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Biomedical subjects

S Kagami

Publications and source records attributed to S Kagami.

At least 55 records · Page 3Linked to original sources
PubMed1996

Possible role for a polysaccharide antigen shared between Streptococcus pyogenes and S. mutans in the pathogenesis of poststreptococcal glomerulonephritis.

Streptococcus mutans has been shown to share a polysaccharide (PS) antigen with S. pyogenes strains isolated from patients with acute poststreptococcal glomerulonephritis (PSGN), using a monoclonal antibody f-77 reactive with the PS. To investigate the pathogenetic role of the shared PS in PSNG, experimental nephritis was induced in animals. Rats were immunized thrice with heat-killed cells of S. mutans or S. pyogenes, followed by an intravenous injection of live cells of S. pyogenes. Histologic examination showed that both animal groups had comparable degrees of diffuse proliferative nephritis characterized by immune deposits. The shared PS antigen was detected in glomeruli of all nephritic rats by immunofluorescence using monoclonal antibody f-77. Furthermore, all nephritic rats had an elevated antibody titer to the shared PS antigen. These results suggest that prior sensitization (infections such as dental caries) to S. mutans modulates immune responses to subsequent S. pyogenes infections and induces immune-complex disease (PSGN) through the shared PS antigen.

Acute Disease↗
PubMed1996

Detection of hepatitis C virus core protein in the glomeruli of patients with membranous glomerulonephritis.

Two Japanese patients suffered from membranous glomerulonephritis associated with hepatitis C virus (HCV) infection. Renal histologic changes were characterized by granular deposits of IgG and C3 along the capillary wall and numerous subepithelial deposits in glomeruli. Hypocomplementemia was present in one patient, but both cryoglobulins and rheumatoid factors were absent. HCV RNA was detected in both their sera by RT-PCR, both free and in the form of circulating immune complexes. The HCV core protein was found in the glomeruli from both patients by indirect immunofluorescence. These results suggest that in some patients chronic HCV infection causes membranous glomerulonephritis through immune complex deposition involving HCV proteins.

Aged↗
PubMed1995

Acute interstitial nephritis and uveitis with bone marrow granulomas and anti-neutrophil cytoplasmic antibodies.

Acute interstitial nephritis (AIN) and uveitis of unknown etiology developed in a 15-year-old girl. Symptoms and urinary abnormalities improved spontaneously but moderate renal dysfunction and anterior uveitis persisted. A repeat biopsy performed 2 years later showed focal tubulointerstitial changes, while bone marrow examination revealed granulomas. Simultaneously, antineutrophil cytoplasmic antibodies (ANCA) were detected, and decreases in T cell population and lymphocyte function were found. These immunological abnormalities normalized in parallel with clinical improvement with corticosteroid therapy, strongly suggesting that in some patients autoimmune disorders contribute to the pathogenesis of the disease.

Acute Disease↗
PubMed1995

Streptokinase gene variable region classification in streptococci: lack of correlation with post-streptococcal glomerulonephritis.

To investigate a possible causal role of streptokinase (SKase) in acute post-streptococcal glomerulonephritis (APSGN), the major variable region of SKase genes of Streptococcus pyogenes strains isolated from patients with and without APSGN were analyzed using the polymerase chain reaction, restriction enzyme analysis and the direct sequencing of SKase genes. In the APSGN-associated strains, six of nine revealed mutant classes corresponding to the nephritogenic classes I and II proposed by Johnston et al. [1992], the remaining three belonged to non-nephritogenic classes. In twenty strains not associated with APSGN, seventeen belonged to classes I and II, while three were from other classes. The major variable region of the SKase gene shows no apparent relation with induction of APSGN in humans, suggesting that unique classes of streptococcal SKase do not play a role in the pathogenesis of APSGN.

Adolescent↗
PubMed1994

Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor-beta expression in rat glomerular mesangial cells.

