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T Sugisaki

Publications and source records attributed to T Sugisaki.

At least 19 recordsLinked to original sources
PubMed2001

[A case of Sjögren's syndrome presenting with hypokalemic myopathy due to renal tubular acidosis].

A 37-year-old woman was admitted to our university hospital because of severe flaccid quadriplegia. Her laboratory data, lip biopsy and muscle biopsy findings were compatible with hypokalemic myopathy due to renal tubular acidosis(RTA) type I associated with primary Sjögren's syndrome. Kidney biopsy revealed chronic tubulointerstitial nephritis(TIN), consisting of focal mononuclear cell infiltration with tubulitis, interstitial fibrosis and tubular atrophy. Immunohistochemical analysis of the renal biopsy specimens showed that the infiltrating mononuclear cells were predominantly CD8+T cells, and CD68+ cells(macrophages), whereas CD4+ T cells were fewer in number. Following potassium administration and alkali therapy, hypokalemia and metabolic acidosis were ameliorated and limb palsy gradually subsided. Finally, RTA improved with prednisolon and short term cyclophosphamide treatment without supplemental potassium and alkali therapy.

Acidosis, Renal Tubular↗
PubMed2000

[Serum sickness].

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Anti-Inflammatory Agents↗
PubMed1999

A case of primary antiphospholipid antibody syndrome with acute renal failure showing thrombotic microangiopathy.

An 18-year-old woman complained of fever and edema and was admitted to Showa University Hospital for treatment of thrombocytopenia and deteriorating renal function. Laboratory studies demonstrated the presence of lupus anticoagulant (LA), prolongation of prothrombin time, hemolytic anemia, a negative Coombs' test, the absence of antinuclear antibodies, and a normal fibrinogen level. Renal biopsy revealed mesangial hypercellularity, severe endocapillary cell damage, and double contour of the basement membrane walls. Immunofluorescence studies demonstrated focal, peripheral, and finely granular deposits for IgG, IgM, and IgA but were negative for fibrinogen. Electron microscopy showed glomerular capillary loops with subendothelial widening and subendothelial deposits, mesangiolysis, mesangial interposition, and marked luminal narrowing. Biopsy findings were consistent with thrombotic microangiopathy. The patient was treated with hemodialysis, methylprednisolone pulse therapy, and dipyridamole. After treatment, LA disappeared, the prothrombin time became normal, and renal function improved. The renal lesions in this patient were caused by primary antiphospholipid antibody syndrome. This case strongly suggests an important causal relationship between LA and renal lesions in thrombotic microangiopathy. We present this case to promote understanding of the pathogenesis of primary antiphospholipid antibody syndrome.

Acute Kidney Injury↗
PubMed1998

A case of immunotactoid glomerulopathy with unusual microtubular deposits.

A 57-year-old man with monoclonal gamma-globulinemia was admitted because of edema and proteinuria. A renal biopsy specimen showed lobular glomerulonephritis associated with deposition of material that was positive for IgG, C3, C1q, fibrin, kappa light chain, and lambda light chain but was not stained by Congo red. Glomeruli showed massive electron-dense deposits with two kinds of unusual, highly organized crystalline structures in the mesangial matrix and peripheral capillary loops. Clinically, the patient had nephrotic syndrome, microscopic hematuria, and hypertension. No Bence-Jones protein or cryoglobulin was found in the urine or serum. Immunoelectrophoresis of blood and urine revealed increased IgG-lambda paraprotein, but no free light chains were found. This case was not associated with amyloidosis, systemic lupus erythematosus, light chain deposition disease, cryoglobulinemia, or multiple myeloma. Immunotactoid glomerulopathy was diagnosed. Treatment with oral prednisone was effective for the management of nephrotic syndrome and renal dysfunction. Glomerular deposition of two kinds of microtubular structure in immunotactoid glomerulopathy has rarely been reported.

Glomerulonephritis↗
PubMed1997

[Cryoglobulinemia].

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Cryoglobulinemia↗
PubMed1996

The relationship of adhesion molecules and leukocyte infiltration in chronic tubulointerstitial nephritis induced by puromycin aminonucleoside in Wistar rats.

We studied the expression of adhesion molecules on infiltrating leukocytes and tubular cells in chronic tubulointerstitial nephritis associated with puromycin aminonucleoside (PA) nephrosis. Rats received injections of PA (2 mg/100 g body wt) weekly for the first 3 weeks and every other week thereafter. Rats were killed at 0, 3, 5, 8, and 12 weeks after the start of injections. From the third to the fifth week, the initial infiltrating cells in interstitial tissue were mainly CD4+ T lymphocytes. At the fifth week, ICAM-1, CD44, and hyaluronate were expressed on infiltrating cells in interstitial tissue. At the eighth week, the number of infiltrating cells reached a peak and consisted of T lymphocytes (CD4, CD8) and macrophages (ED1, MHC class II, CD11b, and CD18). The severity of interstitial infiltration was correlated with the degree of proteinuria and with ICAM-1 expression. Our results suggest that CD4+ T lymphocytes may contribute to the production of initial tubular injury. Expression of ICAM-1 helps mononuclear cells migrate to the interstitium. In addition, expression of CD44 and hyaluronate may play important roles in the chronicity of tubulointerstitial nephritis.

