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T Ootaka

Publications and source records attributed to T Ootaka.

30 records · Page 2Linked to original sources
PubMed1991

[Minimal change nephrotic syndrome with predominant mesangial IgA deposits: clinicopathological study].

It has been reported that minimal change nephrotic syndrome (MCNS) shows no deposit of immunoglobulins or complement components in the glomeruli. We found 6 patients with IgA deposits in the glomeruli among 101 patients with MCNS, and examined the clinicopathological features of these cases. In all cases, light microscopy showed minor glomerular abnormalities. However, immunohistochemical study demonstrated marked IgA deposits in the glomerular mesangium. IgM was detected in 5 cases, IgG in 2, C3 in 2, and Clq in 1. On electron microscopy, small mesangial deposits were found in all cases and foot process effacement was partially demonstrated. There were no abnormalities in the glomerular basement membrane. The renal functions were within normal ranges in all 6 cases. In three cases, biopsies were performed within a month after the initiation of profuse proteinuria. In the other three cases, frequent relapses had been observed for 6 to 15 years before the biopsies. However, all patients ultimately revealed complete remission with corticosteroid treatment. Serum IgA levels were within normal range in examined 4 cases. Hematuria was negative in all of them. The clinical findings seem to be identical to MCNS rather than IgA nephropathy, and IgA deposits may have no pathogenetic significance, although the pattern of deposition looks quite similar to that of IgA nephropathy. These results indicate that the renal lesions in the 6 patients may belong to the subtype of MCNS, rather than IgA nephropathy.

Adolescent↗
PubMed1990

Analysis of leukocyte surface antigens on ethanol-fixed paraffin-embedded tissue material.

Ethanol-fixed paraffin-embedded specimens of human tissues were studied whether the surface antigens of leukocytes in these tissues can be stained and analyzed. Three-layer indirect immunoperoxidase staining was performed on the ethanol-fixed paraffin-embedded sections by the use of several monoclonal antibodies for whole human leukocytes (Dako LC), B cells (Dako CD-22, 4KB5, and L26; Leu 14), T cells and their subsets (Dako UCHL-1, T1, T3, T4 and T8; Leu 4, 3a and 2a) and monocyte/macrophage lineage (Dako macrophage, Leu M1, M3 and M5). The results were compared with those on fresh-frozen sections. No essential differences were obtained between the paraffin-embedded and the fresh frozen sections stained by the following antibodies; Dako LC for whole human leukocytes; Dako UCHL-1, T3 and Leu 4 for T cells; Dako CD22, 4KB5, L26 and Leu 14 for B cells; Dako macrophage, Leu M1 and M5 for monocyte/macrophage lineage. On the other hand, the subsets of T cells could only be detected on the fresh-frozen sections. The results of the leukocyte analysis on the paraffin-embedded specimens of several renal diseases were very similar to those reported by other investigators on fresh-frozen sections or PLP-fixed materials. Thus, by the use of appropriate monoclonal antibodies, the ethanol-fixed paraffin-embedded material can be used for leukocyte analysis except for the definition of T cell subsets.

Antibodies, Monoclonal↗
PubMed1990

[The effect of captopril on proteinuria in glomerular diseases].

We evaluated the efficacy of an ACE inhibitor captopril (CAP) for the reduction of proteinuria in glomerular diseases, and tried to find the conditions in which urinary protein excretion was significantly decreased by this drug. Renin provocation test by CAP (C-test) was performed, and the result was compared to the effect on proteinuria. In 33 patients with proteinuria, ranging from 1.1 to 14.1 g/day, CAP was administered. Urinary protein excretion was reduced from 3.6 +/- 0.6 to 2.8 +/- 0.4 g/day (mean +/- SEM, p less than 0.01) after 2 weeks. The decrease in urinary protein was significant when renal function was moderately impaired (30 less than or equal to Ccr less than 60 ml/min) or patients were on a salt diet less than 7 g of NaCl daily. Reduction of urinary protein excretion by 2-week treatment of CAP was correlated with the result of C-test (r = 0.874, p less than 0.025). The long-term follow up for more than 6 months also suggested that CAP delayed the deterioration of renal function. Thus, CAP was proved effective in treating proteinuria, and C-test might give us an information of its proteinuria-suppressing effect in an individual case. But its efficacy was observed only in patients with moderately-reduced renal function or on low-salt diet. Therefore, we should select the cases carefully to expect the effect of CAP for the reduction of proteinuria.

Adult↗
PubMed1989

Histologic localization of terminal complement complexes in renal diseases. An immunohistochemical study.

Histologic localizations of terminal complement complexes (TCCs) were examined and compared with clinical findings in 154 patients with various renal diseases. Immunohistochemical demonstration of TCCs was carried out on ethanol-fixed paraffin-embedded renal biopsy specimens by indirect immunoperoxidase technique. In glomerular diseases that are thought to be immune-complex glomerulonephritis (IC-GN), such as IgA-nephropathy, membranous nephropathy, and systemic lupus erythematosus (SLE), TCCs were demonstrated in a pattern similar to that of immunoglobulins and C3, indicating that TCCs were induced by immune complexes. The intensity of TCC deposition was correlated with the morphologic destruction of glomeruli or serum creatinine levels in IgA-nephropathy, with urine protein in membranous nephropathy, and with serum C4 in SLE. TCC deposits without IC were also observed in tissue damages without disease specificity such as glomerular or vascular sclerosis and tubulointerstitial lesions. These findings suggested the existence of various roles of TCCs in renal injury, according to IC-mediated or non-IC-mediated mechanism acting in individual diseases.

Antibody Specificity↗
PubMed1988

Renal lesions in Cockayne's syndrome.

A nine-year-old boy who exhibited mild proteinuria and severe renal dysfunction with short stature, mental retardation, retinitis pigmentosa, deafness, and intracranial calcification was presented. Clinical features of the patient were in the most part consistent with those of Cockayne's syndrome. On the renal biopsy, two-thirds of the glomeruli had fallen into global sclerosis. The remaining one-third showed thickening of the capillary walls and expansion of the mesangial matrix. Immunofluorescence study proved no significant deposition of immunoglobulins or complements. Electron microscopy revealed diffuse homogeneous thickening of the glomerular basement membrane. These histological findings were thought to be characteristic of the Cockayne's syndrome. Although the pathogenesis of Cockayne's syndrome is yet unknown, its renal lesions resembled those of an aged kidney, and a prematurely aged metabolic state was supposed as a principal cause of the disease.

Aging↗
PubMed1987

Dense deposit disease: its possible pathogenesis suggested by an observation of a patient.

A girl, aged 8, was admitted to a hospital in a state of nephrotic syndrome of one year's duration. The renal biopsy showed mesangial and endocapillary proliferations with lobulation. Dense deposit was not demonstrated by electron microscopy, but lamellation of the lamina densa was found in most of the capillary loops. Her condition was improved by steroid treatment in a few months, but moderate proteinuria persisted. Five and half years later, follow-up biopsy showed typical pathological features of dense deposit disease. It is suggested that the lamellation of the lamina densa in the first biopsy could be related to the dense alteration of glomerular basement membrane in the second biopsy.

Basement Membrane↗