PubMed Health⌕ Search

Biomedical subjects

N Akano

Publications and source records attributed to N Akano.

35 records · Page 2Linked to original sources
PubMed1987

Glomerular deposition of cross-linked fibrin in human kidney diseases.

The immunofluorescent localization of cross-linked fibrin (XFb) in kidneys from 87 patients with renal diseases was evaluated using a monoclonal antibody that discriminates XFb from fibrinogen and its derivatives. Glomerular deposition of XFb, along the endothelial surface and in the mesangium, was frequently observed in patients with IgA nephropathy, Henoch-Schönlein purpura nephritis (HSPN), lupus nephritis, and hemolytic uremic syndrome (HUS), which was confirmed by immunoelectron microscopy. Dual-label immunofluorescent studies showed that XFb was deposited in limited areas among the sites reactive with anti-fibrinogen antibodies; XFb was not present in the crescents, Bowman's capsule or interstitium. The localization of XFb was generally discordant with that of the platelet membrane antigen and von Willebrand factor (factor VIII-related) antigen. Subendothelial co-deposition of XFb and immunoglobulins (IgA with or without IgG) occasionally accompanying C3 was found in the glomeruli of some of the patients with IgA nephropathy and HSPN. The distribution of XFb observed by immunoelectron microscopy was similar to that of electron dense deposits. The glomerular population of monocytes/macrophages in patients with XFb deposition was similar to that of those without deposition. Urinary XFb derivatives were detected by the latex agglutination test in three of the 16 patients with glomerular XFb deposition, and in two of the 18 patients without it. These data indicate that the coagulation system is activated in the kidney of patients with IgA nephropathy, HSPN, lupus nephritis and HUS, and support the concept that glomerular fibrin deposition is associated with endothelial/subendothelial and mesangial injury. The activation of the coagulation system in IgA nephropathy and HSPN seems to be mediated by immune complexes rather than monocytes/macrophages. Determination of urinary XFb derivatives is not helpful for assessing glomerular XFb deposition.

Antibodies, Monoclonal↗
PubMed1987

Cellular and non-cellular compositions of crescents in human glomerulonephritis.

The composition of glomerular crescents was examined on the frozen kidney sections obtained from 10 patients (5 patients with IgA nephropathy, two with Henoch-Schönlein purpura nephritis and three with glomerulonephritis due to undetermined etiology) using well-defined monoclonal and polyclonal antibodies to coagulation proteins, extracellular matrices, intermediate filament proteins and immune cells. Fibrinogen/fibrin related antigens (FRA), which were stained with anti-fibrinogen serum, were positive in the crescents of all the patients, but monoclonal antibody to crosslinked fibrin or von Willebrand factor (factor VIII related) antigen did not bind to the crescents. This suggests that the FRA deposited in the crescents is fibrinogen or its degradation products rather than fibrin. Staining for intrinsic components of renal basement membrane, including type IV and V collagens, laminin and fibronectin, were consistently positive in all stages of the crescents. Cytokeratin, showing cytoplasmic staining of the glomerular parietal epithelium and tubular epithelium in the normal kidney, was demonstrated in three patients with cellular crescents. Vimentin, which is normally distributed in parietal and visceral epithelial cells in the glomeruli and interstitial cells, was found at all stages of the crescents. These findings suggest that in the early stage of crescent formation, glomerular epithelial cells play an important role, and that the accumulation of intrinsic basement membrane constituents is associated with the formation and progression of the crescents. None of the crescent cells reacted with either of two monoclonal antibodies (Mo2 and FMC 32) to monocytes/macrophages or with nonspecific esterase staining. It seems that, at least in our patients, monocytes are a minor factor contributing to the formation of glomerular crescents.

Collagen↗
PubMed1987

Immunohistochemical studies of reflux nephropathy. The role of extracellular matrix, membrane attack complex, and immune cells in glomerular sclerosis.

Renal tissue obtained from 8 patients with reflux nephropathy was studied by immunofluorescence with well-defined mono- and polyclonal antibodies to extracellular matrix, intermediate filament proteins, membrane attack complex of complement (MAC), and immune cells. In both unscarred and scarred areas of the tissue, intrinsic components of the human glomeruli, such as Type IV collagen, laminin, and fibronectin, accumulated in the expanded mesangium of the glomeruli. Those components were diminished or absent in the hyalinized glomeruli. Type III collagen was occasionally localized to the mesangium and synechiae in the glomeruli and was frequently observed within the nearly hyalinized glomeruli. MAC was co-deposited with C3, C5, C9, and properdin in the sclerotic area of the glomeruli, along with a decrease in the reactivity of podocytes with anti-vimentin antibody. Numerous suppressor/cytotoxic T cells were identified in the glomeruli and widened interstitum. Monocytes/macrophages also infiltrated the glomeruli. The present study suggests that accumulation of extracellular matrix, activation of the complement system, and infiltration of suppressor/cytotoxic T cells and monocytes/macrophages are closely associated with the glomerular obsolescence and the progression of reflux nephropathy.

Adolescent↗
PubMed1982

Urinary fibrinogen and fibrin fragments in children with renal disease.

Fibrinogen fragments (X, Y, D and E) and fibrin fragments (D-dimer and E) were examined in the urine of 52 patients with various types of renal diseases. One or more of the fibrinogen fragments were detectable in all the urine specimens. D-Dimer together with fibrinogen fragments was found in 38 of the 52 patients. The clearance ratio of D-dimer to IgG, which indicates D-dimer generated in the kidney, was lower than 1 in all the patients with the minimal changes nephrotic syndrome, and was greater than 1 in the majority of patients with acute glomerulonephritis, rapidly progressive glomerulonephritis, mesangial proliferative glomerulonephritis and membranoproliferative glomerulonephritis. Our results suggest that urinary fibrin/fibrinogen degradation products (FDP) in renal diseases are derived primarily from increased filtration of FDP from the plasma through a damaged glomerular basement membrane, and that the mechanism of lysis of cross-linked fibrin deposited in the glomeruli occurs simultaneously in some types of glomerulonephritis. It seems that the determination of the clearance ratio of D-dimer to IgG may be useful in assessing the activation of the coagulation and fibrinolysis systems in the kidney in patients with renal diseases.

Adolescent↗