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K Kanatsu

Publications and source records attributed to K Kanatsu.

At least 37 records · Page 2Linked to original sources
PubMed1987

Clinicopathological study of patients with mesangial isolated C3d deposition in various glomerular diseases.

The clinicopathological findings of isolated mesangial C3d deposition in the absence of other complement components or immunoglobulins are summarized. 55 out of 242 individual human renal biopsies examined by immunoperoxidase microscopy had isolated C3d deposition. This group consisted of 12 patients with chronic glomerulonephritis, 8 with minimal-change nephrotic syndrome, 32 with benign recurrent hematuria, 2 with Bartter's syndrome and 1 with Raynaud's syndrome. None of these patients had a disorder of the renal function and in all the patients the disease took a benign clinical course. Light-microscopic findings indicated injuries ranging from minor glomerular abnormality to mild diffuse mesangial proliferative glomerulonephritis, and there were no other remarkable findings such as cellular crescents, global sclerosis or interstitial infiltration. By immunoperoxidase microscopy, fine granular deposits of C3d were identified only in the mesangium, and arteriolar C3 staining was seen in 31 of the 55 patients. In 38 of the 42 patients examined by electron microscopy, electron-dense deposits were identified in the mesangial matrix. These findings suggest that isolated C3d deposition is a new entity with benign features both clinically and pathologically.

Adolescent↗
PubMed1986

Dynamic changes in plasma inactive renin levels in Bartter's syndrome after administration of captopril and angiotensin II.

Changes in plasma active and inactive renin concentration (ARC and IRC) after captopril administration and angiotensin II (AII) infusion were studied in six patients with Bartter's syndrome. A single oral dose of captopril (8-25 mg) lowered the blood pressure and increased both ARC and IRC. AII infusion elevated blood pressure, suppressed ARC and increased IRC. In this syndrome of high renin levels, infused AII appeared to increase inactive renin secretion by reducing its conversion to active renin. On the other hand, an acute fall in AII levels and/or renal perfusion pressure by captopril increased both active and inactive renin. This indicates that the increase in the secretion of inactive renin, stimulated by captopril, might exceed any increase in its conversion to active renin in patients with Bartter's syndrome, in whom the production of renin is accelerated, and conversion of inactive renin to active renin probably already operates near its maximum.

Adolescent↗
PubMed1984

Detection of IgA class circulating immune complexes bound to anti-C3d antibody in patients with IgA nephropathy.

IgA class circulating immune complexes (CIC) were detected by solid-phase fluorescent enzyme immunoassay of F(ab')2 anti-C3d antibody in the serum of 52 patients with IgA nephropathy. Conglutinin (Kg) binding IgA class CIC were also measured, and results by these assays were compared. Kg binding IgA class CIC and anti-C3d binding IgA class CIC were detected in 27% and 44%, respectively, of the patients with IgA nephropathy. Either or both of the two were found in 65% of the patients. There was no significant correlation between IgA class CIC detected by these methods and serum IgA. Although all samples with a very high level of anti-C3d binding IgA class CIC did not also have a very high level of Kg binding IgA class CIC, there was a slight quantitative correlation between the 2 assays. Ultracentrifugation analysis showed that anti-C3d binding IgA class CIC were of various sizes between polymeric (21 S) and monomeric IgA (7 S), whereas Kg binding IgA class CIC were mostly monomeric IgA (8 S) with a minor component of heavy fractions (14 S). Both IgA class CIC fixed iC3b and IgA class CIC fixed C3d are present in IgA nephropathy. These observations suggest that the different types of complement bound to IgA class CIC have different roles in IgA nephropathy.

Antigen-Antibody Complex↗
PubMed1984

Immunoelectron microscopic studies of IgA nephropathy.

