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A Yusa

Publications and source records attributed to A Yusa.

12 recordsLinked to original sources
PubMed1998

Significance of leukocyte infiltration in membranous nephropathy with segmental glomerulosclerosis.

AIM: To clarify the role of leukocyte subsets in the development of glomerulosclerosis (GS) and interstitial lesions which may contribute to the prognosis of membranous nephropathy (MN), we investigated infiltrating cells in both glomeruli and interstitium in biopsy specimens. METHODS: Forty-one cases of MN were divided into two groups: MN with segmental GS (MN+GS; n = 21) and MN without GS (MN-GS; n = 20). There was no significant difference between both groups regarding clinical data at the time of the renal biopsy. The cells were analyzed with a three-layer indirect immunoperoxidase method using monoclonal antibodies against leukocyte common antigen, T cells, B cells, and monocytes/macrophages (Mo/Mstraight phi). RESULTS: Renal function tended to deteriorate during the final follow-up period in group MN+GS, but not in group MN-GS. The number of glomerular and interstitial leukocytes in group MN+GS were significantly higher than those in group MN-GS. Leukocytes were mostly Mo/Mstraight phi in the glomerulus, while T cells and Mo/Mstraight phi were predominant in the interstitium. In group MN+GS, there was a significant correlation in number of Mstraight phi (CD68+) between glomeruli and interstitium, but not in group MN-GS. CONCLUSION: The results suggest that Mo/Mstraight phi may play an important role in the development of segmental GS and interstitial lesions in MN which may be responsible for the incurability and poor prognosis.

Adult↗
PubMed1998

[A case of hepatitis C virus associated membranous glomerulonephritis ameliorated by corticosteroid therapy].

We report a 50-year-old male patient with hepatitis C virus (HCV)-associated membranous glomerulonephritis (MN), for which he had been treated with corticosteroid therapy for one and a half years. This patient received blood infusion at 38 years of age. He visited our hospital because of liver dysfunction at 42 years. One year later, proteinuria and microhematuria were pointed out (43 years). Renal biopsy revealed MN with focal fibrocellular crescents. HBsAg, cryoglobulin, rheumatoid factor were all negative. Prednisolone was administered at the dose of 30 mg/day for 4 weeks and tapered subsequently. The steroid treatment was effective (urinary protein excretion: 4.2-->0.3 g/day, serum albumin: 2.4-->4.0 g/dl, 3 months later), and transaminase slightly elevated (GPT 50-->60-80 IU/l). One and a half years later he proved to be positive for HCV antibody, and corticosteroid administration was terminated. Subsequently proteinuria increased, and reached 3.0 g/day 6 years later. However, serological markers and ultrasonographic study for chronic hepatitis revealed mild changes of the liver. These findings suggest that corticosteroid therapy is not contraindicated against HCV-associated MN, and may possibly be used as the treatment for this condition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Mechanism of infiltration and activation of glomerular monocytes/macrophages in IgA nephropathy.

Glomerular deposits of fibrin-related antigens (FRA), C3c, membrane attack complex (MAC) were examined by the immunoperoxidase method on 176 renal biopsy specimens from 120 cases with IgA nephropathy including 56 cases with sequential biopsies. On 47 sets of repeated renal biopsy specimens, the glomerular infiltration of the following immune cells was examined by the indirect immunoperoxidase method; immune cells positive for C3bi receptor (C3biR; CR3/CD11b, CR4/CD11c), HLADR antigen and several leukocyte surface markers (CD45R, CD3, CD15 and CD68). Twenty-four-hour urine protein (UP) at the renal biopsy was also evaluated. The glomerular deposition of FRA was inversely correlated with C3c/MAC deposition (p < 0.00001). Most cases (163 of 176) were classified into the following two types; type C with dominant deposition of C3c (97 cases) and type F with dominant deposition of FRA (66 cases), except for 13 cases with equivalent deposits of C3c and FRA (7 cases, type B) and without C3 or FRA deposits (6 cases, type O). In 56 rebiopsied cases, apparent conversion from type F or C into the other was observed only in one case though a few cases in type C lost or reduced C3c deposition to an equivocal type at the follow-up biopsy, which were included in type C', an expanded category of type C. In the whole cases, the glomerular infiltration of immune cells was significantly correlated with FRA deposition (p < 0.0002) but not with C3c. Glomerular CD11c+ cells were significantly correlated with C3c deposition in type C' (p < 0.0001), but not in type F. Glomerular HLADR positive immune cells were significantly correlated with glomerular CD3+ T cells in type F (p < 0.001), but not in type C'. In type C', UP was significantly correlated with glomerular CD11c+ cells (p < 0.0001) but not with CD 15+ or HLADR+ cells. On the other hand, in type F, UP was significantly correlated with CD 15+ and HLADR+ cells (p < 0.001) but not with CD11c+ cells. These results suggested that there are multiple pathways in inducing glomerular infiltration of immune cells in IgA nephropathy. In type C, local activation of complements might primarily induce immune cell infiltration through C3biR and these C3biR+ cells are involved in inducing proteinuria. On the other hand, in type F, in which complement activation is weak, immune cells might infiltrate directly through their Fc receptor or MHC class II antigens, and might be activated by T-cell/macrophage interaction to induce proteinuria.

