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Biomedical subjects

O Matsumura

Publications and source records attributed to O Matsumura.

At least 19 recordsLinked to original sources

Influences of Helicobacter pylori on serum pepsinogen concentrations in dialysis patients.

BACKGROUND: Patients with impaired renal function have been known to have elevated concentrations of serum pepsinogens, which are raised by Helicobacter pylori infection of the stomach. The present study was performed to examine the effect of H. pylori infection on serum pepsinogen concentrations in dialysis patients. METHODS: Forty nine patients on dialysis and 48 subjects with no known kidney disease were examined for upper gastroduodenal endoscopy, H. pylori infection and serum concentrations of pepsinogen I and II. The status of H. pylori infection was evaluated from results of a urease test, histology and culture of biopsy specimens of the gastric mucosa. Serum pepsinogen levels were measured by radioimmunoassay. RESULTS: Serum concentrations of pepsinogen I and II were elevated in the dialysis patients in comparison with those in the controls (277.4+/-24.2 vs 52.6+/-4.0 pg/ml, P<0.01 for pepsinogen I, and 30.2+/-2.9 vs 14.9+/-1.3 pg/ml, P<0.01 for pepsinogen II). In both the dialysis patients and controls, those with H. pylori infection had significantly higher concentrations of serum pepsinogen I and II and a lower ratio of pepsinogen I to pepsinogen II than those without infection. Among the controls, 15 of 25 subjects with atrophic gastritis had a pepsinogen I/pepsinogen II ratio < or = 3.0, while only two out of 17 patients on dialysis fell into this range. CONCLUSIONS: We conclude that H. pylori status should be taken into account when serum pepsinogen concentrations are evaluated in dialysis patients.

Female↗

Changes in phenytoin concentrations in blood and cerebrospinal fluid caused by direct hemoperfusion in a patient intoxicated with phenytoin.

We performed direct hemoperfusion (DHP) 5 times on a patient with consciousness disorder and phenytoin intoxication. We then measured the phenytoin concentrations in her cerebrospinal fluid (CSF) and blood at various times. After the first DHP session, consciousness began to improve, and it normalized after the fourth DHP session when the blood concentration of phenytoin had decreased from 54.0 microg/ml to 16.5 microg/ml. The average plasma phenytoin elimination rate of DHP was 18.0% over 120-180 min. The concentration of phenytoin in the CSF decreased as that in the blood was lowered by DHP. The average reduction rate of phenytoin in the CSF after a DHP session was 23.7%, which was similar to the rate of elimination from the blood. The CSF/blood phenytoin ratio was 0.17, and no marked changes were detected before or after a DHP session.

Acute Disease↗

Eradication of Helicobacter pylori restores elevation of serum gastrin concentrations in patients with end-stage renal disease.

In order to explore the role of Helicobacter pylori (H. pylori) infection in hypergastrinemia in patients on dialysis, the changes in serum gastrin concentration were examined before and after eradication treatment for H. pylori. Twenty-seven patients on dialysis were treated for the eradication of H. pylori. Fasting serum gastrin concentrations were measured by a radioimmunoassay which detects gastrin 17. Ammonia and pH levels of the gastric juice were also measured. The serum gastrin concentrations were significantly decreased following eradication of H. pylori, and the mean value reached the normal range. The restoration of hypergastrinemia was associated with marked reductions of gastric juice ammonia and pH levels. In contrast, patients in whom H. pylori was not eradicated showed no changes in these parameters. In conclusion, the elevation of the fasting serum gastrin 17 concentration seen in dialysis patients appeared to be attributable to H. pylori infection in the stomach.

Ammonia↗

[Effects of folic acid supplementation on hyperhomocysteinemia in CAPD patients: effects on unsaturated fatty acids].

Hyperhomocysteinemia has been recognized as one of the risk factors for atherosclerosis and premature vascular disease. Patients on dialysis and end-stage renal disease also manifest high plasma concentrations of homocysteine. We performed this study to evaluate the effects of folic acid supplementation on hyperhomocysteinemia in CAPD patients. Twenty-three CAPD patients (8 males, 15 females, 49.1 +/- 14.2-years-old) dialyzed for 22.7 +/- 19.2 months participated in the study. Daily 5-mg doses of folic acid supplementation for 4 weeks significantly reduced plasma concentrations of total homocysteine (p < 0.01) and serine (p < 0.001). This observation suggests that the reduction of plasma concentrations of total homocysteine results from activation of homocysteine remethylation to methionine. On the other hand, folic acid supplementation also revealed significant correlations between changes in serum concentrations of both dihomo-gamma-linolenic acid and arachidonic acid and changes in plasma concentrations of total homocysteine (r = -0.517, p < 0.05, r = -0.451, p < 0.05, respectively). In addition, serum concentrations of both dihomo-gamma-linolenic acid and arachidonic acid in 11 CAPD patients with hyperhomocysteinemia (> or = 35 micromol/litter) were significantly lower than those of 12 CAPD patients with normohomocysteinemia (< 35 micromol/litter) (p < 0.05, p < 0.05, respectively). Serum concentrations of both dihomo-gamma-linolenic acid and arachidonic acid in CAPD patients with hyperhomocysteinemia increased significantly (p < 0.01, p < 0.05, respectively) and reached similar levels of CAPD patients with normohomocysteinemia, while plasma concentrations of total homocysteine decreased after folic acid supplementation. These findings suggest that correction of hyperhomocysteinemia in patients on dialysis produces an increase in unsaturated fatty acids.

