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Biomedical subjects

F Gejyo

Publications and source records attributed to F Gejyo.

At least 145 records · Page 8Linked to original sources
PubMed1997

Significance of glomerular deposition of apolipoprotein (a) in various glomerulopathies.

Apolipoprotein (a) [apo(a)] may interfere with the fibrinolytic system because of its structural similarity to plasminogen. In the present study, we evaluated the effect of glomerular deposition of apo(a) on coagulation and fibrinolysis in patients with glomerular diseases. Twenty-four patients (13 males and 11 females) with various glomerulopathies were studied. We examined renal biopsy specimens for the presence of apo(a), and investigated the relationship between the glomerular deposition of apo(a) and coagulation and fibrinolysis within the glomeruli. The patients who exhibited the deposition of apo(a) (group A) had a significantly higher incidence of deposition of apo B-100 and low-density lipoprotein (LDL) receptor, and a significantly lower incidence of deposition of plasmin-alpha 2-plasmin inhibitor complexes (PIC) and tissue-type plasminogen activator than did patients without apo(a) deposition (group B). Patients in group A had a significantly higher level of serum total cholesterol and lipoprotein (a) than did patients in group B. Plasma levels of PIC and D-dimer in group A were significantly lower than those in group B. The plasma level of thrombin-antithrombin III complexes in group A was significantly higher than that in group B. These findings suggest that glomerular apo(a) deposition plays a part in coagulation and fibrinolysis within the glomeruli in patients with glomerular diseases.

Adolescent↗
PubMed1997

Histological localization of advanced glycosylation end products in the progression of diabetic nephropathy.

We studied the immunohistochemical localization of advanced glycosylation end products (AGEs) in the progression of diabetic nephropathy. Fourteen NIDDM patients with diabetic nephropathy were evaluated: 2 patients with normoalbuminuria, 4 with microalbuminuria (MA) and 8 with overt proteinuria (OP). Three patients with minor glomerular abnormalities were used as nondiabetic controls. Immunoreactivity to a monoclonal anti-AGE antibody (6D12) was recognized on the internal elastic membranes of arterial walls in every diabetic group. Hyaline lesions of arterioles of the MA and OP groups demonstrated strong reactions with 6D12. A portion of the nodular and exudative lesions in glomeruli of OP group patients also revealed immunoreactivity to 6D12. No immunoreactivity to 6D12 was observed in nondiabetic control specimens. We confirm that the accumulation of AGEs began in arterial walls of the early stage and presented in glomerular lesions of the late stage of the progression of diabetic nephropathy.

Adult↗
PubMed1997

Chronic erythropoietin treatment enhances endogenous nitric oxide production in rats.

To examine the effect of chronic administration of recombinant human erythropoietin (rHuEPO) on endogenous nitric oxide (NO) activity, we treated Sprague-Dawley rats with rHuEPO (100 IU kg-1 or 300 IU kg-1) or a corresponding vehicle for 2 weeks, administered subcutaneously on alternate days. Treatment elicited increases in haematocrit and systolic blood pressure in a dose-dependent fashion. Simultaneous administration of NG-nitro-L-arginine methyl ester (L-NAME, 20 mg dl-1 of drinking water), but not aminoguanidine (400 mg dl-1), induced a further significant rise in blood pressure. The effect of L-NAME was inhibited by a large dose of L-arginine (2.0 g dl-1). Polycythaemia and hypertension induced by chronic rHuEPO therapy were associated with increased urinary NO2- and NO3- (NOx-) excretion, while co-administration of L-NAME, but not aminoguanidine, reduced NOx- excretion. Our results indicate that chronic rHuEPO treatment has a significant pressor effect, but induces a compensatory increase in the steady-state release of NO by constitutive NO synthase in normal rats. Such enhanced NO synthesis may act as a protective mechanism against the hypertensive effect of rHuEPO.

Animals↗
PubMed1997

[Pathogenesis of IgA nephropathy: role of outer membranes of Haemophilus parainfluenzae antigens].

