Biomedical subjects
Publications and source records attributed to T Suga.
Two patients with ectopic kidney are described here. One was a 33-year-old male with hypertension and heavy proteinuria. The other was a 30-year-old male who had hypospaedia complained of dysuria for 30 years. These two cases were correctly diagnosed after radiographical examinations. Early detection of this disease can be achieved by using some radiographical techniques which is important in managing the future course of patients with ectopic kidney.
Exacerbation of urinary abnormalities after upper respiratory tract infections in patients with IgA nephropathy was examined. Twenty patients with IgA nephropathy and fourty patients with other glomerular diseases were evaluated in this study. The incidence of exacerbation in microhematuria after upper respiratory tract infections was significantly higher in patients with IgA nephropathy than those with other glomerular diseases. The improvement of microhematuria after upper respiratory tract infections was significantly delayed in some patients with IgA nephropathy. It is indicated that upper respiratory tract infections might be a risk factor of exacerbation in patients with IgA nephropathy.
Polymeric IgA in sera was determined by thin-layer gel filtration in patients with IgA nephropathy, other glomerular diseases, IgA myeloma and healthy adults to determine whether serum IgA is composed of a monomeric and/or larger polymers in these patients. The levels of IgA in sera were also quantitated by laser nephelometer in these patients. Eleven patients with IgA nephropathy (Berger's disease), six patients with other glomerular diseases, three patients with IgA myeloma and four healthy adults were examined. It was shown that the polymerized IgA in sera from patients with IgA nephropathy was significantly higher than that in sera from patients with other glomerular diseases and healthy adults. Levels of IgA in sera from patients with IgA nephropathy are significantly higher than that in sera from patients with other glomerular diseases and healthy adults. These findings suggest that an increase in serum IgA from patients with IgA nephropathy may be mainly due to an increase in polymers rather than the monomer of IgA.
A 22-year-old male patient with focal segmental glomerulosclerosis(FSGS) associated with a pheochromocytoma is reported. Immunofluorescence study of the kidney biopsy specimen demonstrated segmental depositions of IgM, C3 and fibrinogen. Alteration of glomerular basement membrane(GBM) with fibrin strands and platelet aggregates was observed by electron microscopic examination. Administration of prednisolone had no effect on massive proteinuria, but surgical removal of the tumor promptly reduced proteinuria. It was suggested that FSGS can develop in patients with pheochromocytomas, and local hypercoagulation might be responsible for the development of this lesion.
A 35-year-old female patient with Behçet's disease associated with nephrotic syndrome is described. Renal biopsy specimens revealed typical features of membranous nephropathy in light microscopical, electron microscopical and immunofluorescent microscopical examinations. Circulating immune complexes (IC) phagocytized by polymorphonuclear leukocytes (PMN) in this patient were significantly increased compared with those in healthy adults. Recurrent oral aphthous ulcers had persisted for 14 years. In the course of Behçet's disease, nephrotic syndrome due to membranous nephropathy was observed. Depositions of IgA, IgM, C3 and C4 were observed in the subcutaneous arteriolar walls by immunofluorescence. It is suggested that the pathogenesis of Behçet's disease and membranous nephropathy might be due to a deposition of circulating immune complexes in various types of vascular vessels in this patient.
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The activities of antimycin A-insensitive palmitoyl-CoA oxidation and of palmitoyl-CoA oxidase in peroxisomes from chicken liver were similar to those of rat liver. Catalase and D-amino acid oxidase activities in peroxisomes from chicken liver were lower than those of rat liver, and urate oxidase was not detected. Carnitine acetyl-transferase and palmitoyltransferase levels in chicken liver were 18- and 2-fold higher, respectively, than those of rat liver. Peroxisomal palmitoyl-CoA oxidation of chicken liver was inhibited by cyanide, in contrast to that of rat liver, although it was insensitive to antimycin A. Subcellular distribution of this enzyme was similar to that of rat liver; i.e., it was located only in the peroxisomes. The fatty acyl-CoA oxidase had a higher affinity toward medium- to long-chain fatty acyl-CoAs (C8 to C16) than shorter-chain analogs. The fatty acyl-CoA dehydrogenase had a broad affinity toward fatty acyl-CoAs (C4 to C18). Carnitine acetyltransferase was distributed equally in both peroxisomes and mitochondria. Carnitine palmitoyltransferase was distributed in the proportion of 20 and 80% in peroxisomes and mitochondria, respectively.
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The structures of cysteine conjugates of 3,5-di-tert-butyl-4-hydroxytoluene (BHT) and the binding sites of BHT metabolites on microsomal protein were investigated by 13C nuclear magnetic resonance (13C-NMR) and gas-liquid chromatography/mass spectrometry. The cysteine conjugates of 2,6-di-tert-butyl-4-hydroxymethylphenol (BHT-alcohol) and 2,6-di-tert-butyl-4-methylene-2,5-cyclohexadienone (quinone methide), which are metabolites of BHT found in rat liver and specifically reacts with thiol compounds, were prepared as alcoholic aqueous solutions. The molecular structure of the cysteine conjugate of BHT-alcohol agreed completely with that of quinone methide in 13C-NMR spectra or mass spectra. These spectra of both conjugates further showed that the conjugates are due to thioether binding between the 4-methyl group of metabolites and the sulfhydryl group of cysteine. When [14C]BHT-bound microsomes prepared in vitro were enzymatically hydrolyzed with Pronase E, the major radioactive material that eluted with methanol from a column of Amberlite XAD-2 and gave a positive ninhydrin reaction was identified as a cysteine conjugate of BHT by comparing its Rf values on TLC and mass spectrum. On the basis of the results, it was apparent that the binding site of activated substituents of BHT on protein was mainly the sulfhydryl group of cysteine residue.
