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Biomedical subjects

I Shirato

Publications and source records attributed to I Shirato.

At least 91 records · Page 5Linked to original sources
PubMed1991

Increased steady-state levels of mRNA coding for extracellular matrix components in kidneys of NZB/W F1 mice.

The present study was carried out to determine how mRNA levels of extracellular matrix (ECM) components including alpha 1(IV) chain, laminin A, B1 and B2 chains, heparan sulfate proteoglycan (HSPG), alpha 1(I) chain, and alpha 1(III) chain are regulated in the kidney of NZB/W F1 mice. Messenger RNA levels for ECM genes except for laminin A chain increased significantly with the progression of nephritis in NZB/W F1 mice. In the NZW kidneys, however, the mRNA levels for alpha 1(IV) chain, laminin B1 and B2 chains, and HSPG declined markedly with age, whereas those for alpha 1(I) and alpha 1(III) chains showed little difference throughout the experimental period. Messenger RNA levels of beta-actin remained constant, and those of laminin A chain could not be detected in either control or diseased kidneys. Immunofluorescent microscopy showed that the intensity and distribution of staining of collagen IV, laminin, and HSPG in the glomeruli of NZB/W F1 mice increased markedly with the progression of disease. Types I and III collagen were not detected in the glomeruli of NZB/W F1 mice by immunofluorescence until 24 weeks of age, after which increased amounts of these collagens were found in the glomeruli and interstitium with progression of disease. These results suggest that increased levels of mRNA coding for ECM components and increased accumulation of these proteins may contribute to a cascade of events, leading to chronic renal injury in lupus nephritis.

Animals↗
PubMed1991

Modulation of basement membrane component gene expression in glomeruli of aminonucleoside nephrosis.

The present studies were designed to analyze mRNA levels of basement membrane components including collagen IV, laminin, and heparan sulfate proteoglycan (HSPG) in the course of puromycin aminonucleoside (PAN) nephrosis. mRNA levels for alpha 1 (IV) chain; laminin A, B1, and B2 chains; and HSPG were measured in glomeruli of PAN nephrotic rats 0, 2, 8, 14, and 20 days after PAN injection. In the nephrotic stage of PAN nephrosis (on the 8th day), mRNA levels for alpha 1 (IV) chain and laminin A, B1, and B2 chains increased, whereas those for HSPG decreased. The anionic sites in glomerular basement membrane stained by polyethyleneimine were smaller in size and fewer in number in PAN nephrotic rats than they were in control rats. In the remission stage of PAN nephrosis (on the 20th day), however, mRNA levels for alpha 1 (IV) chain and laminin A, B1, and B2 chains decreased, whereas mRNA levels for HSPG increased. Polyethyleneimine aggregates in this stage appeared to be larger and more intense than those in the nephrotic stage. These results indicate that the expression of basement membrane genes for alpha 1 (IV), laminin, and HSPG was abnormally regulated in PAN nephrosis and that this abnormal gene regulation might contribute to the development of proteinuria.

Animals↗
PubMed1990

Detection of 'activated platelets' in the urinary sediments using a scanning electron microscope in patients with IgA nephropathy.

The presence of 'activated platelets' in the urinary sediments was studied by scanning electron microscopy (SEM) in patients with IgA nephropathy. The aim of the present study was to determine if the presence of activated platelets in the urinary sediments is correlated with glomerular injuries in patients with IgA nephropathy. Eleven patients with IgA nephropathy, 5 patients with thin basement membrane syndrome and 5 patients with membranous nephropathy were examined. The presence of platelets in glomeruli was also examined by immunofluorescence (IF). This study showed a correlation between the presence of activated platelets in the urinary sediments and the severity of glomerular injuries in patients with IgA nephropathy. The platelets were observed focally in glomeruli from such patients. It was suggested that the detection of activated platelets in the urinary sediments is useful in evaluating the degree of histopathological changes and/or prognosis of IgA nephropathy.

Blood Platelets↗
PubMed1990

[A case of Alport syndrome diagnosed by immunofluorescence using a newly defined monoclonal antibody].