IgA nephropathy is characterized by IgA deposits, predominantly in the glomerular mesangium and mesangial proliferative glomerulonephritis. Concerning its pathogenesis, several investigators suggest that the deposited IgA is an antibody to viral, bacterial, or dietary antigens. Such reports strengthen the possibility of a relationship between mucosal immunity and the pathogenesis of IgA nephropathy. We previously observed that Haemophilus parainfluenzae (HP) is more commonly isolated from the pharynx of patients with IgA nephropathy than from those with other diseases. We have also identified the glomerular deposition of the outer membranes of HP antigens (OMHP) and an increased serum concentration of IgA antibodies against OMHP in patients with IgA nephropathy. These findings suggest that HP has a role in the etiology of IgA nephropathy.

Antibodies, Bacterial↗
PubMed1997

Apolipoprotein E and alpha 1-antichymotrypsin in dialysis-related amyloidosis.

Dialysis-related amyloidosis as represented by carpal tunnel syndrome is a serious complication of long-term dialysis treatment of patients with chronic renal failure. beta 2-microglobulin has been identified as a structural component of the amyloid deposits, but other factors also are associated with amyloid formation. We recently demonstrated the presence of apolipoprotein E and alpha 1-antichymotrypsin in the amyloid deposits. We therefore analyzed how polymorphic variants of both genes were related to the onset of amyloidosis. Among the apolipoprotein E genotypes, allele epsilon 2 represented a protective factor that delayed the onset of disease. In contrast, polymorphic alpha 1-antichymotrypsin alleles had no effect on the onset of amyloidosis. Thus, the apolipoprotein E epsilon 2 allele can be added to the list of factors that determine the onset of dialysis-related amyloidosis, which include patient age at initiation of dialysis therapy, dialysis duration, and the dialysis membrane used.

Amyloidosis↗
PubMed1996

High prevalence of serum apolipoprotein E4 isoprotein in rheumatoid arthritis patients with amyloidosis.

OBJECTIVE: To determine whether serum Apolipoprotein E (Apo E) type 4 isoprotein is a risk factor for the development of amyloidosis in patients with rheumatoid arthritis (RA). METHODS: Using isoelectric focusing, we studied Apo E phenotype expression and the corresponding allele frequencies (epsilon 2, epsilon 3, and epsilon 4) in 35 patients with RA and amyloidosis, 65 patients with RA and without amyloidosis, and 63 healthy controls. RESULTS: The Apo E3/4 phenotype was significantly more common in the group with amyloidosis (31.4%) than in the patients without amyloidosis (12.3%; P < 0.05) or in healthy controls (12.7%; P < 0.05). The frequency of the epsilon 4 allele was significantly greater in the group with amyloidosis (0.16) than in the patients without amyloidosis (0.07; P < 0.05) or in healthy controls (0.07; P < 0.05). CONCLUSION: The presence of Apo E4 isoprotein may be a risk factor for the development of amyloidosis in patients with RA.

Adult↗
PubMed1996

Circulating IgA, IgG, and IgM class antibody against Haemophilus parainfluenzae antigens in patients with IgA nephropathy.

We previously demonstrated a close relationship between the outer membranes of Haemophilus parainfluenzae (HP) antigens (OMHP) and IgA nephropathy (IgAN). Our objective was to clarify the relationship among IgA, IgG, and IgM class antibody against OMHP in the sera of 44 patients with IgAN and 62 patients with other glomerular diseases (OGD) by ELISA. Patients with IgAN showed a significantly higher level of IgA antibodies (P less than 0.0005) and IgG antibodies (P less than 0.001) against OHMP, than did patients with OGD. Positive correlations were observed between IgA and IgG antibodies, between IgA and IgM antibodies, and between IgG and IgM antibodies against OMHP in the sera of patients with IgAN. Immunoblotting showed that IgA, IgG, or IgM antibodies against OMHP in the sera of all patients with IgAN bound to components of OMHP. Amino acid sequences of three components of OMHP recognized by the sera from patients with IgAN revealed homology with those reported for outer membrane protein (OMP) P6 precursor, OMP P5, and P2 porin protein of H. influenzae. Results suggest that patients with IgAN have glomerular deposits of OMP P6 precursor, OMP P5, or P2 porin protein of HP, and a specific increase in the production of IgA antibodies against OMHP via polyclonal activation against these, with switching of production from one isotype to another, e.g. from IgM to IgA.

