furuichi K, Segawa C, Shimizu M, Kobayashi K, Su SB, Mukaida N, Matsushima K. Urinary levels of chemokines (MCAF/MCP-1, IL 8) reflect distinct disease activities and phases of human IgA nephropathy. J Leukoc Biol 1998 ; 63 : 493-9. 25. Schwarz M, Radeke H, Resch K, Uciechowski P. Lymphocyte derived cytokines induce sequential expression of monocyte- and T cell specific chemokines in human mesangial cells. Kidney Int 1997 ; 52 :1521-31. 15. World Health Organization (WHO) Monograph. Classification of glomerular diseases. In : Churg J, Bernstein J, Glassock RJ (eds) Renal disease. Tokyo : Igaku-Shoin, 1995 : 3. 10. Rovin BH, Phan LT. Chemotactic factors and renal inflammation. Am J Kidney Dis 1998 ; 31 : 1065-84. 2. Takeda S, Kida H, Yokoyama H, Tomosugi N, Kobayashi K. Two distinct types of crescentic glomerulonephritis. Clin Nephrol 1992 ; 37 : 285-93. 23. Rehan A, Johnson KJ, Wiggins RC, Kunkel RG, Ward PA. Evidence for the role of oxygen radicals in acute nephrotoxic nephritis. Lab Invest 1984 ; 51: 396-402. 7. Wada T, Furuichi K, Segawa C, Shimizu M, Sakai N, Takeda S, Takasawa K, Kida H, Kobayashi K, Mukaida N, Ohmoto Y, Matsushima K, Yokoyama H. MIP-1 ar and MCP-1 contribute to crescents and interstitial lesions via the cognate chemokine receptor in human crescentic glomerulonephritis. Kidney Int 1999 ; 56 : 995-1003. 9. Matsushima K, Larsen CG, DuBois GC, Oppenheim JJ. Purification and characterization of a novell monocyte chemotactic and activating factor produced by a human myelomonocytic cell line. J Exp Med 1989 ; 169 : 1485-90. 14. Wada T, Yokoyama H, Sakai N, Izumiya A, Shimizu M, Misaki T, Furuichi K, Segawa C, Kobayashi K. Cytokine up regulation in tubulointerstitial nephritis associated with membranous nephropathy. Clin Exp Nephrol 1999; 3 : 130-2. 16. Tervaert JWC, Limburg PC, Elema JD, Huitema MG, Horst G, The TH, Kallenberg CGM. Detection of autoantibodies against myeloid lysosomal enzymes : A useful adjunct to classification of patients with biopsy-proven necrotizing arteritis. Am J Med 1991 ; 91 : 59-66. 12. Wada T, Yokoyama H, Su SB, Mukaida N, Iwano M, Dohi K, Takahashi Y, Sasaki T, Furuichi K, Segawa C, Hisada Y, Ohta S, Takasawa K, Kobayashi K, Matsushima K. Monitoring urinary levels of monocyte chemotactic and activating factor reflects disease activity of lupus nephritis. Kidney Int 1996 ; 49 : 761-7. 5. Wada T, Yokoyama H, Furuichi K, Kobayashi K, Harada K, Naruto M, Su SB, Akiyama M, Mukaida N, Matsushima K. Intervention of crescentic glomerulonephritis by antibodies to monocyte chemotactic and activating factor (MCAF/MCP-l). FASEB J 1996 ; 10 : 1418-25. 22. Baud L, Hagege J, Sraer L, Ronsdeau E, Perez J, Ardaillou R. Reactive oxygen production by cultured rat glomerular mesangial cells during phagocytosis is associated with stimulation of lipoxygenase activity. J Exp Med 1983 :158 : 1836-42. 4. Atkins RC, Paterson DJN, Song Q, Lan HY. Modulators of crescentic glomerulonephritis. J Am Soc Nephrol 1996 ; 7: 2271-8. 8. Luster AD. Chemokines-chemotactic cytokines that mediate inflammation. N Engl J Med 1998 ; 338 : 436-45. 21. Schena FP, Gesualdo L, Grrandaliano G, Montinaro V. Progression of renal damage in human glomerulonephritis : Is there sleight of hand in winning the game? Kidney Int 1997 ; 52 : 1439-57. 1. Glassock RJ, Cohen AH, Adler SG. Primary glomerular diseases. In : Brenner BM (ed) The Kidney 5th ed. Philadelphia : WB Saunders, 1996 :1402-10. 3. Takeda S, Kida H, Yokoyama H, Takazakura E, Kobayashi K. Methylprednisolone pulse therapy in two clinical types of crescentic glomerulonephritis. Intern Med 1998 ; 37 : 585-91. |