We report a case of Alport syndrome. The patient, a nine-year-old boy, showed macroscopic hematuria after an upper respiratory infection seven years ago. Microscopic hematuria with proteinuria was pointed out in routine urinalysis at school. He had no apparent familial history of either progressive renal diseases or deafness. Renal biopsy was performed at the age of eight, and he was diagnosed as focal segmental glomerulonephritis (mild) by light microscopy. Slight irregular thickening of the glomerular basement membrane (GBM) was observed focally by electron microscopy. Both light microscopy and electron microscopic examinations did not indicate a hereditary nephritis. The 28-kilodalton (kDa) monomers of the non-collagenous globular domain (NC-1) of type IV collagen were absent along renal glomerular capillary walls from the patient by indirect immunofluorescence while they were normally observed in glomerular capillary walls from healthy subjects and patients with a variety of non-hereditary glomerulonephritis. It was suggested that immunofluorescence using a monoclonal antibody for the NC-1 domain of type IV collagen is useful in the precise diagnosis of the patients with Alport syndrome.

Antibodies, Monoclonal↗
PubMed1990

A case of Wegener's granulomatosis showing a dramatic response to corticosteroid and cyclophosphamide therapy--evaluation of anticytoplasmic antibodies (ACPA) in serum samples.

A case of Wegener's granulomatosis with renal dysfunction is described. Granulomatous lesions of the lung, left eyelid and left leg, and chronic sinusitis were observed at the time of admission. Renal and skin biopsy specimens revealed typical features of Wegener's granulomatosis on light microscopy and immunofluorescence microscopy. A dramatic response occurred following corticosteroid and cyclophosphamide therapy, characterized by improvement of proteinuria and renal function, and disappearance of the granulomas and 67gallium citrate accumulations in both the eyes and nose. Furthermore, the levels of anticytoplasmic antibodies (ACPA) in the serum samples were significantly decreased after such therapy. It appears that combined therapy with corticosteroid and cyclophosphamide can be effective in improving proteinuria and renal dysfunction, and in reducing of ACPA in patients with Wegener's granulomatosis.

Autoantibodies↗
PubMed1989

Detection of anionic sites and immunoglobulin A deposits in the glomerular capillary walls from patients with IgA nephropathy.

A study of anionic sites in the glomerular basement membrane (GBM) from patients with immunoglobulin A (IgA) nephropathy is described. The relationship between the deposition of IgA and the detection of glomerular extracellular components, i.e., noncollagenous (NC-1) domain of Type IV collagen, in the glomerular capillary walls was examined by double immunofluorescence. Renal biopsy specimens from patients with IgA nephropathy were immersed in polyethyleneimine (PEI) as a cationic probe and then examined by electron microscopy. Renal specimens were also incubated with mouse monoclonal anti-NC-1 domain of Type IV collagen and then stained with fluorescein isothiocyanate (FITC)-labelled goat antimouse Ig antiserum. After these reactions, sections were stained with rhodamine-labelled rabbit antihuman IgA antiserum. GBM subepithelial anionic sites marked by PEI were altered by the deposition of electron-dense deposits (EDD) in patients with IgA nephropathy and there was a significant correlation between the levels of proteinuria and the incidence of EDD in the GBM in such patients. Marked proteinuria was observed in patients who showed loss of anionic sites in the GBM by electron microscopy. By double immunofluorescence, IgA was shown to be focally deposited outside the NC-1 domain of Type IV collagen-detected regions in the same patients. The authors concluded that high levels of proteinuria might be due to alterations of the size barrier and/or anionic sites of GBM in the moderate stage of IgA nephropathy.

Basement Membrane↗
PubMed1989

Computer imaging analysis of glomerular extracellular components in patients with IgA nephropathy.

Computer imaging analysis was used for quantitative evaluation of the extents, amounts and distributions of glomerular extracellular components, such as the 7S and NC-1 domains of type IV collagen, laminin (LN), fibronectin (FN) and IgA, in glomeruli from patients with IgA nephropathy. Renal biopsy specimens from 13 patients with IgA nephropathy were incubated with mouse monoclonal antibodies against the FN or non-collagenous (NC-1) domain of type IV collagen or polyclonal antiserum against the LN or 7S domain of human type IV collagen, and then stained with appropriate dilutions of FITC-labeled anti-mouse Ig antisera. Marked staining of the 7S or NC-1 domain of type IV collagen, LN or FN was detected in the glomerular capillary walls and/or mesangial areas in patients with IgA nephropathy. In particular, a prominent increase of FN was observed in the subendothelial regions of glomerular capillary walls, i.e. mesangial interposition, in the moderate or advanced stage of IgA nephropathy. Therefore, computer imaging analysis was shown to be useful for the quantitative determination of such components distributed in glomeruli from patients with IgA nephropathy.

