Nobuki Maki

Yuri General Hospital, Honjō, Saitama, Japan

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Publications (26)48.72 Total impact

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    ABSTRACT: A 62-year-old splenectomized woman was admitted because of upper respiratory tract symptoms, general fatigue, and purpura. Laboratory data demonstrated microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure, and a positive Streptococcus pneumoniae (SP) urinary antigen test. A renal biopsy showed thrombotic microangiopathic changes. She was diagnosed with hemolytic uremic syndrome (HUS) secondary to SP infection. Methylprednisolone pulse therapy in addition to antibiotic therapy led to prompt improvement of her symptoms and laboratory abnormalities. This is the first adult case of SP-associated HUS successfully treated without hemodialysis. SP infection should be considered as a causative etiology in all splenectomized patients with HUS.
    Internal Medicine 01/2012; 51(15):2001-5. DOI:10.2169/internalmedicine.51.7916 · 0.97 Impact Factor
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    ABSTRACT: Proliferative glomerulonephritis with monoclonal IgG deposits (PGNMID) associated with membranoproliferative features is an extremely rare entity. Information on clinicopathological features and prognosis in this entity is limited. We reviewed 5,443 renal biopsies processed at our department, and identified 4 patients with PGNMID associated with membranoproliferative features. We evaluated clinicopathological features and outcomes in these patients, and characterized paraprotein deposits by immunofluorescence studies. Three out of 4 patients had nephrotic syndrome with renal insufficiency at presentation. Cryoglobulin or monoclonal protein in serum and urine was not detected. Renal biopsy showed membranoproliferative features with or without nodular formation. Tubulointerstitial and vascular alterations were mild in three patients. All patients had glomerular IgG-kappa deposits. Heavy chain subclass analysis performed in 3 patients showed IgG3 deposits. Immunofluorescence studies using antibodies specific for gamma-heavy chain C(H)1, C(H)2, and C(H)3 domains and gamma3 hinge did not show any apparent deletion. Confocal microscopy revealed glomerular colocalization of light and heavy chains. On electron microscopy, granular deposits were predominantly mesangial and subendothelial. All patients were treated with steroids and cytotoxic agents, but no effect on proteinuria was observed. The renal outcome was progressive in all patients. Early death was observed in two elder patients. No patient had overt myeloma or lymphoma at presentation or over the course of follow-up (mean 43 months). Our study suggests a predominance of IgG3-kappa glomerular deposits of nondeleted whole immunoglobulin molecules in PGNMID associated with membranoproliferative features. The clinical outcome in patients with this entity appears to be poor.
    Clinical nephrology 08/2009; 72(1):46-54. DOI:10.5414/CNP72046 · 1.23 Impact Factor
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    ABSTRACT: An imbalance of Th1 and Th2 cytokines has been reported in MCNS. Interleukin-13 (IL-13: Th2 cytokine) has been implicated in the pathogenesis of MCNS, but Th1/Th2 regulators such as T-bet (Th1-specific transcription factor) and GATA-3 (Th2-specific transcription factor) have not been examined. We isolated PBMC from 25 patients with MCNS during nephrosis and remission phases, from 17 nephrotic patients with membranous nephropathy (MN), and from 25 healthy subjects. We measured mRNA expression levels of T-bet, GATA-3, Stat5A (regulator of Th2 priming), IFN-gamma (Th1 cytokine), IL-2 (Th1 cytokine and activator of Stat5), IL-4 (Th2 cytokine), and IL-13 in PBMC, using real-time RT-PCR. GATA-3, Stat5A, and IL-13 mRNA expression levels were higher in the nephrotic MCNS group compared to the others. IL-2 mRNA expression levels were higher in nephrotic patients with MCNS and MN than in MCNS patients in remission and healthy controls. There were no differences in mRNA expression levels of T-bet, IFN-gamma, and IL-4 between MCNS and MN patients and healthy controls. This study is the first to reveal increased mRNA expression levels of GATA-3 and Stat5A in PBMC from MCNS patients in nephrosis. This study also supports recent findings suggesting the role of IL-13 in the development of MCNS. A predominant Th2 type of T cell activation may be involved in the pathogenesis of MCNS.