| References_xml | – reference: 14. Wada T, Yokoyama H, Sakai N, Izumiya A, Shimizu M, Misaki T, Furuichi K, Segawa C, Kobayashi K. Cytokine up regulation in tubulointerstitial nephritis associated with membranous nephropathy. Clin Exp Nephrol 1999; 3 : 130-2. – reference: 16. Tervaert JWC, Limburg PC, Elema JD, Huitema MG, Horst G, The TH, Kallenberg CGM. Detection of autoantibodies against myeloid lysosomal enzymes : A useful adjunct to classification of patients with biopsy-proven necrotizing arteritis. Am J Med 1991 ; 91 : 59-66. – reference: 4. Atkins RC, Paterson DJN, Song Q, Lan HY. Modulators of crescentic glomerulonephritis. J Am Soc Nephrol 1996 ; 7: 2271-8. – reference: 24. Diamond JR, Folts DK, Ding G, Frye JE, Restrepo NC. Macrophages, monocyte chemoattractant peptide 1, and TGF-?A1 in experimental hydronephrosis. Am J Physiol 1994 ; 266 : F926-33. – reference: 17. Gross WL, Schmitt WH, Csernok E. ANCA and associated diseases : immunodiagnostic and pathogenetic aspects. Clin Exp Immunol 1993 ; 91: 1-12. – reference: 9. Matsushima K, Larsen CG, DuBois GC, Oppenheim JJ. Purification and characterization of a novell monocyte chemotactic and activating factor produced by a human myelomonocytic cell line. J Exp Med 1989 ; 169 : 1485-90. – reference: 12. Wada T, Yokoyama H, Su SB, Mukaida N, Iwano M, Dohi K, Takahashi Y, Sasaki T, Furuichi K, Segawa C, Hisada Y, Ohta S, Takasawa K, Kobayashi K, Matsushima K. Monitoring urinary levels of monocyte chemotactic and activating factor reflects disease activity of lupus nephritis. Kidney Int 1996 ; 49 : 761-7. – reference: 23. Rehan A, Johnson KJ, Wiggins RC, Kunkel RG, Ward PA. Evidence for the role of oxygen radicals in acute nephrotoxic nephritis. Lab Invest 1984 ; 51: 396-402. – reference: 7. Wada T, Furuichi K, Segawa C, Shimizu M, Sakai N, Takeda S, Takasawa K, Kida H, Kobayashi K, Mukaida N, Ohmoto Y, Matsushima K, Yokoyama H. MIP-1 ar and MCP-1 contribute to crescents and interstitial lesions via the cognate chemokine receptor in human crescentic glomerulonephritis. Kidney Int 1999 ; 56 : 995-1003. – reference: 3. Takeda S, Kida H, Yokoyama H, Takazakura E, Kobayashi K. Methylprednisolone pulse therapy in two clinical types of crescentic glomerulonephritis. Intern Med 1998 ; 37 : 585-91. – reference: 8. Luster AD. Chemokines-chemotactic cytokines that mediate inflammation. N Engl J Med 1998 ; 338 : 436-45. – reference: 20. Tang WW, Feng L, Mathison JC, Wilson CB. Cytokine expression, up regulation of intercellular adhesion molecule-1, and leukocyte infiltration in experimental tubulointerstitial nephritis. Lab Invest 1994 ; 70 : 631-8. – reference: 25. Schwarz M, Radeke H, Resch K, Uciechowski P. Lymphocyte derived cytokines induce sequential expression of monocyte- and T cell specific chemokines in human mesangial cells. Kidney Int 1997 ; 52 :1521-31. – reference: 22. Baud L, Hagege J, Sraer L, Ronsdeau E, Perez J, Ardaillou R. Reactive oxygen production by cultured rat glomerular mesangial cells during phagocytosis is associated with stimulation of lipoxygenase activity. J Exp Med 1983 :158 : 1836-42. – reference: 2. Takeda S, Kida H, Yokoyama H, Tomosugi N, Kobayashi K. Two distinct types of crescentic glomerulonephritis. Clin Nephrol 1992 ; 37 : 285-93. – reference: 15. World Health Organization (WHO) Monograph. Classification of glomerular diseases. In : Churg J, Bernstein J, Glassock RJ (eds) Renal disease. Tokyo : Igaku-Shoin, 1995 : 3. – reference: 1. Glassock RJ, Cohen AH, Adler SG. Primary glomerular diseases. In : Brenner BM (ed) The Kidney 5th ed. Philadelphia : WB Saunders, 1996 :1402-10. – reference: 6. Yang N, Isbel NM, Paterson DJN, Li Y, Ye R, Atkins RC, Lan HY. Local macrophage proliferation in human glomer ulonephritis. Kidney Int 1998 ; 54 : 143-51. – reference: 19. Stahl RAK, Thaiss F, Disser M, Helmuchen U, Hora K, Schlondorff D. Increased expression of monocyte chemoattractant protein-1 in anti-thymocyte antibody-induced glomerulonephritis. Kidney Int 1993 ; 44 : 1036-47. – reference: 18. Yokoyama H, Takaeda M, Wada T, Ohta S, Hisada Y, Segawa C, Furuichi K, Kobayashi K. Glomerular ICAM-1 expression related to circulating TNF-a in human glomerulonephritis. Nephron 1997 ; 76 : 425-33. – reference: 5. Wada T, Yokoyama H, Furuichi K, Kobayashi K, Harada K, Naruto M, Su SB, Akiyama M, Mukaida N, Matsushima K. Intervention of crescentic glomerulonephritis by antibodies to monocyte chemotactic and activating factor (MCAF/MCP-l). FASEB J 1996 ; 10 : 1418-25. – reference: 10. Rovin BH, Phan LT. Chemotactic factors and renal inflammation. Am J Kidney Dis 1998 ; 31 : 1065-84. – reference: 13. Yokoyama H, Wada T, Furuichi K, Segawa C, Shimizu M, Kobayashi K, Su SB, Mukaida N, Matsushima K. Urinary levels of chemokines (MCAF/MCP-1, IL 8) reflect distinct disease activities and phases of human IgA nephropathy. J Leukoc Biol 1998 ; 63 : 493-9. – reference: 21. Schena FP, Gesualdo L, Grrandaliano G, Montinaro V. Progression of renal damage in human glomerulonephritis : Is there sleight of hand in winning the game? Kidney Int 1997 ; 52 : 1439-57. – reference: 11. Schlondorff D, Nelson PJ, Luckow B, Banas B. Chemokines and renal disease. Kidney Int 1997 ; 51 : 610-21. |
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| Snippet | To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocytechemoattractant protein (MCP) -1 in the pathogenesis of rapidly progressive... To elucidate the role of monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein(MCP)-1 in the pathogenesis of rapidly progressive... |
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| SubjectTerms | Anti-Inflammatory Agents - administration & dosage Biomarkers - analysis Chemokine CCL2 - analysis Chemokine CCL2 - physiology Chemokine CCL2 - urine Disease Progression Female Glomerulonephritis - classification Glomerulonephritis - drug therapy Glomerulonephritis - etiology Humans Kidney - metabolism Male MCAF/MCP-1, chemokine, rapidly progressive glomerulonephritis, crescentic glomerulone phritis Methylprednisolone - administration & dosage Middle Aged |
| Title | The role of monocyte chemotactic and activating factor (MCAF)/monocyte chemoattractant protein (MCP) -1 in subgroups of rapidly progressive glomerulonephritis |
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| ispartofPNX | The Japanese Journal of Nephrology, 1999, Vol.41(7), pp.704-711 |
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