Immunoelectron microscopy was used in this study of IgA nephropathy to examine the relationship between immune deposits and electron-dense deposits seen by electron microscopy, and these findings were correlated with the severity of mesangial proliferation. Immunoelectron microscopic studies for antihuman gamma-chain, alpha-chain, mu-chain, C3, and C3d were performed by the method of Nakane in 16 patients with IgA nephropathy. The patients with minimal glomerular involvement and focal proliferative glomerulonephritis showed electron-dense reaction products of IgA in the paramesangial area, while the patients with diffuse proliferative glomerulonephritis showed electron-dense reaction products of IgA throughout the enlarged mesangial matrix. Immunoelectron microscopy showed electron-dense reaction products of IgA at the same locations as the electron-dense deposits seen on electron microscopy. C3 deposits were identified in 15 out of the 16 patients, but were less dense than IgA deposits. Electron-dense reaction products of C3 contained both positive and negative sites in 7 patients. Extensive C3d deposits were found in all cases in association with IgA deposits. The locations of these deposits were the same as those of the IgA deposits. These findings suggest that C3 deposits dissociate from the immune deposits and that the locations of the immune deposits correlate well with the severity of mesangial proliferation.

Biopsy↗
PubMed1984

Demonstration of C3d deposits in membranous nephropathy.

An immunoperoxidase technique for light microscopy was carried out in 16 patients with idiopathic membranous nephropathy in order to determine the role of the complement system in glomeruli. Although C3 deposits are found in 50% of the cases, C3d deposits are identified in all cases in association with IgG deposits. This suggests that C3 deposits are degraded and dissociated from immune complexes. Patients with glomerular C3 deposits showed more proteinuria than those without glomerular C3 deposits. The presence of C3 deposits indicates the importance of proteinuria in human membranous nephropathy.

Antigen-Antibody Complex↗
PubMed1984

High level of plasma inactive renin in Bartter's syndrome.

In 10 cases of Bartter's syndrome, plasma active and inactive renin (AR and IR) were measured by two different methods. First, plasma renin activity (PRA), and total renin activity (TRA) after activating IR with trypsin, were measured by radioimmunoassay (RIA) of angiotensin I (AI) generated from endogenous substrate. And secondly, plasma active renin concentration (ARC) and total renin concentration (TRC) were measured by RIA of AI generated in the presence of an excess of exogenous substrate. The difference between TRA and PRA, and between TRC and ARC were designated as inactive renin activity (IRA) and inactive renin concentration (IRC), respectively. Small amounts of IRA were found only in 2 cases and no IRA in 8 cases. However, the existence of large amounts of IR in Bartter's syndrome was revealed by the IRC determination. This suggests that the shortage of endogenous renin substrate, consumed by the markedly increased AR, may have interfered with the detection of IRA in Bartter's syndrome, though the IR is markedly increased as well. The molecular weights of AR and IR were determined by Sephadex G-100 gel filtration in 3 cases. Both AR and IR seemed to be smaller than those of normal subjects.

Adolescent↗
PubMed1984

Distribution of IgG subclasses in membranous nephropathy.

The distribution of human IgG subclasses among the glomerular deposits in human membranous nephropathy was examined by immunofluorescence with subclass specific monoclonal antibodies. Large amounts of granular deposits of IgG4 were identified along the capillary loops in all 12 patients, and seven patients had small amounts of IgG1 deposits. Neither IgG2 nor IgG3 deposits were detectable in any of the patients. On the contrary, all four IgG subclasses were detected in membranoproliferative glomerulonephritis and lupus nephritis with a predominance of IgG1 and IgG3. The results indicate that IgG4 is predominant in the glomerular deposits in membranous nephropathy and may play an important role in its pathogenesis.

Complement System Proteins↗
PubMed1984

Correlation of C3d fixing circulating immune complexes with disease activity and clinical parameters in patients with systemic lupus erythematosus.