Angiotensin II (Ang II) has been implicated in the development of progressive glomerulosclerosis, but the precise mechanism of this effect remains unclear. In an experimental model, we have shown previously that TGF-beta plays a key role in glomerulosclerosis by stimulating extracellular matrix protein synthesis, increasing matrix protein receptors, and altering protease/protease-inhibitor balance, thereby inhibiting matrix degradation. We hypothesized that Ang II contributes to glomerulosclerosis through induction of TGF-beta. Ang II treatment of rat mesangial cells in culture increased TGF-beta and matrix components biglycan, fibronectin, and collagen type I at both the mRNA and protein levels in a time- and dose-dependent manner. Saralasin, a competitive inhibitor of Ang II, prevented the stimulation. Ang II also promoted conversion of latent TGF-beta to the biologically active form. Coincubation of mesangial cells with Ang II and neutralizing antibody to TGF-beta blocked the Ang II-induced increases in matrix protein expression. Continuous in vivo administration of Ang II to normal rats for 7 d resulted in 70% increases in glomerular mRNA for both TGF-beta and collagen type I. These results indicate that Ang II induces mesangial cell synthesis of matrix proteins and show that these effects are mediated by Ang II induction of TGF-beta expression. This mechanism may well contribute to glomerulosclerosis in vivo.

Angiotensin II↗
PubMed1994

Evaluation of laboratory parameters reflecting activity of lupus nephritis in children: indicators of severe renal lesions.

Assessment of activity of lupus nephritis is critical in the management and ultimate prognosis of patients. Clinical and laboratory data of 18 children with lupus nephritis were examined to determine what factors reflect activity of renal lesions. Using a histologic scoring system with an activity index (AI) and a chronicity index (CI), correlations between histologic scores and laboratory parameters were analyzed. Serum total protein, albumin and complement at the time of renal biopsy inversely correlated with the AI, but not parameters correlated with the CI. Serum complement levels correlated inversely with the amount of glomerular immune deposits, while the AI and CI correlated with the amount of immune deposits. These results suggest that hypoalbuminemia and hypocomplementemia are indicators of severe, active lupus nephritis, pointing to the need for early renal biopsy and intensive therapy.

Adolescent↗
PubMed1994

[Clinico-pathological study of carried-over patents with Henoch-Schönlein nephritis].

Fifty-two (49.5%) of 105 children with Henoch-Schönlein purpura developed nephritis. Eleven (21.1%) of 52 nephritic patients were carried over beyond childhood, while 21 (40.4%) cases had normalized urinalyses in childhood. The carried-over patients had a higher incidence of severe proteinuria and tubular atrophy compared to those of patients with normalized urinalyses (p < 0.05). These results suggest that patients with severe proteinuria and tubular atrophy tend to have persistent urinary abnormalities beyond childhood.

Adolescent↗
PubMed1994

Integrins.

Explore the source record for details and available documents.

Amino Acid Sequence↗
PubMed1993

Coordinated expression of beta 1 integrins and transforming growth factor-beta-induced matrix proteins in glomerulonephritis.

BACKGROUND: Extracellular matrix remodeling after tissue injury involves both cell-cell and cell-matrix interactions. Integrins are matrix receptors that play a central role in such interactions, and transforming growth factor-beta (TGF-beta) is known to be a strong modulator of their expression. Our previous work has shown that in the anti-thymocyte serum-induced model of glomerulonephritis in the rat, elevated glomerular production of TGF-beta is a causal factor in matrix accumulation. Here we present data on the expression and distribution of glomerular beta 1 integrins in experimental glomerulonephritis. EXPERIMENTAL DESIGN: Metabolic labeling, immunohistochemical, and immunoprecipitation techniques were used on kidney glomeruli from normal rats and from rats over the course of glomerulonephritis induced by administration of anti-thymocyte serum. Changes in beta 1 subunit-containing integrins and the extracellular matrix components that serve as ligands for these integrins were characterized. RESULTS: The data indicate that expression in glomeruli of alpha 1, alpha 5, and beta 1 subunits paralleled both mesangial content of the ligands for the alpha 1 beta 1 and alpha 5 beta 1 integrins, laminin, collagen and fibronectin, and TGF-beta 1 protein; increasing on day 7 of disease and decreasing toward normal by day 28. The alpha 3 subunit displayed the opposite pattern. Exogenous TGF-beta, but not other cytokines, stimulated synthesis of alpha 1 beta 1 and alpha 5 beta 1 integrins by normal glomeruli. CONCLUSIONS: The data indicate that glomerular beta 1 integrin expression is altered in a manner that would promote cell adhesion to the matrix proteins known to accumulate in this disease model. The data further suggest that TGF-beta is responsible for these changes.

