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T Ideura

Publications and source records attributed to T Ideura.

At least 19 recordsLinked to original sources
PubMed2001

Acquisition of the monocyte/macrophage phenotype in human mesangial cells.

The function of intrinsic glomerular cells in active glomerular inflammation may be similar to that of monocytes/macrophages. Mesangial cells have phagocytic properties and release numerous mediators. In this study we examined whether human mesangial cells (hMCs) express a monocyte/macrophage phenotype in active glomerular inflammation. We report that the proto-oncogene c-fms, the macrophage colony-stimulating factor (M-CSF) receptor, which is a characteristic gene of monocytes/macrophages, is expressed in hMCs. Normal unmanipulated hMCs express weak c-fms mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR), and its expression increases after stimulation with platelet-derived growth factor-BB (PDGF-BB) and epidermal growth factor (EGF). The expression of c-fms was also demonstrated by flow cytometry with a specific polyclonal antibody. By immunohistochemistry, c-fms was prominently detected in acute glomerulonephritis, IgA nephritis, and lupus nephritis. These results indicate that hMCs express c-fms in active glomerular inflammation and are consistent with mesangial cells acquiring some macrophage-like characteristics in diseased states.

Acute Disease↗
PubMed2001

Reversible nephrotic syndrome in a patient with amyloid A amyloidosis of the kidney following methicillin-resistant Staphylococcus aureus infection.

A common form of methicillin-resistant Staphylococcus aureus (MRSA) associated glomerulonephritis is either an endocapillary proliferative glomerulonephritis or a crescentic glomerulonephritis. This report describes the development of reversible nephrotic syndrome following MRSA infection in a patient with amyloid A amyloidosis. The patient had been diagnosed as having rheumatoid arthritis for 50 years. Suppurative arthritis due to MRSA became complicated 2 years prior to admission to our hospital. In the meantime, a nonnephrotic-range proteinuria developed. Two weeks before admission, nephrotic syndrome developed. The serum creatinine level remained unchanged throughout the course, but common features characteristic of MRSA-associated glomerulonephritis were observed in this patient, such as elevated serum IgG and IgA levels. A renal biopsy specimen showed glomerular amyloid A amyloidosis of a nodular type, infiltrated mononuclear cells in the mesangium, deposition of IgG, IgA, and C3, and swelling of glomerular endothelial cells. There were no crescentic glomeruli. Following surgical eradication of the MRSA focus in the right knee joint, nephrotic syndrome disappeared. Hence, it was highly possible that MRSA infection induced a reversible nephrotic syndrome by causing reversible injuries to glomerular endothelial cells. The description of this case serves to illustrate the range of MRSA infections that may cause various forms of glomerulonephritides.

Aged↗
PubMed2001

[A case of paroxysmal nocturnal hemoglobinuria combined with focal segmental glomerular sclerosis].

A 81-year-old woman was admitted to our hospital because of edema and massive proteinuria on September 26, 1995. On admission, the palpebral conjuctiva were slightly anemic, and edema of the eyelids and legs was observed. Laboratory findings were as follows, urine protein(3+), occult blood(3+), WBC 2,600/microliter, Hgb 10.0 g/dl, reticulocytes 20@1000, TP 5.0 g/dl, Alb 2.7 g/dl, T-Cho 376 mg/dl, TG 194 mg/dl, LDH 763 U/l, haptoglobin < 93 mg/dl, Ham's test(+), sugar water test(+), and indirect coombs (+). The erythrocytes of this patient showed a negative population consisting of double negative erythrocytes evaluated by flow cytometric two-color analysis using monoclonal antibodies specific to CD55 and CD59. From these findings, the diagnosis of paroxysmal nocturnal hemoglobinuria(PNH) was made. The patient showed nephrotic syndrome and a renal biopsy was performed. The histological findings of renal biopsy showed focal and segmental sclerosis and adhesion of glomerular tufts. Interstitial fibrosis with atrophic tubules and lymphocyte infiltration were also observed. There was no specific staining of immunoglobulins and complement by immunofluorescence. The diagnosis of focal segmental glomerular sclerosis(FSGS) was made. There have been only three case reports of glomerular disease in patients with PNH, such as purpura nephritis, IgA nephropathy and membranous nephropathy. The complication of FSGS and PNH is every rare and there has been no report of FSGS in a case with PNH. The onset of PNH resulted from the loss of CD55 and CD59, which was critical in the onset of FSGS in the present case.

Aged↗
PubMed2001

[A case report of chronic chyluria probably due to Bancroftian filariasis, which showed hypoproteinemia].

