Publications by authors named "Katsuhiko Yonemura"

Objective: Severe urinary tract infection may lead to sepsis in some cases. In these cases, treatment must not only include drainage of the source of infection, but also management of systemic inflammatory response syndrome (SIRS). Blood purification therapy focused on endotoxin adsorption is thought to be a useful treatment method for this purpose.

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We encountered a 49-year-old Japanese man in whom tumor-like renal lesions developed as a result of chronic Staphylococcus aureus pyelonephritis. The patient complained of general fatigue, weight loss, and anorexia for 6 months. Contrast-enhanced computed tomography (CT) of the abdomen revealed multiple low-density lesions in both kidneys and paraaortic lymphadenopathy.

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The purpose of this study was to evaluate whether upregulated p21, a cell cycle-inhibitory protein, contributes to cisplatin (CDDP)-induced acute renal failure (ARF) and to acquired resistance to rechallenge injury with CDDP in rats. ARF was induced in rats by injection of CDDP (5 mg/kg) and rechallenge injury to CDDP by the same dose of CDDP 14 days after the first CDDP injection. Rats were treated with p21 antisense oligodeoxynucleotide (ODN) or its vehicle, p21 sense ODN, every 36 h from days 0 to 5 for single CDDP and from days 13 to 19 for rechallenge injury and killed at day 3, 5, 16, or 19.

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Background: Establishment of non-invasive urinary biomarkers for the prediction of acute renal failure (ARF) is important. We evaluated whether urinary oxidative stress markers reflect intrarenal oxidative stress in cisplatin (CDDP)-induced ARF, and whether these markers can be used for the prediction of future ARF.

Methods: Urinary malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured up to day 14 post-CDDP (6 mg/kg) injection in rats.

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A 53-year-old man with nephrotic syndrome and severe renal failure was diagnosed with light- and heavy-chain deposition disease (LHCDD) by renal biopsy. The patient had no monoclonal protein and mild marrow plasmacytosis (6%), but marrow plasma cells expressed CD19(-)CD56+ and predominant monoclonal kappa-chain, indicating plasma cell dyscrasia. Conventional chemotherapy was ineffective and did not improve renal failure.

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To investigate the mechanisms of myofibroblast differentiation of interstitial fibroblastic cells (FCs) in rats with uranyl acetate-induced acute renal failure (ARF), we examined the relationship between the expression of alpha-smooth muscle actin (alpha-SMA), myofibroblast phenotype and tubular dilatation as well as cell shape and adhesion of FCs. Peritubular alpha-SMA-positive myofibroblasts appeared after induction of ARF and extended along the damaged, dilated proximal tubules and then almost disappeared after proximal tubular recovery. The perimeter of proximal tubules correlated with fractional areas stained for alpha-SMA (P<0.

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Background: We investigated the clinical and pathological findings relevant to the efficacy of corticosteroid treatment in IgA nephropathy patients with 0.5 to 2.0 g/day of proteinuria at the initiation of corticosteroid treatment.

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The purpose of this study was to evaluate the expressions and the roles of proteins involved in cell cycle regulation and DNA repair in cis-diamminedichloroplatinum (II) (cisplatin or CDDP)-induced acute renal failure (ARF). Treatment with CDDP (6 mg/kg, iv) induced tubular damage and increased serum creatinine (Scr) and the number of TUNEL-positive cells in the outer stripe of the outer medulla in rats, which reached peak levels at 5 days after CDDP. The expressions of cyclin-dependent kinase inhibitors (p21 and p27), cyclin B1, cyclin D1, PCNA, GADD 45, and GADD 153 were significantly increased in the outer medulla, reaching peak levels at 3 days after CDDP.

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A 71-year-old man with bilateral renovascular disease was admitted to Hamamatsu University hospital because of appetite loss and acute shortness of breath due to acute pulmonary edema (APE) with accelerated hypertension and renal failure. Hypertension and APE were controlled by an angiotensin converting enzyme inhibitor (ACEI) and four sessions of hemodialysis with reduction of 1.8 kg bodyweight.

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Background: Cardiovascular mortality is extremely high in patients on hemodialysis. Among a variety of pathophysiological conditions, deranged calcium homeostasis including secondary hyperparathyroidism may be one of the factors contributing to cardiovascular disease in patients on hemodialysis. This study was designed to evaluate the role of the serum parathyroid hormone (PTH) concentration and its regulatory factors in serum on arterial stiffness in patients on maintenance hemodialysis.