Animals↗
PubMed1996

Morphological studies on avian spinal cord chimeras.

Spinal cord chimeras were constructed by orthotopic grafting of quail embryonal neutral folds, neural crest and neural tube into chicken embryos. The spinal cord xenografts were accepted for varying lengths of time, but most chimeras eventually rejected the quail transplant. This was associated with perivenular cuffing and demyelination with preservation of most neurons, as well as clinical neurological symptoms. Twenty-four chimeras were studied to delineate the time of first appearance of glial deposits of immunoglobulin and to identify the subpopulations of T cells in spinal cord infiltrates. The results suggested that deposits of immunoglobulins on glial elements preceded inflammatory cell infiltration. The perivenular cuffs consisted predominantly of T cells and showed a preponderance of CD8- over CD4-positive cells (CD4/CD8 ratios around 0.6). Further, CD4+ cells were found almost exclusively in the central portions of the infiltrate, with the periphery consisting almost only of CD8+ cells. The diffuse cellular infiltrate of the parenchyme contained T and plasma cells. The T cells were almost exclusively CD8+. Plasma cells were seen only at the outer borders of the cuffs and dispersed throughout the quail-derived spinal cord tissue. It seemed that rejection of quail-derived melanocytes in feathers ('quail-like feathers'), described by us earlier, often preceded neurological symptoms and showed a histopathological pattern comparable to spinal cord lesions, i.e., predominantly perivascular cuffing. In preliminary studies, enhancement of disease by immunization with quail organ suspension and decreased intensity of disease by combined immunosuppressive treatment with FK 506 and cycylophosphamide were suggested. The data presented here are compatible with the hypothesis that rejection of CNS quail tissue by chimeras is preceded in the periphery by rejection of melanocytes in segments of skin and in feathers, and that the spinal cord rejection relies on xenoantibodies and on cytotoxic as well as delayed hypersensitivity-type T cells. Finally, these data strengthen the analogy between the histopathologic presentation and immune effector composition of the xenograft rejection lesions in the chimeras and the plaques seen in patients with multiple sclerosis.

Animals↗
PubMed1996

Antibodies to quail erythrocytes in quail-chicken spinal cord chimeras.

Quail-chicken spinal cord chimeras are a model for temporary acceptance followed by rejection of xenografts and also for demyelinating lesions of the central nervous system. The antiglobulin test with quail erythrocytes was employed to detect antibodies in sera of quail-chicken spinal cord chimeras. Sera of all 46 chimeras tested gave positive results. In virtually all instances, antibodies were detected within 10 weeks after hatching and they persisted for all the observation time up to 8 months. The antibodies detected in these tests were directed against species antigens of the quail. They were apparently identical with xenoantibodies described in a previous study, which were detected by indirect immunofluorescence with quail tissue sections; on the other hand, mixed agglutination tests with quail embryonal cell monolayers employed previously had detected a broader spectrum of antibodies that did the antiglobulin tests with quail erythrocytes. The antiglobulin test with quail erythrocytes seems the most cost-efficient and convenient test to monitor xenoantibody formation in this animal model.

Agglutination Tests↗
PubMed1996

Arteritis in a novel congenic strain of mice derived from MRL/Lpr lupus mice: genetic dissociation from glomerulonephritis and limited autoantibody production.

An MRL/Mp strain of mice bearing the Fas deletion mutant gene, lpr (MRL/lpr), spontaneously develop systemic vasculitis and glomerulone phritis in the same individual, and both have been thought to be associated with an increase in circulating immune complexes and autoantibodies. However, the genetic basis of these diseases is poorly understood. A novel recombinant congenic mouse strain, McH5-lpr/lpr, which was established by rearrangement of the genetic background of MRL/lpr mice by hybridization with C3H/HeJ-lpr/lpr mice, developed severe granulomatous polyarteritis, as did the MRL/lpr strain, but not glomerulonephritis. Serum levels of anti-DNA and anti-myeloperoxidase antibodies in these mice were significantly reduced, as compared with MRL/lpr mice, although rheumatoid factors were not. These results indicate that each of these two diseases, arteritis and glomerulonephritis, is under the control of different background gene(s), suggesting a different pathological basis of these diseases, and that anti-DNA and anti-myeloperoxidase autoantibodies appear to have a limited pathogenic role in granulomatous arteritis in the mouse strain described.

Animals↗