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Biomedical subjects

S Koshikawa

Publications and source records attributed to S Koshikawa.

At least 109 records · Page 6Linked to original sources
PubMed1983

Attachment of polymorphonuclear leukocytes to glomeruli in IgA nephropathy.

It has been reported that depressed phagocytic activity of polymorphonuclear leukocytes (PMN) and cytoplasmic inclusion bodies containing IgA was observed in PMN from patients with IgA nephropathy. Peripheral blood PMN obtained from 19 patients with IgA nephropathy and 19 healthy subjects is investigated to determine whether or not they adhere to glomeruli in frozen sections of specimens from patients with IgA nephropathy. The average number of PMN from patients with IgA nephropathy that attached to glomeruli was significantly lower than the number seen with PMN obtained from healthy subjects. The results suggest that PMN function is depressed in patients with IgA nephropathy; it is postulated that these abnormalities may play an important role in the pathogenesis and/or progression of IgA nephropathy.

Adult↗
PubMed1983

Phagocytic activity of polymorphonuclear leucocytes in patients with IgA nephropathy.

The phagocytic activity of polymorphonuclear leucocytes (PMN) in 57 patients with IgA nephropathy was investigated using Immunobeads. Depressed activity was detected in 41 patients (72%). A significant correlation existed between the ingestive function of neutrophils and glomerular histological abnormalities, such as the degree of mesangial proliferation. In addition, 25 patients with IgA nephropathy were studied to detect the presence of immunological inclusions in the PMN by a direct immunofluorescent technique (anti-IgG, IgA, IgM and C3). Intracytoplasmic inclusions containing IgA were frequently detected in the PMN, and a negative correlation was found between the percentage of IgA-positive PMN and the phagocytic activity of neutrophils in patients with IgA nephropathy. These results suggest that the activity of neutrophils represents one of the important factors in the pathogenesis of IgA nephropathy and that mesangial IgA deposition is partly caused by decreased clearance activity of PMN.

Antigen-Antibody Complex↗
PubMed1981

Plasma beta-thromboglobulin levels in chronic renal failure patients.

Impaired platelet function is commonly recognized in uremia. It is partially improved by dialysis. However, in regular hemodialysis patients (RD), platelet function is not fully evaluated. This study investigated platelet activity in chronic renal failure (CRF) using beta-thromboglobulin (BTG) as a marker. BTG in RD were significantly higher than those in non-dialyzed CRF patients (P less than 0.05), and BTG in non-dialyzed CRF were higher than in normal controls (P less than 0.01). In non-dialyzed CRF, BTG were correlated to serum creatinine value (P less than 0.01). Arteriovenous fistula did not affect BTG. Hemodialysis and direct hemoperfusion with charcoal beads increased BTG but neither peritoneal dialysis nor hemofiltration altered BTG. RD treated over one year showed higher BTG than those treated for less than one year (P less than 0.01). In RD who showed elevated BTG, platelet aggregation and retention rates were depressed and bleeding times were prolonged. These results indicate that BTG can be used as the marker of impaired platelet function in CRF and of the blood compatibility of artificial kidneys.

Beta-Globulins↗
PubMed1981

Glomerular deposition of antihemophilic factor antigen in various renal diseases.

Glomerular localization of antihemophilic factor (AHF, Factor VIII) antigen was studied by immunofluorescent microscopy in 114 diseased and in 3 normal kidneys. Deposition of AHF was detected in the endothelial cells of glomeruli and in blood vessels in renal tissues. These deposits were not eluted by acid buffer treatment. In the group with minimal change nephrotic syndrome and in some cases of proliferative glomerulonephritis, deposition of AHF was limited to the endothelial cells. In cases of the nephrotic syndrome with proliferative changes, deposits were confined to endothelial cells but were increased because of proliferation and/or swelling of the endothelial cells. In some cases of IgA glomerulonephritis, membranous glomerulonephritis, membranoproliferative glomerulonephritis and lupus nephritis, deposition of AHF was detected not only in the glomerular endothelial cells but also in the immune deposits. However, after acid buffer treatment, it remained only in the endothelial cells. In other cases of membranous glomerulonephritis (7/9), membranoproliferative glomerulonephritis (5/8), lupus nephritis (5/14) and Henoch-Schönlein nephritis (1/3), deposits of AHF were confined to the immune deposits. These findings suggest that deposition of AHF is closely related to the immune reaction, and that functional impairment of endothelial cells may occur in some cases with massive immune deposits along the glomerular capillary walls. The glomerular endothelial cells may be affected by massive immune complexes that pass through the endothelial fenestrae or cytoplasm and remain in the glomerular basement membrane for a long time.

Antigens↗