Adult↗
PubMed1996

Intercellular adhesion molecule-1/leukocyte function associated antigen-1-mediated and complement receptor type 4-mediated infiltration and activation of glomerular immune cells in immunoglobulin A nephropathy.

Glomerular expression of intercellular adhesion molecule-1 (ICAM1) (CD54) and membrane cofactor protein (MCP; CD46) and positive infiltrating cells in leukocyte function associated antigen-1 (LFA1)alpha (CD11a) and C3bi receptors (CR3/CD11b, CR4/CD11c) were examined by the indirect immunoperoxidase method on 43 sets of repeated renal biopsy specimens from patients with immunoglobulin A nephropathy. Twenty-four-hour urine protein at the time of renal biopsy was also evaluated. Glomerular infiltration of LFA1alpha+ cells was significantly correlated with glomerular expression of ICAM1 (r = 0.494, P < 0.0001). Glomerular complement receptor type 4 (CR4)+ cells were significantly correlated with glomerular expression of MCP (r = 0.405, P < 0.0001). The glomerular expressions of ICAM1 and MCP were significantly correlated with each other (r = 0.700, P < 0.00001). The glomerular infiltrations of LFA1alpha+ and CR4+ cells were highly correlated with each other (r = 0.884, P < 0.00001), and both cell types were significantly correlated with urine protein (respectively, r = 0.426 and 0.478, P < 0.001 and 0.0001). When the change in these parameters between the time of the initial and follow-up biopsies was evaluated, there was a significant correlation between the change in glomerular expression of ICAM1 (DeltaICAM1) and MCP (DeltaMCP) as well as between the change in glomerular infiltration of LFA1alpha+ cells (DeltaLFA1alpha+) and CR4+ cells (DeltaCR4+). Both DeltaLFA1alpha+ and DeltaCR4+ were significantly correlated with the change in urine protein. These findings suggest that ICAM1/LFA1 interaction and MCP-mediated C3bi/C3biR interaction cooperate and participate in persistent glomerular infiltration of immune cells in immunoglobulin A nephropathy, and that these LFA1alpha+ and C3biR+ cells contribute to the induction of proteinuria.

Adult↗
PubMed1996

[Analysis of intraglomerular and interstitial infiltration of leukocytes in membranous nephropathy with focal segmental glomerulosclerosis].

We investigated infiltrating cells in the glomeruli and interstitium in biopsy specimens from 41 cases with membranous nephropathy (MN) and found that 21 had focal segmental glomerulosclerosis (FGS) and 20 did not. There was no significant difference between groups MN +FGS and MN regarding age, interval from onset, serum creatinine level and urine protein excretion when the biopsy was performed. The cells were analyzed with 3-layer indirect immunoperoxidase techniques using monoclonal antibodies to leukocyte common antigen, T cells, B cells and monocytes/macrophages (Mo/M phi). The numbers of leukocytes in both glomeruli and interstitium increased significantly in group MN+FGS as compared to those in group MN, respectively. Most of the leukocytes infiltrating the glomeruli were Mo/M phi, while T cells and Mo/M phi were predominant in the interstitium. There was a significant correlation between the numbers of intraglomerular and interstitial Mo/M phi in group MN+FGS, but not in group MN. Follow-up periods after the biopsy were not significantly different between the groups. At the final points of follow-up, urine protein excretion significantly decreased in group MN, but not in group MN+FGS. In group MN+FGS, serum creatinine levels were twice the level found at the biopsy in 5 cases, and 2 required hemodialysis therapy. Renal functions were not deteriorated in any cases of group MN. These findings suggest that FGS may be one the deleterious factors in MN, which may facilitate the infiltration of Mo/M phi in both glomeruli and interstitium and T cells in the interstitium.

Adult↗
PubMed1995

Participation of CR1 (CD35), CR3 (CD11b/CD18) and CR4 (CD11c/CD18) in membranoproliferative glomerulonephritis type I.