    Clinical nephrology 07/2009; 71(6):608-16. DOI:10.5414/CNP71608 · 1.23 Impact Factor
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    ABSTRACT: There are three subtypes of monoclonal immunoglobulin deposition disease: light chain deposition disease (LCDD), light and heavy chain deposition disease (LHCDD), and heavy chain deposition disease (HCDD). Although it has been considered that LHCDD is a variant of LCDD, information on clinicopathological features and prognosis in LHCDD is presently limited. We reviewed 5,443 renal biopsies, and evaluated clinicopathological features and outcomes in patients with LHCDD, in comparison with those in patients with LCDD and previously reported patients with HCDD. We also characterized paraprotein deposits in patients with LHCDD. We identified 6 patients with LHCDD, 6 patients with LCDD, and 1 patient with HCDD. The most common clinicopathological findings in patients with LHCDD were proteinuria, renal insufficiency, and nodular sclerosing glomerulopathy. Three patients had IgG-k deposits and 3 patients had IgG-l deposits. Heavy chain subclass analysis performed in 4 patients showed IgG3 deposits in all patients. Dual immunostaining revealed glomerular colocalization of light and heavy chains. In contrast with LCDD, glomerular C3 and C1q deposits were common findings in LHCDD and HCDD. All patients with LHCDD were treated with steroids and cytotoxic agents, but no effect on proteinuria was observed. Three patients developed end-stage renal disease requiring hemodialysis. The underlying hematological disorders in LHCDD and HCDD were milder than in LCDD. Early renal survival and overall patient survival in our patients appeared to be better in LHCDD than in LCDD. There are apparent differences in clinicopathological features and prognosis between LHCDD and LCDD. LHCDD is probably more similar to HCDD.
    Clinical nephrology 02/2009; 71(1):9-20. DOI:10.5414/CNP71009 · 1.23 Impact Factor
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    ABSTRACT: A 48-year-old man without underlying disease developed mediastinitis and was treated by mediastinal drainage. Methicillin-resistant Staphylococcus aureus (MRSA) was detected in a culture of the abscess material. He was treated with anti-MRSA antibiotics and the MRSA infection improved. Four weeks after the onset of MRSA infection, he developed rapidly progressive glomerulonephritis (RPGN) with nephrotic syndrome (NS). A renal biopsy showed endocapillary proliferative glomerulonephritis with IgA-predominant glomerular deposition. These clinicopathological findings were consistent with those in glomerulonephritis following MRSA infection (post-MRSA infection glomerulonephritis). The level of serum creatinine increased to 6.3 mg/dl, 7 weeks after the onset of RPGN. At that time, the eradication of MRSA infection was considered. He was given middle-dose steroid therapy. Thereafter, his RPGN with NS improved. MRSA infection did not recur. If the disease activity of post-MRSA infection glomerulonephritis persists after the disappearance of MRSA infection, the application of immunosuppressive therapy with steroids may be useful.
    Clinical nephrology 11/2008; 70(4):344-7. DOI:10.5414/CNP70344 · 1.23 Impact Factor
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    ABSTRACT: A 70-year-old woman with an 11-year history of indeterminate inflammatory bowel disease developed rapidly progressive glomerulonephritis (RPGN) 3 months after the initiation of infliximab therapy. A renal biopsy showed Congo red-positive homogenous deposits in the mesangial area, glomerular capillary walls and arterial walls. Cellular and fibrocellular crescents were observed in 7 of 28 functioning glomeruli. There were findings of active tubulointerstitial nephritis and vasculitis of the small arteries. On electron microscopy, amyloid fibrils were observed in the deposits. Immunohistochemistry showed positive staining for amyloid A (AA) protein. After cessation of infliximab therapy, she was treated with methylprednisolone pulse therapy followed by oral prednisolone therapy. Thereafter, her RPGN was improved. This is a rare case of co-existent focal extracapillary glomerulonephritis with vasculitis and AA renal amyloidosis. Considering the temporal association of drug use with new onset of RPGN in our patient, we suggest a causal link between infliximab and RPGN due to extracapillary glomerulonephritis and vasculitis.
    Clinical nephrology 10/2008; 70(3):240-4. DOI:10.5414/CNP70240 · 1.23 Impact Factor
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    ABSTRACT: A 19-year-old Japanese woman with a 4-year history of Crohn's disease (CD) developed high fever, polyarthralgia, and painful subcutaneous nodules of the legs. A skin biopsy showed panarteritis with fibrinoid necrosis in the deep dermis. Endoscopic examination showed aphthous lesions in the entire colon. She was diagnosed with cutaneous polyarteritis nodosa (PAN) associated with CD. Steroid therapy improved her symptoms. To our knowledge, this is the first Japanese case of cutaneous PAN associated with CD.