Adolescent↗
PubMed1996

Renal functional measurements in young rats with chronic inhibition of nitric oxide synthase.

The purpose of the present study was to examine renal functional changes caused by chronic blockade of nitric oxide (NO) synthesis in young rats. Two types of NO synthase inhibitor were used: NG-nitro-L-arginine methyl ester (L-NAME) as a non-selective inhibitor and aminoguanidine (AG) as a selective inhibitor of the inducible isoform. Oral administration of L-NAME (20-80 mg/dL of drinking water), not AG (400 mg/dL), for 4 weeks induced systemic hypertension in the treated rats. Both inhibitors caused a significant reduction in urinary excretion of NO2-/NO3-. Rats treated with L-NAME developed proteinuria and tubular enzymuria (high excretion of N-acetyl-beta-D-glucosaminidase) in a dose-dependent fashion, with normal serum levels of creatinine, albumin and cholesterol. Chronic AG administration did not alter the urinary levels of protein and N-acetyl-beta-D-glucosaminidase or serum laboratory values. Overall, these observations highlight the importance of the continuous generation of NO by the constitutive isoform in the control of vascular tone and the maintenance of renal glomerular and tubular function. Oral administration of L-NAME may serve as a model of chronic NO-deficient hypertension with renal injury in young rats.

Animals↗
PubMed1996

[The clinical significance of the measurement of serum soluble interleukin-2 receptors in various diseases].

We measured the serum levels of soluble interleukin-2 receptor (sIL-2R) in patients with collagen disease, viral hepatitis, and chronic renal failure on hemodialysis (HD) by enzyme immunoassay. sIL-2R levels were significantly higher in patients with collagen diseases (rheumatoid arthritis (RA), 843 +/- 509; systemic lupus erythematosus (SLE), 774 +/- 308; Sjögren's syndrome (SjS), 760 +/- 288; progressive systemic sclerosis (PSS), 649 +/- 198U/ml), with the viral markers of hepatitis B or C (HBsAg positives, 911 +/- 589; anti-HCV positives, 664 +/- 455U/ml) or with chronic renal failure on HD(1,431 +/- 406U/ml) than in the controls (302 +/- 57U/ml). In RA patients, there was a significant positive correlation between sIL-2R level and Lansbury's Indice or serum rheumatoid factor level. Patients with viral hepatitis showed a significantly positive correlation between the sIL-2R level and the level of ZTT or TTT. There was a significant difference between the HD patients with the anti-HCV antibody and those without, and between those with the anti human T lymphotrophic virus-I (HTLV-I) antibody and those without. In addition, there was a significant positive correlation between the sIL-2R level and duration of HD. These findings suggest that sIL-2R is a useful marker for disease activity in collagen diseases, especially in RA, and chronic viral infection such as HBV, HCV or HTLV-I in HD patients.

Autoimmune Diseases↗
PubMed1996

[A quantitative of serum biotin with microplate-assay using affinity streptavidin].

We modified Bayer's method of micro-plate assay for quantitation of biotin concentration. Biotin concentration in the solution and serum which cannot be quantitated directly by a microorganism assay (bio-assay), was easily determined by this method, which showed a high affinity of streptavidin for biotin this method and had a wide measurement range (0.9-60,000 pg/ml). We measured the concentration of biotin in 150 sera from 44 patients (21 males and 23 females) with active hepatitis (high level of both GOT and GPT, over 100 IU/l), 15 patients (7 males and 8 females) with inactive hepatitis (positive HCV-Ab but within normal limits of both GOT and GPT level), 17 patients (8 males and 9 females) with hepatoma and liver cirrhosis and 71 healthy persons (34 males and 37 females). The biotin concentration of sera in the healthy persons was 243.5 +/- 184.6 pg/ml, there being no sex difference. The biotin concentration in sera was higher in the patients than in healthy persons. It was high in the hepatoma and cirrhosis group (4,394.0 +/- 6,176.3), the active hepatitis group (2,397.4 +/- 2,785.5), and the inactive hepatitis group (1,873.2 +/- 1,523.7). These findings suggest that the biotin concentration is not significantly correlated with an escape enzyme such as GOT and GPT. These findings suggest that a high biotin concentration reflects other mechanisms such as escape from damaged liver cells.