Administration, Oral↗

[A case with rheumatoid arthritis complicated with ANCA-associated vasculitis].

A 50-year-old woman with rheumatoid arthritis (RA) developed constitutive symptoms such as fever and weight loss, mononeuritis multiplex and rapidly progressive glomerulonephritis (RPGN). The renal biopsy revealed crescentic glomerulonephritis (CrGN) with few immune deposits such as IgG and C 3 and necrotizing vasculitis, which led to the pathological diagnosis of microscopic polyangiitis (MPA). Moreover the high serum level of anti-myeloperoxidase (MPO) antibody, one of the anti-neutrophil cytoplasmic antibody (ANCA), suggested that she had ANCA-associated vasculitis. The renal prognosis of the ANCA-associated vasculitis is said to be poor unless patients were treated in the early phase of the disease. As we started to treat the patient when her serum creatinine level (sCr) was 1.7 mg/dl and creatinine clearance (CCr) was 27 ml/min, her renal function returned to the almost normal level (sCr = 0.6, CCr = 91). It is well known that patients with RA may develop various kinds of extraarticular manifestations which are usually related to immune-complex mediated vasculitis, what we call malignant RA. We emphasize that ANCA-associated vasculitis is another important complication of RA. When we see a RA patient with constitutional symptom, abnormal urinary sediments and other clinical signs of vasculitis such as mononeuritis multiplex, ANCA-associated vasculitis should be considered. Since the early diagnosis and treatment of ANCA-associated vasculitis is a key to prevent renal failure, it is encouraged to measure the serum ANCA titer for not only the diagnosis of such patients but the evaluation of their clinical course.

Antibodies, Antineutrophil Cytoplasmic↗

Eradication of Helicobacter pylori in patients with end-stage renal disease under dialysis treatment.

The efficacy and safety of combination therapy with amoxicillin, lansoprazole, and plaunotol for the eradication of Helicobacter pylori in patients on dialysis were evaluated. The study subjects comprised 15 dialysis patients in whom H pylori had been found in the gastric mucosa. The patients were given 500 mg amoxicillin once a day for 3 weeks, 30 mg lansoprazole once a day for 8 weeks, and 80 mg plaunotol three times a day for 24 weeks. Endoscopy was performed on entry and at 4 and 24 weeks after cessation of amoxicillin. The concentrations of serum gastrin and gastric juice ammonia also were measured. Fourteen patients completed the treatment protocol, one having dropped out because of nausea and diarrhea. H pylori was eradicated in 11 of the 14 patients 4 weeks after the end of amoxicillin therapy (eradication rate, 78.6%). All but one patient was free of H pylori 24 weeks after the amoxicillin was discontinued. Patients who became negative for H pylori had significantly decreased serum gastrin and gastric juice ammonia concentrations. Our findings indicate that a combination of amoxicillin, lansoprazole, and plaunotol can be used to eradicate H pylori in patients on dialysis.

2-Pyridinylmethylsulfinylbenzimidazoles↗

A family with two sisters with collagenofibrotic glomerulonephropathy.

Collagenofibrotic glomerulonephropathy is a recently recognized disease entity. Although an autosomal recessive inheritance pattern has been suggested for this condition, there are few reports of familial cases. Only four pairs of child siblings, with histological confirmation of the glomerular lesions, have been reported. The current report describes a family including two sisters with histological evidence of collagenofibrotic glomerulonephropathy. Serum concentrations of the procollagen III peptide were elevated in the affected sisters, whereas their parents and other siblings demonstrated neither proteinuria nor increased blood levels of the procollagen III peptide. Our findings support an autosomal recessive pattern of inheritance for this type of glomerulonephropathy. They also suggest that the serum concentration of the procollagen III peptide is a useful marker for collagenofibrotic glomerulonephropathy.

Adult↗

Jak3 expression in glomerular epithelia of IgA nephropathy (IgA-N) patients.