    Modern Rheumatology 09/2008; 18(6):639-42. DOI:10.1007/s10165-008-0110-8 · 2.21 Impact Factor
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    ABSTRACT: Very few cases of non-organized and non-Randall-type monoclonal immunoglobulin deposition disease (MIDD) associated with membranous features have been reported. Information on clinicopathological features and prognosis in this entity is limited. We reviewed 5443 renal biopsies processed at our department, and identified three patients with MIDD associated with membranous features. We evaluated clinicopathological features and outcomes in these patients. All patients had proteinuria, and one patient developed nephrotic syndrome. Renal insufficiency was not observed. Cryoglobulin or monoclonal protein in serum and urine was not detected. A renal biopsy showed thickening of the glomerular capillary walls and spike formation. Tubulointerstitial and vascular alterations were mild or absent. Immunofluorescence studies revealed granular IgG3-kappa deposits in two patients and IgG1-kappa deposits in one patient, along the glomerular capillary walls. Immunofluorescence studies using antibodies specific for gamma-heavy chain Fab containing C(H)1 domain, C(H)2 domain and C(H)3 domain did not show any apparent deletion. On confocal microscopy, glomerular colocalization of light and heavy chains was observed. Electron microscopy showed predominant subepithelial granular deposits without distinct ultrastructural organization. All patients were treated with steroids, and good effects were observed. A follow-up renal biopsy performed in one patient showed histological improvements. No patient developed myeloma or other haematological malignancy during the course of follow-up (mean 44 months). MIDD associated with membranous features is an extremely rare but distinctive entity. Our study suggests glomerular deposition of a nondeleted whole immunoglobulin molecule. Patients with this entity appear to respond well to steroid therapy.
    Nephrology Dialysis Transplantation 08/2008; 23(12):3888-94. DOI:10.1093/ndt/gfn363 · 3.49 Impact Factor
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    ABSTRACT: Recent studies in animal models for systemic lupus erythematosus (SLE) have shown that Toll-like receptors (TLR-7 and TLR-9) and interferon (IFN)-alpha are involved in the pathogenesis of murine lupus. Recent studies using flow cytometry have also shown increased expression of TLR-9 in peripheral blood mononuclear cells (PBMCs) from SLE patients. In this study, we performed quantitative real-time reverse transcription-polymerase chain reaction analyses of PBMCs from 21 SLE patients and 21 healthy subjects, to estimate TLR2, TLR3, TLR4, TLR5, TLR7, TLR8, TLR9, IFN-alpha and LY6E (a type I IFN-inducible gene) mRNA expression levels. Expression levels of TLR2, TLR7, TLR9, IFN-alpha and LY6E mRNAs in SLE patients were significantly higher than those in healthy controls. Expression levels of TLR7 and TLR9 mRNAs correlated with that of IFN-alpha mRNA in SLE patients. These results suggest that up-regulated expression of TLR7 and TLR9 mRNAs together with increased expression of IFN-alpha mRNA in PBMCs may also contribute to the pathogenesis of human lupus.
    Clinical & Experimental Immunology 07/2008; 152(3):482-7. DOI:10.1111/j.1365-2249.2008.03646.x · 3.28 Impact Factor
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    ABSTRACT: A 63-year-old man presented with chronic headache and bilateral hearing loss. A physical examination showed bilateral conjunctivitis. Circulating anti-Cogan peptide antibodies were detected by dot blot analysis. He was diagnosed as having Cogan's syndrome (CS). Steroid therapy led to dramatic improvement of his symptoms and abnormal laboratory findings. During a tapering course of steroid therapy, he suffered from headache. An ophthalmoscopic examination revealed papillary edema. Magnetic resonance imaging of the brain showed hypertrophic cranial pachymeningitis (HCP). After steroid pulse therapy, HCP was improved. To our knowledge, this is the first case of CS complicated with HCP.