Proteinuria is commonly observed in patients with chyluria due to Bancroftian filariasis. However, whether or not hypoalbuminemia is caused by chyluria alone is still a matter of debate. This is because various forms of glomerulonephritis are complicated in such patients. Herein, we report a case we have recently encountered. A 72-year-old male was admitted to our division for further evaluation of nephrotic syndrome. He was from the Southernmost part of Japan, where Bancroftian filariasis has been epidemic, and had developed persistent chyluria over a period of nearly 50 years. There was no other past history of illness except for diabetes mellitus(DM) pointed out 3 months prior to admission. The physical and laboratory examinations on admission fulfilled the diagnostic criteria for nephrotic syndrome. Lymphoscintigraphy showed an intense tracer accumulation in both kidneys. A renal biopsy was performed. At the light microscopic level, the glomeruli looked normal. Edema of the tubulointerstitium was noted. At the electron microscopic level, effacement of podocyte foot processes was not observed. Immunofluorescent study did not show glomerular deposition of immunoglobulins and complements. He also had persistent microscopic hematuria. Automated urinary sediment analysis by real-time confocal scanning laser microscopy revealed red blood cells of the non-glomerular type. Taken together, these findings strongly indicated that hypoalbuminemia of this patient was caused by chyluria alone. In conclusion, a report of the present case provides strong evidence that hypoalbuminemia of a patient with Bancroftian filariasis could be caused by chyluria alone.

Aged↗
PubMed2000

[Two cases of idiopathic membranous nephropathy with focal and segmental glomerulosclerotic lesions in which renal function progressively deteriorated].

Previous reports have clarified that focal and segmental glomerulosclerosis(FSGS) appearing in membranous nephropathy(MN) is associated with a poorer prognosis than that of MN without FSGS. However, the etiology and pathogenesis of such FSGS lesions may show substantial individual differences. In some patients, hemodynamic alterations secondary to hypertension and vascular disorders seem to play a crucial role in the development of such FSGS lesions. In such instances, steady regulation of blood pressure might slow down further progression of FSGS lesions. Here we describe two cases of biopsy-proven MN with FSGS. Case I was a 44-year-old man who had shown massive proteinuria with hematuria at the age of 39 years. Renal biopsy specimens obtained at the age of 40 and 41 years showed MN without FSGS and MN with FSGS, respectively. His blood pressure control was fairly good throughout the course. Although he was on a steroid, an immunosuppressant, a low protein diet, and an ACE inhibitor, his renal function declined in 5 years. Case 2 was a 61-year-old woman who showed nephrotic syndrome at the age of 39 years. A renal biopsy specimen obtained at the age of 58 years showed MN with FSGS and remarkable atherosclerotic changes of the interlobular arteries. Her blood pressure control was rather poor throughout the course. Her renal function gradually declined over 22 years. Since parts of the FSGS lesions of the second case may have been caused by hypertension, it is tempting to speculate that day-to-day control of blood pressure could improve the long-term prognosis. We believe that, at least in some patients of MN with FSGS, careful management may lead to a more favorable course of decline in renal function.

Adult↗
PubMed1999

Effect of simvastatin on proliferative nephritis and cell-cycle protein expression.

BACKGROUND: Mesangial cell proliferation is important in subsequent mesangial matrix expansion in glomerular injury. Therefore, the regulation of mesangial cell proliferation may be critical in the treatment of glomerulonephritis. Inhibition of 3-hydro-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibits the production of mevalonate and has been shown to suppress proliferation in many cell types, including mesangial cells in vitro. It is expected that HMG-CoA reductase inhibitor may suppress mesangial cell proliferation and subsequent progression of glomerulonephritis. Recently, the tight relationship between cell-cycle regulatory protein expression and mesangial cell proliferation in experimental glomerulonephritis was demonstrated. The aim of the present study is to examine the effect of simvastatin, one of the HMG-CoA reductase inhibitors, on the glomerular cell proliferation and on the expression of CDK2 or p27Kip1 in mesangial cells in experimental glomerulonephritis in vivo. METHODS: The effect of simvastatin on a rat mesangial proliferative glomerulonephritis induced by antithymocyte antibody (anti-Thy 1.1 GN) was studied. Administration of simvastatin or vehicle (for control GN) were started from two days before disease induction, and was continued to the day of nephrectomy. Nephrectomy was done at days 0, 2, 4, 7, 12 and 20 after disease induction. Immunohistochemistry for proliferating cells, macrophages, alpha-smooth muscle actin, type IV collagen and PDGF-B chain was performed, respectively, in addition to conventional periodic-acid Schiff staining. Double immunostaining for CDK2/OX-7 or p27Kip1/OX-7 was also done, respectively. RESULTS: There was no difference in the degree of the initial injuries between simvastatin-treated and control GN rats. The most pronounced feature of simvastatin-treated GN was the suppression of the early glomerular cell proliferation (about 70% of proliferation was suppressed at day 4). At day 4, alpha-smooth muscle actin expression was also decreased in simvastatin-treated GN rats. Inhibition of macrophage recruitment into glomeruli by simvastatin was also a prominent feature (about 30% decrease in the number of glomerular macrophages at day 2). Simvastatin significantly suppressed subsequent mesangial matrix expansion and type IV collagen accumulation in glomeruli. Although it might simply reflect the reduction in mesangial cells, glomerular PDGF-B chain expression was reduced. There was no significant difference in plasma lipids levels at day 2 and day 4. In vehicle-treated GN rats, the number of CDK2+/OX-7+ cells (CDK2-expressed mesangial cells) in glomeruli increased significantly from day 4 to day 7. Although simvastatin suppressed mesangial cell proliferation, the increase in the number of glomerular CDK2+/OX-7+ cells was also attenuated by simvastatin treatment. There was no difference in the number of p27Kip1+/OX-7+ cells (p27Kip1-expressed mesangial cells) in the glomerulus between vehicle-treated and simvastatin-treated GN rats. CONCLUSION: Simvastatin suppressed mesangial cell proliferation and subsequent matrix expansion, and macrophage infiltration into glomeruli in anti-Thy 1.1 GN rats. The antiproliferative effect of simvastatin in this model was also associated with the reduction of CDK2 expression in mesangial cells.