Acute Disease↗
PubMed1992

A monoclonal antibody (1G10) recognizes a novel human mesangial antigen.

We have identified a unique mesangial matrix protein of the human glomerulus by using a monoclonal antibody, 1G10, generated against culture human glomerular cells. By immunofluorescence, the antigen recognized by 1G10 (1G10 antigen) is present in mesangium and smooth muscle tissue and cannot be detected in any other tissue examined. Immunoelectron microscopy of glomeruli indicated that 1G10 antigen is present exclusively in the mesangial matrix at the endothelial-mesangial interface. The 1G10 antigen is also expressed by cultured mesangial cells, but not by cultured glomerular epithelial cells, umbilical endothelial cells or fibroblasts. 1G10 did not react with the mesangial matrix proteins [fibronectin (FN), laminin (LAM), collagen types I, III, IV, V, and VI (Col I, III, IV, V, VI), heparin sulfate proteoglycan (HSPG), or thrombospondin (TS)] present under normal and diseased states or smooth muscle antigens (myosin, actin), but did react with a 4 M urea extract of renal cortex and a 0.3% deoxycholate extract of isolated glomeruli. Two dimensional immunoblot analysis using the urea extract demonstrated the binding of 1G10 to an approximately 200 KDa polypeptide with pI 6.0. On one dimensional immunoblot this band did not show cross react with polyclonal antisera to FN, LAM, Col IV, V, VI, HSPG or TS. This mesangial matrix component is trypsin and periodate sensitive, suggesting that it has the character of glycoprotein. In renal biopsy specimens from patients with mesangial proliferative glomerulonephritis (GN) and membranoproliferative GN, the expression of the 1G10 antigen increased along with mesangial hypercellularity or increased accumulation of mesangial matrix, but decreased in completely sclerosed glomeruli. No significant changes in 1G10 antigen expression was observed in membranous GN or minimal change nephrosis compared to normal glomeruli. This study suggests that the 1G10 antigen may not only be a useful marker for the clinical assessment of GN, but may also serve as a potential tool for the study of the pathogenesis of glomerular diseases characterized by cellular proliferation and mesangial matrix expansion.

Animals↗
PubMed1991

Acute tubulointerstitial nephritis associated with Yersinia pseudotuberculosis infection.

Two siblings infected with Yersinia pseudotuberculosis suffered from acute renal failure about 2 weeks after the onset of the disease. Renal histology in both siblings showed acute tubulointerstitial nephritis. Yersinia pseudotuberculosis type VB was isolated from feces of one of them, antibodies to Yersinia pseudotuberculosis type VB in their sera were elevated. The results of the present study suggest that acute renal failure complicating infections with Yersinia pseudotuberculosis is due to acute tubulointerstitial nephritis.

Acute Kidney Injury↗
PubMed1990

IgA nephropathy in Japanese children and adults: a comparative study of clinicopathological features.

A comparative clinicopathological study was retrospectively performed in 61 children and 51 adults with IgA nephropathy. Hematuria and/or proteinuria as a chance finding was the most common initial clinical sign, being observed in 82.0% of the children and in 52.9% of the adults. At renal biopsy, hypertension and severe proteinuria were found in 9.8 and 33.3% of the adults and in 0 and 14.8% of the children (both p less than 0.05), respectively. Elevations of blood urea nitrogen and serum creatinine were found at this time of biopsy in 21.6 and 9.8% of the adults, but in none of the children (p less than 0.001 and p less than 0.05, respectively). Histologically, focal glomerulosclerosis and tubular atrophy were found in 52.9% of the adults and in 32.8% of the children (p less than 0.05). However, some features of the disease seen in both groups were similar, including the incidences of IgA nephropathy, sex ratio, the mode of onset, incidences of gross hematuria, and high IgA levels in the sera. Furthermore, the relationships between the severity of proteinuria and renal lesions were similar: mesangial proliferation, glomerulosclerosis, and tubular atrophy increased with the degree of the severity of proteinuria. These results suggest that IgA nephropathy is essentially identical in children and adults, although adult patients tend to be further advanced in their disease course at the time of diagnosis, and that focal glomerulosclerosis with tubular atrophy is correlated with deterioration of renal function.