    Clinical Rheumatology 06/2008; 27 Suppl 1:S33-5. DOI:10.1007/s10067-008-0841-0 · 1.77 Impact Factor
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    ABSTRACT: We aimed to clarify the relationship between HLA-DRB1(*)1501 and anti-glomerular basement membrane (GBM) antibody-mediated disease in Japanese patients. Samples were collected from 16 anti-GBM antibody-positive patients who were admitted to our department or related hospitals from December 1990 to October 2005. We analysed clinical and laboratory data, kidney biopsy findings, and the HLA-DR phenotypes and HLA-DRB1 alleles of the patients. Among the 16 patients, 15 had HLA-DR15 [the phenotype frequency (PF) was 93.8%], 7 were positive for DR4 (the PF was 43.8%) and 5 were positive for DR9 (the PF was 31.3%). The allele frequency of HLA-DRB1(*)1501 was 46.4% (13/28), which was significantly different from Japanese controls (11.6%) (P < 0.001). In contrast, the frequency of HLA-DRB1(*)1502 was not different from controls (0/28). The odds ratio of HLA-DRB1(*)1501 in these patients was 6.4 (95% CI: 2.4-16.5). The present study demonstrated that Japanese patients with anti-GBM antibody-mediated disease are very likely to carry the HLA-DRB1(*)1501 but not the HLA-DRB1(*)1502 allele.
    Nephrology Dialysis Transplantation 05/2008; 23(10):3126-9. DOI:10.1093/ndt/gfn179 · 3.49 Impact Factor
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    ABSTRACT: It is recently suggested that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is involved in the pathogenesis of systemic lupus erythematosus (SLE). In this study, we examined whether expression levels of TRAIL depend on SLE activity. To estimate TRAIL mRNA expression levels in peripheral blood mononuclear cells (PBMC), we performed quantitative real-time reverse transcription-polymerase chain reaction analyses of PBMC from 18 SLE patients and 20 healthy subjects. Serum soluble TRAIL (sTRAIL) concentrations were measured by an enzyme-linked immunosorbent assay. The mean TRAIL mRNA expression level and serum sTRAIL concentration in SLE patients were significantly higher than those in healthy controls. Expression levels of TRAIL mRNA correlated with the SLE disease activity index and circulating immune complexes levels, while serum sTRAIL concentrations did not. These results indicate that increased expression of TRAIL mRNA in PBMC closely correlates with SLE activity and suggest an important role for TRAIL in the pathogenesis of SLE.
    Clinical Immunology 11/2007; 125(1):26-9. DOI:10.1016/j.clim.2007.05.019 · 3.99 Impact Factor
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    ABSTRACT: Increased serum levels of S100A12, a proinflammatory protein secreted by activated neutrophils, have recently been shown in patients with active inflammatory diseases, such as rheumatoid arthritis and Kawasaki disease. In this study, we investigated serum levels of S100A 12 in patients with small-vessel vasculitis, myeloperoxidase anti-neutrophil cytoplasmic antibodies- (MPO-ANCA) associated pauci-immune glomerulonephritis. Serum S100A12 concentrations were measured by a sandwich enzyme-linked immunosorbent assay (ELISA) in 46 patients with MPO-ANCA-associated glomerulonephritis and 29 healthy controls. We analyzed correlations between serum S100A12 levels and a clinical index of vasculitis activity, the Birmingham Vasculitis Activity Score (BVAS), various laboratory parameters, and pathological activity scores in the patients. We also analyzed changes of serum S100A12 levels in 10 patients after treatment. ELISA showed about 4-fold higher levels of serum S100A12 in patients with MPO-ANCA-associated glomerulonephritis than healthy controls. Serum S100A12 levels correlated with the BVAS scores, the peripheral white blood cell count, levels of serum C-reactive protein and creatinine, and pathological activity scores in the patients, but did not correlate with serum MPO-ANCA titers. Serum S100A12 levels after treatment decreased in all the 10 patients examined. We demonstrated that increased serum S100A12 levels correlate with clinical, laboratory and pathological parameters of disease activity in patients with MPO-ANCA-associated glomerulonephritis. Serum S100A12 level may be one of the useful markers of disease activity in MPO-ANCA-associated glomerulonephritis.
