Biomedical subjects
Publications and source records attributed to Y Nomoto.
The cold-reacting antinuclear factor, specific to kidney tissues, was detected transiently in serum specimens from a diabetic patient during an episode of papillary necrosis. Determination of the cold-reacting antinuclear factor is suggested as being useful in evaluating the degree destruction in kidney tissues.
A study on double immunofluorescent staining of immunoglobulins and complement in IgA-associated immune-complexes of glomerular deposits in patients with IgA nephropathy is described. The components of immune-complexes deposited in kidney tissues included IgA, IgG, IgM, IgE, C3, C3A, properdin, Clq and C4. Although the majority of the deposits consisted of IgA and C3, some deposits showed the coexistence of other classes of immunoglobulins and C3 as well as other types of complement. It was suggested that the immune-complexes deposited in the glomeruli of patients with IgA nephropathy have a polyclonal nature.
One hundred seven cases of open renal biopsy using KAWAMURA-modified forceps have been performed over the past two years under general anesthesia. A sufficient amount of renal tissues for routine histology, immunofluorescence staining and electronmicroscopy were obtained in all 107 cases. There were no complications attributable to the procedure. It is concluded that this procedure using the "KAWAMURA-modified forceps" can be performed easier and faster than the previous techniques of open renal biopsy.
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Follow-up studies on 113 patients with various types of primary glomerular diseases were performed for one to 33 months to determine the clinical spectrum of primary glomerulonephritis. Of those studied, six patients exhibited scleritis. All of these six patients with scleritis were identified as having "IgA nephropathy." None of the patients other than those with IgA nephropathy showed scleritis during the study period. It is suggested that some autoimmune mechanisms similar to the manifestation of IgA nephropathy may be involved in the development of scleritis.
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Aberration of IgA-bearing B lymphocytes in patients with IgA nephropathy has been investigated. Twelve patients with IgA nephropathy demonstrated a marked increase of IgA-bearing lymphocytes in peripheral blood, while ten patients with chronic proliferative glomerulonephritis without mesangial deposition of IgA showed normal amounts of IgA-bearing lymphocytes. The increase of IgA-bearing lymphocytes reflected that of IgA-producing lymphocytes, since lymphocytes obtained from patients with IgA nephropathy restored a high percentage of IgA-bearing cells in vitro after treatment with trypsin. Quantitation of IgA-bearing lymphocytes in peripheral blood is a useful method for screening of patients with IgA nephropathy.
IgA-bearing peripheral blood lymphocytes, serum IgA, urinary sediments and HLA types of patients with IgA nephropathy and members of their families were examined to elucidate whether some familial factors might be related to the development of IgA nephropathy. Ten patients with IgA nephropathy, 31 family members and 36 age-matched healthy persons were examined. All families included certain members with increased amounts of IgA-bearing peripheral blood lymphocytes. The pattern of the emergence of family members with increased IgA-bearing lymphocytes was vertical. Some family members who had increased IgA-bearing lymphocytes showed microhematuria at the time of the study. There was no significant correlation between the amounts of IgA-bearing peripheral blood lymphocytes and levels of serum IgA. HLA types of the ten patients did not show significant deviation from those in the general population. It is suggested that the measurement of IgA-bearing peripheral blood lymphocytes among family members is useful for the screening of patients with IgA nephropathy.
Forty Japanese patients with IgA nephropathy were typed for HLA-A and HLA-B using local antisera. Thirty-seven of these patients were typed for HLA-D using homozygous cells "En", now known to be strongly related to DRw6. Forty-six patients with chronic hemodialysis were used as patient controls for renal disease and 115 healthy individuals were used as normal controls. The frequency of HLA-DEn was significantly increased in 17 out of 37 patients with IgA nephropathy, (46%) (normal controls 18.3%) (P less than 0.0007). Although the occurrence of HLA-B12 was high, it was not significant, i.e. 11 out of 40 (27.5%). These results suggest that some abnormality in the genes of patients with IgA nephropathy is more closely associated with the HLA-D region than the HLA-A or B regions.
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ANF was determined in sera from patients with IgA nephropathy to evaluate the autoimmune nature of this disorder. Sera from 33 patients with IgA nephropathy were assayed for ANF by the FANA technique at 37 degrees and 4 degrees C as well as by a hemagglutination technique. In addition, sera from five patients with lupus nephritis and six patients with idiopathic membranous nephropathy were examined. Thirty healthy adults served as controls. Cold-reacting ANF, which was detected predominantly in the class of IgM, was observed in 81.8% of patients with IgA nephropathy. The nuclear staining pattern was "speckled." Sera from healthy adults did not show any positive signs of ANF, whereas those from patients with lupus nephritis demonstrated "shaggy" pattern of ANF. It is suggested that some autoimmune mechanisms may be involved in the development of IgA nephropathy.
The activity of IgA-specific suppressor T cells was lower in eight patients with IgA nephropathy than in six patients with chronic proliferative glomerulonephritis without glomerular deposition of IgA, two patients with acute glomerulonephritis, or five healthy adult controls. It was determined by the quantitation of immunoglobulins produced from pokeweed mitogen-stimulated B cells cultured with the T cell supernatant (TCS) obtained from concanavalin A-stimulated T cells. Results from a study on an identical twin sister with IgA nephropathy suggested that the decreased activity of IgA-specific suppressor T cells might not be a cause but a result of increased IgA-bearing lymphocytes and serum IgA in patients with IgA nephropathy.
The number of Immunoglobulin-bearing and E-rosette forming peripheral blood lymphocytes, serum levels of immunoglobulins and complement and urinary sediments were examined in patients with idiopathic membranoproliferative glomerulonephritis (MPGN) and their immediate family to determine if familial factors might be related to the development of this disease. Twenty-five patients with MPGN (22 Type I and 3 Type II), 24 family members and 36 age-matched healthy persons were examined. All patients showed an increase in the number of IgM-bearing peripheral blood lymphocytes. All families showed some members with increased numbers of IgM-bearing lymphocytes. There were no significant correlations between the numbers of IgM-bearing peripheral blood lymphocytes and the levels of serum immunoglobulins and complement.
Aberration of IgA-bearing peripheral blood lymphocytes in children with Henoch-Schoenlein purpura has been investigated. Eighteen children with Henoch-Schoenlein purpura demonstrated a marked increase of IgA-bearing lymphocytes in peripheral blood during the acute phase of the disease. The levels of IgA-bearing lymphocytes returned to the normal levels after the acute symptoms of Henoch-Schoenlein purpura had subsided. However, in patients who developed purpura nephritis, the increased levels of IgA-bearing lymphocytes in peripheral blood were retained after the disappearance of purpura, and lasted for more than 12 months. It is concluded that the monitoring of IgA-bearing peripheral blood lymphocytes is useful for the screening of patients with Henoch-Schoenlein purpura and purpura nephritis.
From a series of 152 renal biopsy specimens examined by light, immunofluorescence, and electron microscopy, nine specimens were identified as being from patients with BRH. Histopathologic changes in renal biopsy specimens from most of the 9 patients consisted of either normal or slightly proliferative glomerulonephritis. Characteristic alterations were observed by electron microscopy, which showed the presence of small amounts of electron-dense deposits within the mesangium. In addition, immunofluorescent staining of peripheral blood lymphocytes from patients with BRH and their family members showed an increase of IgA-bearing peripheral blood lymphocytes, and the emergence of microhematuria among the families of patients with BRH indicates that some familial factors may be involved in the development of BRH and IgA nephropathy, which suggests that these two disorders may be closely related.
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Explore the source record for details and available documents.