Jak3 is a member of the Janus kinase family which plays an important role in cytokine signal transduction. Jak3 associates the gamma(c) chain of receptors for IL-2, IL-4, IL-7, IL-9 and IL-15, and is essential for the signal transduction of these cytokines. We have isolated Jak3 kinase from renal mesangial cells and demonstrated the constitutive expression of Jak3 in glomeruli in vivo. To investigate the physiological and pathological role of Jak3 in glomeruli, we prepared anti-Jak3 antibody and analysed the localization of Jak3 in glomeruli of renal biopsy samples from various nephritis patients and normal subjects. Among 61 nephritis patients and four normal subjects investigated in the present study, Jak3 was selectively localized to glomerular epithelia of IgA-N patients (14/34 cases) and focal glomerulosclerosis patients (1/5 cases), but not detected in minimal changes (n = 6), membranous glomerulonephropathy (n = 7), crescentic glomerulonephritis (n = 4), lupus nephritis patients (n = 5), and normal subjects (n = 4). The intense immunoreactivity for Jak3 is significantly associated with the decrease in creatinine clearance (81.5 +/- 10.4 ml/min versus 104.3 +/- 29.6 ml/min; P < 0.05, Student's t-test) and the increase in level of serum creatinine (1.13 +/- 0.33 mg/dl versus 0.75 +/- 0.23 mg/dl; P < 0.01, Student's t-test) in IgA-N patients. Furthermore, gamma(c) chain was concomitantly expressed with Jak3 in glomerular epithelia in vivo and in vitro, suggesting that signal transduction via gamma(c)-Jak3 cascade may be involved in the pathogenesis of glomerular injury of IgA-N. Taken together with the recent findings that IL-4-secreting T lymphocytes in affected glomeruli injure glomerular epithelium, the responsiveness of glomerular epithelium for IL-4 may be pathologically enhanced in IgA-N.

Animals↗

[Eradication of Helicobacter pylori in patients with end-stage renal disease undergoing dialysis treatment].

The aim of the present study was to examine the efficacy and safety of combination therapy with amoxicillin (AMPC), lansoprazole, and plaunotol for the eradication of H. pylori in dialysis patients. The subjects consisted of 15 dialysis patients (10 men and 5 women, mean age of 56 +/- 2.4 years) in whom H. pylori was found in the stomach. H. pylori status was evaluated by histology, culture and rapid urease test with biopsy specimens of the gastric mucosa. The patients were treated with AMPC 500 mg once a day for 3 weeks, lansoprazole 30 mg once a day for 8 weeks and plaunotol 80 mg three times a day for 24 weeks. In addition, the concentrations of serum gastrin and gastric juice ammonia were measured. Fourteen patients completed the treatment schedule, while one discontinued treatment because of nausea and diarrhea. Among the 14 patients, H. pylori was eradicated in 11 without any side effects (eradication rate 78.6%). Concentrations of gastric juice ammonia and serum gastrin were reduced significantly in patients who became H. pylori-negative. The present study indicates that combination therapy with AMPC, lansoprazole and plaunotol is safe and efficient for the eradication of H. pylori in dialysis patients. The results also suggested that elevated concentrations of gastric juice ammonia and serum gastrin in dialysis patients can be attributed, at least in part, to H. pylori infection.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Protein tyrosine kinases expressed in glomeruli and cultured glomerular cells: Flt-1 and VEGF expression in renal mesangial cells.

Protein tyrosine kinases play an important role in cellular proliferation and differentiation of various cell types. To identify potential tyrosine kinases involved in glomerular functions we have utilized the polymerase chain reaction (PCR) and degenerate oligonucleotides for isolation of such genes from isolated glomeruli, cultured mesangial cell, and glomerular endothelial cells. Sequence analysis of PCR-amplified cDNAs resulted in the isolation of 24 tyrosine kinases. Here we describe for the first time the constitutive expression of 15 tyrosine kinases, tyro-1, tyro-4, tyro-6, hyk, Ptk-3, Ryk, tie, yes, lyn, tec, Jak1, Jak2, Jak3, c-abl, and flk, in renal glomeruli. In addition, Flt-1, an endothelial cell-specific receptor for vascular endothelial growth factor (VEGF), is expressed in renal mesangial cells and its gene expression is up-regulated upon the stimulation of platelet-derived growth factor (PDGF) with the concomitant up-regulation of VEGF. These data suggest that possible involvement of VEGF/Flt-1 system in cytokine-induced mesangial cell proliferations.

Animals↗

Late-onset renal dysfunction in a patient with non-Hodgkin's lymphoma following an autologous bone marrow transplantation.

