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Naohisa Tomosugi

Researcher at Kanazawa University

Publications -  9
Citations -  415

Naohisa Tomosugi is an academic researcher from Kanazawa University. The author has contributed to research in topics: Glomerulonephritis & Nephritis. The author has an hindex of 5, co-authored 9 publications receiving 404 citations.

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Prevention of Proteinuria by the Administration of Anti-interleukin 8 Antibody in Experimental Acute Immune Complex-induced Glomerulonephritis

TL;DR: Results indicated that IL-8 participated in the impairment of renal functions in experimental acute immune complex-mediated glomerulonephritis through activating as well as recruiting neutrophils.
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Detection of urinary interleukin-8 in glomerular diseases

TL;DR: Elevated urinary IL-8 levels during the acute phase or exacerbations were found to be decreased during spontaneous or steroid pulse therapy-induced convalescence in all patients examined, suggesting local production ofIL-8 in diseased glomeruli might be involved in the pathogenesis of the glomerular diseases.
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Risk factors for infection and immunoglobulin replacement therapy in adult nephrotic syndrome

TL;DR: Data indicate that hypogammaglobulinemia and renal insufficiency are independent risk factors for bacterial infection in adult patients with nephrotic syndrome and the effects of intravenous immunoglobulin suggest that maintenance of serum IgG levels over 600 mg/dL may reduce the risk of infection.
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Up-regulated MHC-class II expression and γ-IFN and soluble IL-2R in lupus nephritis

TL;DR: Overall, glomerular lesions such as HLA-DQ expression, the activity index and leukocyte infiltration correlated positively with serum gamma-IFN levels, but not with serum sIL-2R levels, anti-DNA antibody titers and CH50 titers.
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Role of plasminogen activator inhibitor on nephrotoxic nephritis and its modulation by tumor necrosis factor.

TL;DR: PAI activity was studied in the plasma of rats with nephrotoxic nephritis to imply that PAI may play a role in the local coagulation in the capillaries of the nephritic kidneys, although this is probably not the only mechanism which explains the continued formation of the glomerular fibrin deposits.