Publications by authors named "Kenji Arizono"

Glomerular inflammation is a putative aggravation factor for type 2 diabetic nephropathy and urinary thrombin is a novel marker of glomerular inflammation. To clarify the relationship between glomerular inflammation and progression of the nephropathy, we measured urinary thrombin in 118 patients with type 2 diabetic nephropathy at different stages. To investigate the implications of urinary thrombin in the nephropathy, we compared urinary thrombin with expression of tissue factor, the trigger of blood coagulation activation, in glomeruli and with markers of renal injury (estimated glomerular filtration rate (eGFR) and proteinuria).

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Introduction: Mortality in hemodialysis patients is relatively high; thus, its risk stratification is very important. There are insufficient data describing the current status of the management of serum phosphate and calcium levels.

Methods: We conducted a multicenter, prospective, registry study throughout the Kumamoto Prefecture in Japan.

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A 58-year-old man was referred to our institution for an evaluation of nephrotic range proteinuria. Renal biopsy showed a marked expansion of the mesangial matrix and thickening of glomerular basement membrane (GBM) in periodic acid-silver methenamine (PAM). Immunofluorescence (IF) revealed strong staining for the monoclonal kappa light chain.

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Background: Crescentic glomerulonephritis (CresGN), an uncommon rapidly progressive disease, is characterized by severe glomerular inflammation with fibrin deposition. The lack of specific CresGN biomarkers delays diagnosis and threatens life. Because fibrin deposits in CresGN glomeruli indicate thrombin generation, we hypothesized that thrombin is excreted in urine and is a specific CresGN biomarker.

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We report a Japanese woman with variegate porphyria accompanied by amyloid A (AA) amyloidosis. Arthropathy involving multiple joints occurred at 35 years old and persisted. C-reactive protein was 4.

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A 66-year-old woman with seropositive rheumatoid arthritis (RA) and latent tuberculosis infection developed minimal-change nephrotic syndrome following the initiation of anti-tuberculosis chemoprophylaxis with isoniazid. This is the first reported case of an isoniazid-induced nephrotic syndrome. Isoniazid as a single-drug intervention is widely accepted as a safe and effective means of anti-tuberculosis chemoprophylaxis, particularly for RA patients with latent tuberculosis infection; the present case, however, demonstrates that isoniazid has the potential to induce minimal-change nephrotic syndrome, even when used as a single-drug intervention.

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Background/aims: A dialyzer (APS-EX) with a higher hollow fiber density ratio was manufactured using the highest performance polysulfone hollow fiber from Asahi-Kasei Medical.

Methods: We compared the performance of this device in comparison with hemodialysis (HD; APS-S) and hemodiafiltration (HDF) conditions (APS-S, 10 l post-HDF) to evaluate its merit as an internal filtration-enhanced dialyzer.

Results: With low molecular weight proteins, APS-EX had a reduction ratio of 74.

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Chronic inflammation contributes to the pathogenesis of several complications of hemodialysis therapy. It is thought that backfiltration of bacteria-derived contaminations during dialysis may induce a chronic inflammatory state. High-sensitivity C-reactive protein (hs-CRP) is one of the tools which can take a hold on such a chronic inflammatory condition.

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Background: Mutations of the NPHS2 gene are responsible for autosomal-recessive steroid-resistant nephrotic syndrome. Its product, podocin, faces the slit diaphragm area with its two ends in the cytoplasm of foot processes.

Methods: We generated rabbit polyclonal antibodies against conjugated peptides from human podocin N- and C-termini, and studied podocin and synaptopodin using kidney tissues of normal humans and those with glomerular diseases.

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