Using anti-C3d as a solid phase reagent, C3d fixing circulating immune complexes (CIC) were detected in sera from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis, membranous nephropathy and IgA nephropathy. Particularly, sera from SLE showed the highest CIC levels and highest incidence of positivity among these diseases. In the 51 serum samples from 48 patients with SLE we studied, the CIC detected by the anti-C3d assay correlated well (P less than 0.01) with the CIC detected by the solid phase C1q assay, but not with those detected by the conglutinin assay. In addition, the CIC detected by the anti-C3d assay correlated more significantly (P less than 0.001) with disease activity, as well as some clinical parameters (serum anti-dsDNA antibodies, CH50 and C3 levels) than CIC detected by the other two assays of SLE sera. The anti-C3d binding materials were found to be of intermediate (8-19S) and small (7S) sizes in a small number of SLE sera which we analysed.

Antigen-Antibody Complex↗
PubMed1983

A comparative immunologic study of IgA nephropathy.

A conglutinin binding assay has been used to detect circulating immune complexes (CIC) containing IgA, IgG, or IgM in sera from patients with IgA nephropathy. IgA class CIC were detected in 40.7% of patient. IgG class CIC were detected only in patients with glomercular IgG deposits. IgM class CIC were detected more often in patients with glomerular IgM deposits than in patients without glomerular IgM deposits. These results demonstrate an association between the immunoglobulin in CIC and those in glomerular deposits. CIC were not detected in sera from most patients with IgA nephropathy by a Clq binding assay, however, since this assay does not detect IgA class CIC. Immunoelectronmicroscopic studies of IgA nephropathy have shown that C3 deposits are localized to the same areas as IgA deposits. In conclusion, we suggest that mesangial IgA deposits are composed of immune complexes and may be derived from CIC.

Antigen-Antibody Complex↗
PubMed1983

An overlapping syndrome of IgA nephropathy and membranous nephropathy?

This is the first report of primary glomerular disease with both mesangial IgA and subepithelial IgG deposits in the glomeruli at the same time. This nephropathy, discovered in 3 patients, is either a new disease entity or an overlapping of IgA nephropathy and membranous nephropathy. Follow-up studies may clarify the pathogenesis of IgA nephropathy and/or membranous nephropathy. In 1 patient the clinical findings resembled those of IgA nephropathy, and in the other 2 they were those of membranous nephropathy. Light microscopy showed generalized diffuse increases in mesangial cells and matrix, and there was slight capillary wall thickening. In the glomeruli, immunofluorescence microscopy demonstrated both granular deposits of IgA in the mesangium and granular deposits of IgG along the capillary loops. On electron microscopy, electron-dense deposits were identified not only in the mesangium but also on the epithelial side of the glomerular basement membrane. These findings were confirmed by the immunoperoxidase technique in electron-microscopic studies of these antibody classes. These glomeruli contained both the dense reaction products of IgA deposits in the paramesangium and mesangial matrix and the dense reaction products of IgG deposits on the epithelial side of the basement membrane.

Adult↗
PubMed1982

Circulating immune complexes of IgG, IgA, and IgM classes in various glomerular diseases.

In order to examine the correlation between immunoglobulin (Ig) classes of immunoglobulins in circulating immune complexes (CIC) and immunoglobulins in glomerular deposits, we have measured CIC of IgG, IgA and IgM classes in various glomerular diseases. Serum CIC were measured using a modified conglutinin binding assay (K assay) using 125I-labeled anti-gamma, anti-alpha and anti-mu antisera. IgA class CIC were detected in more patients with IgA nephropathy than patients with non-IgA nephropathy. There was an association between the presence of IgG deposits in kidneys and the presence of IgG in CIC. Patients with IgA deposits in their kidneys also had IgA class CIC. There was also an association between the presence of IgM deposits in kidneys and the presence of IgM in CIC. These results suggest that the Ig class in CIC and the Ig class in glomerular deposits were correlated, and that in IgA nephropathy the mesangial IgA deposits may be derived from IgA class CIC.

Antigen-Antibody Complex↗