Adult↗
PubMed1990

Mechanism of formation of subepithelial electron-dense deposits in active in situ immune complex glomerulonephritis.

The influences of the epitope density on cationic antigens on the fate of immune reactants and the formation of subepithelial electron dense deposits (EDD) were studied in a model of active in situ immune complex glomerulonephritis (ICGN), using a hapten-carrier system. Three weeks after immunization with trinitrophenol conjugated bovine serum albumin (TNP17.3-BSA), the left kidneys of rats were perfused with 500 micrograms of TNP6.2-cationized human immunoglobulin G (C-HIgG) or TNP31.3-C-HIgG. The renal tissues were then examined at intervals by light, immunofluorescence, and electron microscopies. The perfused kidneys of rats given high-valency antigens (TNP31.3) showed marked subepithelial EDDs with foot process retraction associated with proteinuria. In contrast, those of rats given low-valency antigens (TNP6.2) showed only small subepithelial EDDs beneath the slit membrane, which consisted of apparently normal epithelial cells, and did not develop proteinuria. Kinetic studies on immunofluorescence showed that glomerular depositions of immune reactants (TNP-carrier conjugate, rat IgG, and C3) were present longer in rats treated with high-valency antigens than in those treated with low-valency antigens. We conclude that the epitope density on cationic antigens strongly influences the retention of immune reactants and the formation of subepithelial EDDs, as well as development of glomerular injury.

Animals↗
PubMed1990

[Clinical study on norfloxacin in children].

Norfloxacin (NFLX, AM-715), a new synthetic antibacterial agent, was administered to 18 child patients with infectious diseases. The patients included 5 boys and 13 girls from 3 to 14 years of ages. They were given orally dosage ranging 5.2-17.9 mg/kg/day for 4 to 14 days. Clinical efficacies were excellent in 1 case, good in 16 cases, unknown in 1 case, hence the total efficacy rate was determined to be 100%. There were no cases which showed side effects of the drug and no abnormal laboratory test values were observed during the treatment.

Administration, Oral↗
PubMed1989

Hapten-specific cellular immune response producing glomerular injury.

A new model of experimental glomerulonephritis (GN) in which a cell-mediated (delayed-type) reaction predominated was established. Cationized TNP-BSA conjugates were planted in the kidney of rats by perfusion via the renal artery. Rats which had been sensitized with the TNP hapten 7 days previously revealed marked exudative and proliferative changes in their glomeruli, accompanied by transient proteinuria. A cellular influx was seen without deposition of any autologous antibody. The resulting data are compatible with the idea that cell-mediated immune reactions can participate in tissue damage in glomerular disease.

Animals↗
PubMed1989

Ultrastructural alterations of glomerular anionic sites in IgA nephropathy.

The ultrastructural alterations of glomerular anionic sites were studied in biopsy specimens from 34 patients with IgA nephropathy using polyethyleneimine (PEI). Prominent common findings in the glomeruli of the patients were few PEI particles in electron dense deposits in the mesangial and subepithelial area and marked reduction in glomerular anionic sites covered with deposits. The anionic sites of the glomerular basement membrane (GBM) and epithelial cell surface coat (ESC) appeared unaltered in the patients with hematuria and/or mild proteinuria. But in patients with proteinuria in the nephrotic range, focally discrete loss of anionic sites in the lamina rara externa (LRE) was seen and the number of anionic sites of the ESC were decreased with retraction of the foot processes. The anionic sites of the lamina rara interna showed much less change in these patients. Subepithelial deposits were often seen concomitantly with focal loss of anionic sites in the LRE at the site of the deposits, but subendothelial deposits had little influence on the anionic sites of the neighboring GBM. The anionic sites of GBM that showed focal thinning with small GBM projections were appreciably decreased in number, but those in split GBM were not decreased. These results suggest that either loss of the negative charge on the glomerular capillary wall associated with subepithelial immune deposition or morphological changes of the GBM contribute to the progression of proteinuria in IgA nephropathy.

Adolescent↗