Animals↗
PubMed1999

Plasma exchange for acquired hemophilia: a case report.

A patient with acquired hemophilia complicated with chronic renal failure and lung tuberculosis was successfully treated by consecutive plasma exchange (PE). A 71-year-old man with serious bleeding tendency showed low coagulation factor levels and a high titer of factor VIII (FVIII) inhibitor, and he was diagnosed with acquired hemophilia. Because of the complication of active lung tuberculosis, instead of immunosuppressive therapy, he undertook a series of PE with fresh frozen plasma replacement for 3 months. After the start of PE, his bleeding symptoms and activated partial thromboplastin time (APTT) improved gradually according to the decrease in FVIII inhibitor levels. These results suggest that PE is an effective therapeutic tool for refractory acquired hemophilia.

Aged↗
PubMed1999

Effect of plasma exchange on refractory hemophagocytic syndrome complicated with myelodysplastic syndrome.

A case of hemophagocytic syndrome (HPS) refractory to corticosteroid therapy was successfully treated by plasma exchange. The patient was a 56-year-old woman who had undergone regular hemodialysis for 10 years for complicated myelodysplastic syndrome (MDS) and then had had lung tuberculosis. After the onset of tuberculosis, she suffered from HPS and was treated by antituberculosis agents and high dose corticosteroid administration without any effect on the HPS. After adding a series of plasma exchanges, the HPS improved gradually, and her MDS began to respond to corticosteroid therapy. Plasma hypercytokinemia due to HPS was corrected by plasma exchange, and the correction of a high level of plasma inflammatory cytokine was considered to be one of the contributing factors for the improvement of HPS. These results suggest that therapeutic plasma exchange should be considered as a therapeutic tool for HPS refractory to conventional therapy.

Adolescent↗
PubMed1999

Expression of bcl-2 and bax in glomerular disease.

Bcl-2 may account in part for the maintenance of hypercellularity in human glomerular diseases through preventing cell death and by counteracting bax which may be expressed to regulate excessive proliferation. This process is associated with the effect of PDGF B-chain expression. Bax expression may be important in the cell loss leading to glomerulosclerosis and TGF-beta1 participates in this process by increasing bax expression. Thus, the balance of bcl-2/bax expression may be critical in the course of human glomerular diseases.

Animals↗
PubMed1998

Plasma exchange for thrombocytopenia in antiphospholipid syndrome: a case report.

The remarkable effect of plasma exchange (PE) was observed on thrombocytopenia in a patient with antiphospholipid syndrome (APS) associated with systemic lupus erythematosus. Three times PE led to recovery from severe thrombocytopenia refractory to treatment with corticosteroid, anticoagulant, and antiplatelet drugs accompanied by a decrease in the serum cardiolipin beta2 glycoprotein I antibody level. This result suggests that PE is a valuable therapeutic tool for refractory thrombocytopenia in APS.

Adult↗
PubMed1998

Mesangial proliferative nephritis in man is associated with increased expression of the cell survival factor, Bcl-2.

Although most studies suggest that the hypercellularity in mesangial proliferative nephritis is due to increased cell proliferation, we hypothesized that it may also be due to increased expression of survival factors that may block their removal (apoptosis). We therefore studied the expression of apoptosis preventing/delaying the bcl-2 gene product in the glomerulus with various human glomerulonephritides. Immunohistochemistry for Bcl-2, proliferating cell associated protein (Ki-67) and alpha-smooth muscle actin (alpha-SMA) was performed on 55 biopsied kidney tissues: 6 cases of orthostatic proteinuria as a control (OP); 6 cases of diffuse proliferative lupus nephritis (WHO type IV, LN-MPGN); 24 cases of IgA nephropathy (IgA); 9 cases of minimal change nephrosis and 10 cases of idiopathic membranous nephropathy. The number of Ki-67-positive cells and the expression of alpha-SMA in the glomerulus were significantly higher in LN-MPGN and IgA. There was a significant positive correlation between glomerular Bcl-2 expression and glomerular cell proliferation evaluated by the number of Ki-67-positive cells (r=0.605, p < 0.01) or glomerular alpha-SMA expression (r=0.674, p < 0.01). Glomerular expression of Bcl-2 in IgA or LN-MPGN was significantly higher than that in OP (p < 0.01 and p < 0.05 vs. OP, respectively). The Bcl-2-positive cells were present in mesangial locations and demonstrated a perinuclear pattern. These results suggest that maintenance of glomerular hypercellularity in human glomerular diseases is partly due to the prevention of mesangial cell death via Bcl-2 expression.

Actins↗