A study of the solubilization of glomerular immune deposits by sera from patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy and other glomerular diseases. These specimens were incubated with fresh and heated sera from the same patients and healthy adults at 37 degrees C for one hour in plastic tubes. The sections were stained with fluorescein isothiocyanate (FITC)-labeled heavy chain specific anti-human IgA antiserum and then examined with a fluorescent microscope. It was shown that the solubilization of glomerular immune deposits by sera from patients with IgA nephropathy was significantly less than that by sera from healthy adults. It is possible that impaired solubilization of immune complexes in vivo could lead to the accumulation of glomerular immune deposits in patients with IgA nephropathy.
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A B-cell subset with Fc receptors for IgA (B alpha cells) has been observed in human peripheral blood. To investigate aberrations of B cells in a diseased state, the percentages of B alpha cells were enumerated in peripheral blood from patients with IgA nephropathy, which is characterized by preponderant deposition of IgA-dominant immune complexes in the glomerular mesangial area. The present study showed a significant increase in B alpha cells in peripheral blood from patients with IgA nephropathy but not in those with chronic proliferative glomerulonephritis without mesangial IgA deposition. Most Fc alpha R-bearing cells were observed in surface IgA bearing lymphocytes. No linear correlation was observed between the levels of serum IgA and the percentages of B alpha cells. The addition of aggregated IgA to cultures did not induce Fc alpha R-bearing B cells in vitro. It is postulated that B alpha cells might have some pathogenetic role in the development of IgA nephropathy and that some antigenic stimuli might play a role in the increase of peripheral blood B alpha cells in patients with IgA nephropathy.
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A case of Fabry's disease in a 22-year-old male patient who had mild proteinuria and dark-red eruptions is reported. He had been treated as a case of a so-called "chronic glomerulonephritis" for one year. However, histopathological findings of the renal biopsy specimens showed the presence of numerous vacuolated cells in the glomeruli. These vacuolated cells contained numerous electron dense bodies observed by electron microscopy. Skin lesions of this patient were consistent with those of angiokeratoma corporis. The levels of serum alpha-galactosidase were significantly lower than those of healthy controls. The mother of this patient also showed decreased levels of serum alpha-galactosidase. The pedigree of this patient showed a familial history of various types of renal diseases. It was postulated that Fabry's disease occurring in older patients has a worse clinical course. it is concluded that early detection of this disease through biopsy and the assay of serum alpha-galactosidase levels is important in managing the future course of patients with Fabry's disease.
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Hepatic glomerulosclerosis is characterized by depositions of IgA in mesangial areas of glomeruli similar to those found in primary IgA nephropathy. The mechanism of IgA deposition is presently obscure. We have attempted to elucidate histopathological changes of IgA deposition in such patients. Three cirrhotic patients who had abnormal urinalysis underwent renal biopsy in Tokai University Hospital. Renal biopsy specimens obtained from these three patients showed IgA measangial deposition on immunofluorescence staining, and various histopathological changes on light microscopy. It is suggested that these variable renal changes in patients with hepatic cirrhosis may be related to the alteration of the handling of immune complexes in injured liver.
A case of renal granulomatous sarcoidosis that presented with chronic renal failure (CRF) is described. Renal biopsy specimens revealed typical features of sarcoidosis in light microscopy and immunofluorescence microscopy examinations. The absence of bilateral hilar lymphadenopathy (BHL) was a distinctly unusual feature of sarcoidosis although uveitis and rectal granuloma were observed during the clinical course. A dramatic response occurred on corticosteroid and urokinase therapy, characterized by a fall of serum creatinine levels.
A study on autoradiographical analysis of antigenic sites in patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy. These specimens were treated with citrate buffer (pH 3.2) and the 'eluate' was neutralized by sodium hydroxide. The 'eluate' was labelled with 125iodine by the chloramine-T method. 125I-labelled eluate was then applied to the tonsillar cells obtained from the same and other patients with IgA nephropathy as well as to those with other glomerular diseases. The tonsillar cells were dipped into the emulsion (NBT-2) and then examined with a light microscope. It was demonstrated that the antibodies eluted from renal tissues of patients with IgA nephropathy specificially bound with the nuclear regions of tonsillar cells. The binding of eluted antibodies and tonsillar cells was completely inhibited by the addition of anti-human IgA antisera, but not inhibited by human IgA myeloma proteins. The eluted antibodies bound with tonsillar cells from the same patients, but only 10% of them bound with the tonsillar cells obtained from other patients with IgA nephropathy. It is concluded that IgA antibodies deposited in glomeruli specifically bind with tonsillar cells obtained from patients with IgA nephropathy and these antibodies show some heterogeneity among those patients.