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      Platelet-Derived Growth Factor, Interleukin (IL)-1β, IL-6, IL-6R and Tumor Necrosis Factor-α in IgA Nephropathy

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          We clarified the presence of platelet-derived growth factor (PDGF), interleukin (IL)-1β IL-6, IL-6 receptor (IL-6R) and tumor necrosis factor-α (TNF-α) in renal biopsy specimens from 62 patients with IgA nephropathy, and discuss their relationship with mesangial cell proliferation, degree of histological damage and various clinical factors. Mesangial proliferation was determined histologically by PAS staining and the positive rate of proliferating cell nuclear antigen (PCNA). Renal biopsy specimens were stained using an enzyme-antibody method to determine the presence of cytokines and the receptor. PCNA-positive cells in the glomeruli significantly increased in patients positive for PDGF, IL-6, IL-6R and TNF-α. The degree of histological damage increased with the positive rates of PDGF, IL-6 or IL-6R and the number of PCNA-positive cells in the glomeruli. In the PDGF-A-positive patients, total urinary protein (TUP), urinary 1β-microglobulin (u-β<sub>2</sub>-m) and systolic and diastolic blood pressure were significantly higher, and creatinine clearance (C<sub>cr</sub>) was significantly lower than in the PDGF-A-negative patients. In the PDGF-B-positive patients, TUP, serum creatinine (s-Cr) and urinary and serum β<sub>2</sub>-m increased significantly and C<sub>cr</sub> decreased significantly. IL-1β was not related to any clinical factors. In the IL-6-positive patients, TUP was significantly higher than in the IL-6-negative patients. In the IL-6R-positive patients, TUP, s-Cr, urinary β<sub>2</sub>-m and systolic blood pressure were significantly higher than in the IL-6R-negative patients. In conclusion, PDGF, IL-6 and IL-6R may be closely related to mesangial cell proliferation, histological changes and deterioration of various clinical factors in patients with IgA nephropathy.

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          Author and article information

          S. Karger AG
          24 December 2008
          : 74
          : 4
          : 652-660
          Second Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima City, Japan
          189470 Nephron 1996;74:652–660
          © 1996 S. Karger AG, Basel

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          Pages: 9
          Original Paper


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