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Background: We have previously reported that the serum concentration of 2-(alpha-mannopyranosyl)-L-tryptophan (MPT), tryptophan glycoconjugate, is a more accurate measure of renal function than that of serum creatinine concentration. The aim of the present study was to compare the diagnostic value of serum concentrations of MPT and creatinine as a measure of normal renal function.

Methods: A total of 156 subjects with serum creatinine concentration < or =1.

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Background: We have reported that vitamin D deficiency may be implicated in the pathogenesis of hypoalbuminemia observed in patients with end-stage renal disease, but the mechanism remains to be clarified. The aim of the present study was to determine whether supplementation with alfacalcidol might increase protein intake in hemodialyzed patients with hypoalbuminemia.

Methods: Twelve patients with hypoalbuminemia under 3.

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We report on a patient with membranoproliferative glomerulonephritis (MPGN) type III, whose repeated renal biopsies show evolution from a type I-like pattern to a type III pattern of immune complex formation over a 1-year period. Based on the development of experimental in situ immune complex glomerulonephritis, we discuss possible mechanisms for the formation of subepithelial deposits in type III MPGN with reference to an experimental in situ immune complex model of glomerulonephritis.

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Background: Although vitamin K2 has been shown to prevent prednisolone-induced loss of bone mineral density of the lumbar spine in patients with chronic glomerulonephritis, the magnitude of this effect remains to be clarified. The aim of this prospective study is to compare the protective effect of vitamin K2 with that of vitamin D3 on prednisolone-induced loss of bone mineral density in patients with chronic glomerulonephritis.

Methods: Sixty patients (28 men, 32 women) were randomly divided into 4 groups (n = 15 each group): control (group C), vitamin D3 alone (alfacalcidol, 0.

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We describe a 59-year-old man with nephrotic syndrome that was diagnosed as suspected minimal change nephrotic syndrome by the routine examination of renal tissues at first biopsy, because renal histology showed segmental mild mesangial expansion with argyrophilic staining and partial foot process fusion without any deposition. Prednisolone therapy induced complete remission of nephrotic syndrome. Relapse occurred after 4 years of complete remission, and the second renal biopsy revealed amyloid light-chain (AL)-amyloidosis.

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A woman was admitted to the hospital with joint pain. She was also found to have pericardial effusion, renal dysfunction, pancytopenia, and positive antinuclear antibody; a diagnosis of systemic lupus erythematosus (SLE) was made. Although she had neither neurological symptoms nor fever, laboratory tests showed microangiopathic hemolytic anemia, thrombocytopenia, and renal dysfunction.

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The present study was designed to identify the source and kinetics of an alternatively spliced "embryonic" cellular fibronectin EIIIA (cFn-EIIIA) in relation to regenerating renal tubules in uranyl acetate (UA)-induced acute renal failure (ARF) in rats. Damage of the proximal tubules was found as early as day 2 after induction of ARF, peaked at day 5, and was almost substituted by epithelial relining by day 7. Immunohistochemistry showed de novo deposition of cFn-EIIIA in peritubular regions as early as day 2, then on the tubular basement membrane (TBM) after day 4.

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This case report describes 2 patients with chronic myeloid leukemia in whom hemolytic uremic syndrome developed while being treated with interferon-alpha and hydroxycarbamide. Hemolytic uremic syndrome was recognized by progressive renal dysfunction, thrombocytopenia, microangiopathic hemolytic anemia, and histologic features of thrombotic microangiopathy in the kidney. Although renal dysfunction progressed to dialysis-dependent renal failure in one patient despite treatment with prednisolone and plasmapheresis but not in other, withdrawal of the treatment resulted in a prompt resolution of thrombocytopenia and microangiopathic hemolytic anemia in both patients.

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Background: Reduction of body mass index (BMI) significantly affects mortality in haemodialysis (HD) patients, but it remains to be determined which of the body components influences mortality.

Methods: We examined the whole body composition of 262 HD patients by dual-energy X-ray absorptiometry (DEXA) (age: 60+/-12 years; HD duration 9+/-7 years; male/female: 177/85; diabetics, n=50) and subsequently followed mortality for 5 years.

Results: Patient age was significantly correlated with limb/trunk lean mass (LTLM) ratio (r=-0.

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