    Clinical nephrology 12/2006; 66(5):315-21. DOI:10.5414/CNP66315 · 1.23 Impact Factor
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    ABSTRACT: A 46-year-old woman developed nephrotic syndrome at the age of 16 in 1973. On the basis of the histological findings of the first renal biopsy, she was diagnosed as having minimal change nephrotic syndrome. Initial treatment with steroid was effective, but she had several relapses during tapering of the daily dose of steroid. The second renal biopsy, performed in 1997, disclosed glomerular lobulation, mesangial proliferation, nodular mesangial lesions, and mesangiolysis. From 2001, the degree of proteinuria increased, with urinary protein being 5 g/day in January 2003, when a third renal biopsy was performed. On light microscopy, the glomerular lesions were similar to those observed in 1997. Immunofluorescence microscopy revealed coarse granular stainings for IgG, IgA, IgM, kappa, lambda, and C3 in the mesangial area and along the capillary walls. On electron microscopy, fingerprint structures were observed in the mesangial and subendothelial deposits. There were no characteristic fibers in the nodular lesions. On the basis of clinical and laboratory findings in this patient, we excluded disease entities in which nodular mesangial lesions, mesangiolysis, and fingerprint deposits had been reported. To our knowledge, such a unique combination of glomerular lesions has not been described previously in the literature.
    Clinical and Experimental Nephrology 07/2006; 10(2):140-5. DOI:10.1007/s10157-006-0412-0 · 1.71 Impact Factor
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    Nephrology Dialysis Transplantation 03/2005; 20(2):434-7. DOI:10.1093/ndt/gfh545 · 3.49 Impact Factor
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    ABSTRACT: Podocyte alpha-actinin-4 (actinin-4) is an essential component of the glomerular filtration barrier. We recently reported that the central rod spectrin-like repeats (R1-R4) of actinin-4 have a high affinity to puromycin aminonucleoside (PAN), which can induce nephro-sis in animals. The aim of this study was to identify endogenous molecules that interact with the actinin-4 R1-R4 domain. To identify such molecules, we performed a bacterial two-hybrid screening of a human kidney cDNA library using as a bait human actinin-4 R1-R4. We further verified the identified interactions by in vitro affinity assays and immunofluorescent studies of cultured human embryonic kidney HEK293 cells. To investigate the expression of the identified molecules in podocytes, in situ hybridization, and immunohistochemical studies were performed. One isolated cDNA from the library encoded humanin, a recently identified antiapoptotic peptide. In vitro affinity assays showed specific interactions of recombinant actinin-4 R1-R4, R1, R2, R3, and R4 proteins with humanin-Sepharose. PAN had no effect on these interactions. Green fluorescent protein-fused humanin and endogenous actinin colocalized mainly in the perinuclear cytoplasm of HEK293 cells. Altered colocalization was not observed by the addition of PAN. In situ hybridization and immunohistochemistry showed the expression of humanin in podocytes. Our results suggest that humanin is a novel binding partner of the actinin-4 R1-R4 domain in podocytes. Humanin and PAN are unlikely to compete for the same binding surface in actinin-4.
    Clinical and Experimental Nephrology 01/2005; 8(4):331-8. DOI:10.1007/s10157-004-0322-y · 1.71 Impact Factor
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    ABSTRACT: Gitelman's syndrome (GS) is an autosomal recessive disorder resulting from inactivating mutations in the thiazide-sensitive Na-Cl co-transporter (NCCT) gene. To date, almost 90 mutations have been identified. It is possible that there is a population-specific distribution of mutations. In this study, we analysed mutations in the NCCT gene of seven Japanese patients with GS. Peripheral blood mononuclear cells were isolated from patients with GS, their family members and healthy control subjects. A mutation analysis of the NCCT gene was performed completely by direct automated sequencing of polymerase chain reaction-amplified DNA products. In patients with a deletion or splice site mutation, we undertook cDNA sequence analysis. We identified nine mutations. Five of them [c.185C>T (Thr60Met), c.1712C>T (Ala569Val), c.1930C>T (Arg642Cys), c.2552T>A (Leu849His) and c.1932delC] have been reported in Japanese patients, but not in GS patients from other ethnic groups. The remaining four mutations [c.7A>T (Met1Leu), c.1181_1186+20del26, c.1811_1812delAT and IVS16+1G>A] were novel. In cDNA derived from a patient with c.1181_1186+20del26, a deletion of exon 9 and a frameshift at the start of exon 10 were observed. In cDNA derived from patients with IVS16+1G>A, an additional 96 bp insertion between exons 16 and 17 was observed. Six out of seven patients were compound heterozygotes, and the remaining one carried a single heterozygous mutation. We found four novel mutations in the NCCT gene in seven Japanese patients with GS. Moreover, our study suggests that the distribution of mutations in the NCCT gene in Japanese GS patients potentially differs from that in other populations.