Various types of glomerulonephropathy have been reported in patients with malignant lymphoma. The present report describes a 21-year-old man with non-Hodgkin's lymphoma who developed renal insufficiency 4 months after undergoing autologous bone marrow transplantation without combined total body irradiation treatment. At the presentation of renal dysfunction, the malignant lymphoma had been in complete remission. A renal biopsy specimen revealed glomerular changes resembling those seen in patients with hemolytic uremic syndrome. However, hematologic examinations exhibited no evidence of thrombocytopenia or thrombotic microangiopathy, such as red cell fragmentations on the peripheral blood smear. Although the etiology of this nephropathy remains unclear, the chemotherapeutic agents administered in conditioning regimens for bone marrow transplantation were suspected of contributing to the renal insufficiency. Methylprednisolone pulse therapy appeared to be effective in arresting progression of the nephropathy. This case indicates that renal function should be monitored carefully in patients with malignant lymphoma after bone marrow transplantation, even if such patients lack the signs or symptoms of thrombotic microangiopathy.

Adult↗

An autopsy case of light chain deposition disease.

This report describes a case of light chain deposition disease (LCDD) with unusual findings of fibrillar structures in the deposits and marked calcification in several organs. A forty-year-old man was initially diagnosed with LCDD in 1987, and died of sepsis three and one-half-years later. Histological examination of autopsy specimens demonstrated eosinophilic amorphous materials, which differed from amyloid, in vessel walls or around parenchymal cells in almost every organ examined. Ultrastructurally, in addition to granular deposits, fibrillar structures were also seen in the deposits. Marked calcification was present in the myocardium, skeletal muscles, adrenal glands and arteries.

Adrenal Glands↗

An adult case of polycystic kidney disease associated with congenital hepatic fibrosis.

Congenital hepatic fibrosis is often associated with infantile, but not with adult polycystic kidney disease. We report the unusual case of an adult patient with polycystic kidney disease complicated by congenital hepatic fibrosis. A 27-year-old women was admitted to our hospital because of gross hematuria due to hemorrhage from renal cysts. She presented hematemesis from ruptured esophageal varices at the age of 14 years. She was diagnosed as having end-stage renal disease due to polycystic kidney disease at the age of 23 years, and maintenance hemodialysis was initiated the following year. Gross hematuria was managed with supportive therapy. However, the patient developed cholangitis and died of sepsis. Postmortem examinations as well as the patient's clinical course suggested that she had an autosomal dominant type of polycystic kidney disease. Histological findings of the liver were compatible with congenital hepatic fibrosis.

Adult↗

[An adult case of glomerulocystic kidney disease].

A 56-year-old female presented with end-stage renal disease. A CT scan of her kidneys demonstrated that the density of the renal parenchyma was quite low as compared with normal kidneys, and that corticomedullary demarcation was obscured. Magnetic resonance imaging (MRI) disclosed low intensity of the kidneys in T1-weighed images, and high intensity in T2-weighed images. In order to elucidate the etiology of her kidney disease, open renal biopsy was performed. The kidney surface was covered with numerous cysts with a diameter of less than 3 mm. Biopsy specimens from the cortical surface showed multiple cystic lesions. Serial sections of more than 200 slices of the biopsy material demonstrated that traces of collapsed glomeruli were present in most of the cysts. On electron microscopy, some epithelial cells lining the cysts were found to be round-shaped and contained a substantial amount of mitochondria, suggesting proximal tubules. These histological findings were compatible with glomerulocystic kidney disease (GCKD). An adult case of GCKD has rarely been reported, but the CT scan as well as MRI of the kidneys appeared to complement the diagnosis of GCKD. Although the cysts of GCKD have been considered to be dilatations of the Bowman's capsules, our observation suggested that part of the cells lining the cysts consisted of proximal tubular epithelium.

Female↗

[Anti-cardiolipin antibody and renal microthrombi in lupus nephritis].

To evaluate the relationship between anticardiolipin (ACL) antibody and microthrombi in renal tissue, we examined sera and renal biopsies from 47 patients of systemic lupus erythematosus (SLE) with lupus nephritis (LN). ACL antibody was measured by an enzyme-linked immunosorbent assay (ELISA). Their renal tissues were examined for histological types of lupus nephritis according to the WHO classification and appearance of renal microthrombi. Positive ACL had been shown in 28 of 47 patients (60%) with LN and in 15 of 18 patients (83%) with WHO IV (diffuse proliferative LN: DPLN). Incidences of renal microthrombi were significantly higher in patients with DPLN (61%) than in patients with all LN (34%) (p less than 0.01). The prevalence of renal thrombosis in patients with ACL (46%) was significantly higher than without ACL (16%) (p less than 0.05). Incidence of positive ACL was 81% in the cases with renal microthrombi and 48% in the cases without them. These findings suggest that there is strong association between ACL and the renal microthrombi in active LN.

Autoantibodies↗