Complement C3↗
PubMed1989

A case of acute tubulointerstitial nephritis and uveitis syndrome with a dramatic response to corticosteroid therapy.

A 23-year-old female with acute renal failure associated with acute tubulointerstitial nephritis and uveitis is reported. Renal tubular acidosis and inflammatory reactions consisting of markedly increased erythrocyte sedimentation rate and high serum immunoglobulin levels were seen on admission. Light microscopy revealed infiltration of mononuclear cells in the interstitium. Immunofluorescence of renal tissues was negative in staining for immunoglobulins, fibrinogen, and complement components. Bone marrow specimens did not show any granulomatous lesions. The etiology of this tubulointerstitial nephritis and uveitis syndrome was not clear. Immunological evaluation showed a slight decrease of the OKT4/OKT8 ratio in the peripheral blood. OKT8- and OKM1-positive cells had infiltrated diffusely into the renal interstitium. Acute tubulointerstitial nephritis and uveitis responded dramatically to steroid therapy. It was suggested that immunological factors might correlate with the onset and/or development of this syndrome. It is indicated that high-dose steroid therapy might be useful for patients with acute interstitial nephritis and uveitis.

Adult↗
PubMed1989

[An elderly patient with IgD myeloma associated with renal amyloidosis and acute renal failure].

A 83-year-old male patient with IgD myeloma associated with renal amyloidosis and acute renal failure is described. We also reviewed the clinicopathological findings of IgD myeloma in the literature. Although hemodialysis was performed 36 times for acute renal failure, he died of severe gastrointestinal bleeding. Renal necropsy specimens revealed typical features of amyloidosis in light microscopic, electron microscopic and immunofluorescent examinations. The levels of serum IgD (755 mg/dl), immunoelectrophoresis, and immunofluorescence of bone marrow and renal specimens were consistent with IgD myeloma (lambda type). IgD myeloma is generally considered to be a rare disease of juvenile onset and is complicated with extramyelogenic tumors according to previous reports. However, IgD myeloma without extramyelogenic tumors occurred in a 83-year-old patient reported here. It appears that advanced age onset IgD myeloma associated with renal amyloidosis and acute renal failure is rare. This was the oldest case of IgD myeloma we examined.

Acute Kidney Injury↗
PubMed1989

[Comparative studies of clinicopathological findings in patients with adult and juvenile onset of IgA nephropathy].

Comparative studies of clinicopathological findings were carried out in 89 patients with adult and juvenile onset of IgA nephropathy. Among 89 patients with IgA nephropathy, there were 42 patients with juvenile onset, i.e less than 19 years old, and 47 patients with adult onset, i.e. more than 35 years old. Clinical activities of both groups were examined as follows; urinary protein, mean blood pressure renal function (PSP 15 min, Ccr) and serum IgA (s-IgA). The histology of renal tissues was also examined by light microscopy and immunofluorescence in both groups. The levels of mean blood pressure or s-IgA in patients with adult onset group were significantly higher than those in patients with juvenile onset group (p less than 0.001). The levels of Ccr in patients with adult onset group were markedly decreased. The patients with more than 1.0g/day of proteinuria and more than 110 mmHg of mean blood pressure showed severe proliferative glomerular injuries by light microscopy. It is suggested that the patients with adult onset of IgA nephropathy show severe progressive and/or exacerbating factors during the clinical course.

Adolescent↗
PubMedDate not supplied

A case of neuroleptic malignant syndrome with acute renal failure after the discontinuation of sulpiride and maprotiline.

A 46-year-old man developed neuroleptic malignant syndrome with acute myoglobinuric renal failure after the discontinuation of sulpiride and maprotiline treatment. He showed the characteristic features of hyperpyrexia, altered consciousness, muscle rigidity, and autonomic dysfunction. Laboratory data showed lysis of skeletal muscle cells and renal impairment. Muscle biopsy revealed necrosis and regenerative changes in muscle fibers. Renal biopsy showed focal tubulitis and interstitial infiltration of small inflammatory cells. The combination of sulpiride and maprotiline has not previously been reported to be the cause of neuroleptic malignant syndrome and acute myoglobinuric renal failure.

Acute Kidney Injury↗