    Nephrology Dialysis Transplantation 07/2004; 19(7):1761-6. DOI:10.1093/ndt/gfh239 · 3.49 Impact Factor
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    ABSTRACT: Fabry disease is an X-linked recessive disorder resulting from a deficiency of lysosomal alpha-galactosidase A (alpha-Gal A). Chronic renal failure is an important cause of death in patients with Fabry disease. We report on patients with Fabry disease (a hemizygous male and his mother) due to a nonsense mutation (R220X) in the alpha-Gal A gene. The proband, a 41-year-old man, and his 71-year-old mother presented with renal and cardiac manifestations of Fabry disease. Histological examination and molecular analysis of the alpha-Gal A gene were performed. Typical histological findings of Fabry disease were observed in a renal biopsy specimen from the proband and in renal and myocardial necropsy specimens from the mother. Sequencing of a full-length alpha-Gal A cDNA from the proband indicated a C-T transition at codon 220, resulting in substitution of the predictable termination for arginine (R220X). Examination of genomic alpha-Gal A DNA revealed that the proband was a hemizygote and the mother was a heterozygous carrier for the mutation. This is the first detailed report of family members with Fabry disease due to a nonsense mutation (R220X) in the alpha-Gal A gene. Our study indicates that this mutation causes the typical disease in both genders.
    Clinical nephrology 04/2004; 61(3):185-90. DOI:10.5414/CNP61185 · 1.23 Impact Factor
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    ABSTRACT: Several studies have shown a predominant glomerular deposition of IgG4 in patients with idiopathic membranous nephropathy (MN), whereas significant depositions of other IgG subclasses have been shown in patients with lupus-associated MN and bucillamine-induced MN. We examined the distribution patterns of glomerular IgG subclass deposits in 10 patients with malignancy-associated MN (M-MN) and in 15 patients with idiopathic MN by immunofluorescence (IF) microscopy. The glomerular IF intensities of IgG1 and IgG2 were significantly stronger in the malignancy group than in the idiopathic group (P<0.05). In contrast, there were no differences in glomerular IF intensities of IgG3 and IgG4 between the two groups. Our findings suggest that the distribution patterns of glomerular IgG subclass deposits are different in idiopathic MN and M-MN. The strong IF intensity of glomerular IgG1 and IgG2 in M-MN may provide a possible predictor for this condition.
    Nephrology Dialysis Transplantation 04/2004; 19(3):574-9. DOI:10.1093/ndt/gfg616 · 3.49 Impact Factor
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    ABSTRACT: A 61-year-old woman with rheumatoid arthritis (RA) developed small digital ulcers, proteinuria, and hematuria. Serological studies disclosed high titers of antinuclear antibody and rheumatoid factors (RF; IgM-RF and IgG-RF), and an increased level of circulating immune complexes. These findings suggested an active immunological state of RA. A renal biopsy showed periodic acid-Schiff-positive giant deposits in the mesangial area and subepithelial space. Immunofluorescence microscopy revealed strong stainings for IgG, IgA, IgM, Kappa, Lambda, C3, C1q, and fibrinogen in a granular pattern. Electron microscopy showed giant granular deposits (diameter, up to 4.6 micro m) without specific fibrillary structure in the mesangial area and subepithelial space, and partially in the subendothelial space. There were no findings of vasculitis, such as endothelial proliferation or fibrinoid necrosis of small arteries. This is the first report of immune complex-type glomerulonephritis with unusual giant deposits in a patient with RA in an active immunological state.
    Clinical and Experimental Nephrology 04/2004; 8(1):63-7. DOI:10.1007/s10157-003-0262-y · 1.71 Impact Factor

Publication Stats

317 Citations
48.72 Total Impact Points

Institutions

  • 2008–2012
    • Yuri General Hospital
      Honjō, Saitama, Japan
  • 2009
    • Akita General Hospital
      Akita, Akita, Japan
  • 2003–2009
    • Akita University Hospital
      Akita, Akita, Japan
  • 2003–2005
    • Akita University
      Akita, Akita, Japan