A case of chromosome abnormality with 13q-.
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Biomedical subjects
Publications and source records attributed to Y Nomoto.
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Activation of fibrinolysis in patients with diabetic nephropathy was determined by the plasma levels of plasmin-alpha 2 plasmin inhibitor complexes (alpha 2PIC) using a one-step sandwich enzyme immunoassay (EIA). Plasma levels of alpha 2PIC in diabetic patients with persistent proteinuria were significantly higher than those in diabetic patients without proteinuria, patients with chronic glomerulonephritis, and healthy adults. Plasma levels of alpha 2PIC in diabetic patients with intermittent proteinuria were also significantly higher than those of diabetic patients without proteinuria, patients with chronic glomerulonephritis, and healthy adults. Diabetic patients have been suggested to have a hypercoagulable state. The findings obtained from this study indicated that activation of fibrinolysis might counteract the hypercoagulable state in patients with diabetic nephropathy.
Long-term effects of urokinase on the preservation of renal function in patients with diabetic nephropathy were evaluated. Twenty-nine adult patients with non-insulin-dependent diabetes mellitus and overt proteinuria were randomly divided into two groups. One group was treated with daily oral administration of dipyridamole or dilazep dihydrochloride and weekly intravenous administration of urokinase; the other group was treated with dipyridamole alone. There was a significant decrease in the amount of proteinuria in the first group after 3 months of the treatment compared with the second group. There was also a significant preservation of renal function in the first group after three years of treatment compared with the second group. It was concluded that continuous administration of urokinase in addition to antiplatelet agents is useful in the treatment of patients with diabetic nephropathy.
Significance of serum IgA and IgA-class circulating immune complexes (IgA-CIC) elevation in patients with non-insulin-dependent diabetes mellitus (NIDDM) was described. Seventeen patients with NIDDM and 17 patients with diffuse mesangial proliferative glomerulonephritis without deposition of IgA (DPGN) as controls were examined. The levels of serum IgA in patients with NIDDM were significantly higher than those in patients with DPGN (p < or = 0.01). The levels of IgA-CIC in patients with NIDDM were also significantly higher than those in patients with DPGN (p < or = 0.01). Production of IgA derived from B cells and the proportion of IgA bearing B cells in patients with NIDDM were not significantly higher than those in patients with DPGN. Furthermore, the levels of IgA in pharyngeal washings from diabetic patients were not significantly higher than those for DPGN patients. Duration of diabetes, the level of HbA1c, and the presence of hypertension, microalbuminuria, or retinopathy showed no significant correlations with the levels of serum IgA or IgA-CIC in patients with NIDDM. It was postulated that the elevations of serum IgA and IgA-CIC were based on subclinical infection of the mucosa and/or deterioration of IgA clearance in patients with NIDDM.
This is the first report on immunofluorescence staining of renal biopsy samples in human diabetic nephropathy (DN) using monoclonal antibodies to reduced glycated lysine. In order to detect the localization of glycated lysine in the mesangial matrix and/or the glomerular basement membrane (GBM), we examined immunofluorescence staining using antibodies against reduced glycated lysine in the glomeruli of 16 patients with DN and ten age-matched patients with diffuse mesangial proliferative glomerulonephritis without IgA deposition (DPGN) as controls. In the early stage of DN, immunofluorescence microscopy revealed the presence of intense staining for reduced glycated lysine in the GBM as well as in part of the tubular basement membrane, but not in the mesangial area. In contrast, immunofluorescence microscopy revealed less staining for glycated lysine in the GBM in the advanced stage of DN, and no reaction with any part of the renal tissue in patients with DPGN. It was concluded that detection of reduced glycated lysine in GBM in the early stage of DN might be associated with the initial pathogenesis of this disease.
Correlations of renal histopathologic changes, duration of diabetes, and the degree of control of blood glucose in patients with diabetic nephropathy were determined. Biopsies from 17 patients with diabetic nephropathy due to Type II diabetes were examined. Mild histopathologic changes in renal tissues were observed in patients with good blood glucose control, even if their disease was of more than 5 years' duration. Moderate to severe renal histopathology was found in patients with poor blood glucose control regardless of the duration of diabetes. It is concluded that strict control of blood glucose during the course of diabetes is important in inhibiting the progression of renal involvement in patients with Type II diabetes.
A study of double immunofluorescence staining of sialic acids and IgG in the glomeruli from patients with diabetic nephropathy is described. Renal biopsy specimens from seven patients with diabetic nephropathy were stained with rhodamine-labeled tricum vulgaris (WGA), limulus polyphemus (LPA), and FITC-labeled anti-human IgG antiserum. Both binding of WGA and deposition of IgG in glomerular capillary walls were observed in all patients with diabetic nephropathy. However, the binding of LPA in tissue from the same patients was minimal, although deposition of IgG was marked. It is suggested that an accumulation of substances with an affinity for WGA (most probably N-acetyl glucosamine or N-acetyl neuraminic acid) occurs in the glomerular capillary walls of patients with diabetic nephropathy.
Measurement of sialic acid and acute phase reactant (APR) proteins in sera of patients with diabetic nephropathy was performed. Twenty-six patients with non-insulin-dependent diabetes mellitus (NIDDM) were examined. The levels of sialic acid in sera, with or without treatment of neuraminidase, were measured by the thiobarbiturate method. The levels of alpha 1-antitrypsin (alpha 1-AT), alpha 1-acid glycoprotein (alpha 1-AG) or alpha 2-macroglobulin (alpha 2-MG) were measured by laser nephelometry. The levels of sialic acid or APR proteins in sera of patients with diabetic nephropathy were increased markedly. There was a significant correlation between the levels of sialic acid and those of alpha 1-AT in sera of patients with NIDDM. The mobility of alpha 1-AT in sera of patients with NIDDM treated with neuraminidase was decreased markedly in the immunofixation test. It is suggested that the increase of APR proteins in diabetic sera is mainly composed of sialic acid in patients with NIDDM with or without nephropathy.
The levels of IgA and total proteins in pharyngeal washings were examined in patients with IgA nephropathy and other glomerular diseases in order to determine whether secretory IgA, IgA1 and IgA2 were increased in these patients. Thirty patients with IgA nephropathy, 21 patients with other glomerular diseases and 15 healthy adults were examined. The levels of IgA were quantitated by radial immunodiffusion and laser nephelometry. The levels of total proteins in pharyngeal washings were quantitated by Tonein-TP. It was demonstrated that the levels of IgA in pharyngeal washings were significantly increased in patients with IgA nephropathy compared to those with other glomerular diseases and healthy adults. The levels of total proteins in pharyngeal washings were increased in patients with IgA nephropathy, and the ratio of IgA and total proteins in the washings from patients with IgA nephropathy was not significantly different from those healthy adults. There was a significant correlation between the levels of IgA in pharyngeal washings and those of IgA in sera from patients with IgA nephropathy. The IgA observed in pharyngeal washings contained secretory components, IgA1 and IgA2, in patients with IgA nephropathy. It is suggested that the increase of IgA in the pharyngeal washings in parallel with the increase of total proteins might be associated with local inflammation.