Intraglomerular expression of complement receptors (CR) was investigated chronologically in 22 repeatedly biopsied patients with membranoproliferative glomerulonephritis (MPGN) type I by indirect immunoperoxidase staining using MoAbs. Patients were divided into two groups based on whether intraglomerular C3c deposition was decreased at the second biopsy (2nd Bx) (group A, n = 12), or not (group B, n = 10). At the first biopsy (1st Bx), the severity of glomerular injury and the degree of glomerular C3c deposition were compatible between the two groups. Four patterns of CR1 (CD35) expression on podocytes were recognized: normal; generally decreased; focally/segmentally lost; and completely lost. The numbers of CR3 (CD11b/CD18)- and CR4 (CD11c/CD18)-positive cells per glomerular cross-section were counted. At the 1st Bx, no significant difference was found in the number of CR3+ or CR4+ cells between the two groups. At the 2nd Bx, the numbers of both the CR3+ and CR4+ cells were significantly decreased only in group A (P < 0.01). The numbers of CR3+ and CR4+ cells were significantly higher in cases with moderate or marked C3c deposits than in those with no or mild C3c deposits. The intensity of CR1 expression in group B was less than that in group A at both the 1st and 2nd Bx (1st, P < 0.05; 2nd, P < 0.01), and chronological improvement of CR1 expression was observed only in group A. The severity of glomerular injury was increased only in group B (P < 0.01), and was associated with persistent massive proteinuria and hypocomplementaemia. Our results suggest that, in cases with an adverse outcome, a more severe defect of CR1 initially exists and the expression of CR1 is not recoverable chronologically. This irreversible decrease or loss of CR1 may partly contribute to the continuous C3c deposition and intraglomerular infiltration of CR3+ and CR4+ cells.

Adolescent↗
PubMed1993

Systemic amyloidosis in a patient with adult onset Still's disease.

A 39-year-old woman presented clinical features of adult onset Still's disease. Seven years after the onset, she developed renal insufficiency and biopsy studies revealed amyloid deposits involving amyloid A protein, P component, lambda chain and kappa chain in the kidney and rectum. She died in 1992, primarily due to cardiac failure associated with amyloidosis, indicating that amyloidosis should be considered one of the fatal complications in adult onset Still's disease with a long history.

Adult↗
PubMed1991

Anti-DNA idiotypes deposited in renal glomeruli of patients with lupus nephritis.

Idiotypes (Id) of human anti-DNA antibodies, designated as O-81 Id, were specifically detected on the immune deposits of renal glomeruli in 46% of patients with lupus nephritis. Id-binding to anti-Id antibodies was blocked by free O-81 Id and to some extent by free DNA. DNase or acid buffer treatment failed to reveal new Id determinants on the deposits. O-81 Id and NE-1 Id activity were also detected on the renal eluate-derived IgG, but not IgM from the autopsy cases with lupus nephritis. The incidences of O-81 Id were not associated with histological features in the glomeruli, but the distribution patterns were similar to those of IgG deposits. Our study also showed that 65% to 70% of patients with IgG deposits either in the subendothelium or in the subepithelial area of the glomerular basement membrane (GBM) showed positive tests for O-81 Id. It was also noted that most patients with massive proteinuria had O-81 Id in their glomeruli. It is concluded that O-81 Id deposits are relatively specific for active lupus nephritis and that immunofluorescence studies using anti-Id antibodies may be clinically useful for specifying the renal lesions of systemic lupus erythematosus (SLE).

Antibodies, Anti-Idiotypic↗
PubMed1978

[Residual radioactivity measurement for high purity silicon irradiated by pile-neutron (author's transl)].

Residual radioactivity measurement is described for high purity silicon (purer than tennine) irradiated by pile-neutron to produce n-type silicon semiconductor. The silicon samples were irradiated in four different atomic reactors with thermal neutron fluxes of 0.12, 1.48, 1.8 and 5.5 X 10(13) n/cm2. sec. After irradiation, the sample was dissolved in HF-HNO3, and the solution dried. The residual radioactivity was measured by a 2pi gas-flow low background GM counter. The only active species found was 32P, which was formed by the consecutive reaction of 30Si(n, gamma)31Si beta- leads to 31P followed by 31P(N, GAMMA)32P. The observed production rate for 32P was in good agreement with the calculated one. This technique can be applied to estimate amounts of not only doped phosphorus but impurities such as gold in irradiated silicon. Tail part of a float-zone silicon rod contained about 0.01 atomic ppb of Au, but no activity was observed in its middle part. The present technique is suitable for checking and characterizing silicon rods before their neutron-doping.

Neutrons↗