Adult↗
PubMed1996

[The clinical significance of glitter-cells in the urine during urinary tract infection].

To clarify the relationship between glitter-cells and urine osmotic pressure, neutrophils were isolated from venous blood of 4 normal volunteers and incubated in urine specimens with different osmotic pressures. Glitter-cells were detected in the urine with 100-400 mOsm/l. The rate of glitter-cells in neutrophils incubated for 4 hours were significantly less than those incubated for 0 minute (p < 0.05). We clinically investigated the relationship between the presence of glitter-cells in fresh urine and the site of urinary tract infection (UTI) or organisms isolated from urine. Fresh urine samples were obtained from 95 patients (55 male and 40 female). Urine samples were examined for bacteriuria by the quantitative culture method, and significant bacteriuria was defined as more than 10(5)/ml of bacilli for midstream urine or as more than 10(4)/ml for urine collected by catheterization. Leukocytes and glitter-cells in the unspun and unstained urine were counted on a disposable slide using a counting chamber. Patients with upper UTI showed a significantly higher incidence of glitter-cells than patients with lower UTI (p < 0.05). Patients with glitter-cells had a significantly higher incidence of polymicrobial infections than those without glitter-cell (p < 0.05). These findings suggest that patients with glitter-cells in the urine show upper UTI (pyelonephritis) and polymicrobial infections.

Adolescent↗
PubMed1996

Role of IgA, IgG, and IgM antibodies against Haemophilus parainfluenzae antigens in IgA nephropathy.

We have recently demonstrated glomerular deposition of outer membranes of Haemophilus parainfluenzae (HP) antigens (OMHP) and the presence of IgA antibody against OMHP in patients with IgA nephropathy (IgA-N). In this study, we analyzed IgA-, IgG-, and IgM-classes of antibodies against OMHP, and the relationship between these antibodies and renal lesions in IgA-N. The subjects included 44 patients with IgA-N and 62 patients with outer glomerular diseases (OGD); the latter group consisted of 23 patients with predominantly IgG or IgM deposits and small amounts of IgA in the mesangium (group A), and 39 with IgG or IgM deposits without IgA (group B). IgA, IgG, and IgM antibodies against OMHP in patients sera were detected by enzyme-linked immunosorbent assay (ELISA). Immunoblotting demonstrated that the IgA, IgG, and IgM antibodies against OMHP in the sera of IgA-N patients bound to components of OMHP with molecular weights of 19.5, 30, and 40.5 kD. The amino acid compositions of these three OMHP components were similar to those reported for the outer membrane protein (OMP) P6 precursor, OMP P5, and OMP P2 (porin) of Haemophilus influenzae. Both IgA-N and group A patients, (i.e. those with IgA-related renal disease), demonstrated a significantly higher level of IgA antibodies against OMHP than did group B patients. However, only IgA-N patients revealed a significant correlation between the IgA-antibody titer and degree of glomerular changes. IgA-N patients with macroscopic hematuria or arterio(lo)sclerosis had a significantly higher IgA antibody titer than other IgA-N patients. There was no relationship between renal lesions and IgG or IgM antibody titers in any group. These findings suggest that IgA antibodies against OMHP are significantly increased in patients with IgA-related renal disease compared to those without mesangial IgA deposits and that a significant relationship between these antibodies and renal lesions exists only in patients with IgA-N.

Adult↗