Studies of Vascular Permeability Factor derived from T Lymphocytes and Inhibitory Effect of Plasma on Its Production in Minimal Change Nephrotic Syndrome

Tomizawa, Shuichi; Maruyama, Kosçak; Nagasawa, Naoki; Suzuki, Shigeyuki; Kuroume, Takayoshi

doi:10.1159/000183572

Cited by 47 publications

(20 citation statements)

References 4 publications

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“…These 2 cases of minimal change disease therefore lead to considering two mechanisms of the ne phrotic syndrome. One is the classical 'Shalhoub hypothe sis' [16] of lymphokines causing loss of the glomerular polyanion [17][18][19][20][21][22][23], a generalized phenomenon which may also affect red cells and platelets [24,25]. The other mecha nism is secretion by the tumor of some cell product inducing massive proteinuria.…”

Section: Discussionmentioning

confidence: 99%

Minimal Change Nephrotic Syndrome Revealing Solid Tumors

Meyrier

Delahousse

Callard

et al. 1992

Nephron

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In 2 patients with the nephrotic syndrome, unsuspected solid tumors were found. One was a small cell lung carcinoma, accompanied with the syndrome of inappropriate ADH secretion. The other was a cancer of the breast with lymph node and bone metastases. In both, renal biopsy showed minimal change disease without immune complex deposits. There are only 14 other reported cases of paraneoplastic lipoid nephrosis complicating solid tumors. Such cases lead to the discussion on the respective roles of tumor cell gene product(s) inducing proteinuria and of lymphokine secretion by lymphocytes directed against the tumor itself. Cancer should be considered as a possible etiology of the minimal change nephrotic syndrome in the adult.

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Section: Discussionmentioning

confidence: 99%

Minimal Change Nephrotic Syndrome Revealing Solid Tumors

Meyrier

Delahousse

Callard

et al. 1992

Nephron

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“…It has long been thought that a disturbance of T-lymphocyte function underlies MCNS [1,2,3,4,5,6]. T-cell-derived vascular permeability factor may be responsible for the alteration of glomerular permeability in MCNS by modifying the charge barrier [7]. In addition, the relapse of MCNS is frequently preceded by immunological stimuli, including vaccination, infection, and bee stings, which would stimulate sensitized lymphocytes to produce highly active cytokines [8,9,10,11].…”

Section: Introductionmentioning

confidence: 99%

Polymorphism of the Interleukin-4, Interleukin-13, and Signal Transducer and Activator of Transcription 6 Genes in Indonesian Children with Minimal Change Nephrotic Syndrome

et al. 2005

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Background/Aims: Minimal change nephrotic syndrome (MCNS) in children is frequently associated with allergy and immunoglobulin E (IgE) production. T-helper subtype 2 cytokines, such as interleukin (IL)-4 and IL-13, have been implicated in the regulation of IgE production. We investigated the associations of gene polymorphisms of IL-4, IL-13, and signal transducer and activator 6 (STAT6) in Indonesian children with MCNS (n = 84) and controls with neither allergic nor renal disease (n = 61). Methods: Polymerase chain reaction-restriction fragment length polymorphism was used to determine the IL-4 promoter gene polymorphism (–590C/T) and IL-13 gene polymorphism (4257G/A), and direct sequencing was used for the STAT6 3S untranslated region (2964G/A) polymorphism. Results: There was a significant difference between the MCNS group and the controls in the genotypic distribution of IL-4 and IL-13 gene polymorphism. In the case of the IL-4 promoter gene, the frequency of the CC homozygote was significantly lower in the MCNS group than in the controls, while, in the case of IL-13, the frequency of the GG homozygote was significantly lower in the MCNS group. However, there was no difference between the MCNS group and the controls in the STAT6 gene polymorphism. Conclusion: The genetic variations in the IL-4 and IL-13 genes may be associated with predisposition to MCNS.

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“…This beneficial effect on proteinuria is explained by the hemodynamic effects of CsA: CsA increases renal resistance and decreases glomerular filtration rate [19, 20, 21]and by its action on T lymphocytes. Indeed, lymphocytes were shown to be involved in INS: a vascular permeability factor isolated from supernatants of lymphocytes from INS patients stimulated by concanavalin A [35, 36, 37, 38]and a soluble immune response suppressor synthesized by lymphocytes [39]were incriminated in the physiopathology of INS. Moreover, a factor synthesized by T cell hybridomas [16]and supernatants of mononuclear cells from INS patients were shown to induce proteinuria in rats [17, 18].…”

Section: Discussionmentioning

confidence: 99%

Increased Glomerular Cell Heparan Sulfates in vitro by Ciclosporin A: A Possible Explanation of Its Beneficial Effect in Idiopathic Nephrotic Syndrome

Birmelé

Agostini²,

Girardin³

2001

Nephron

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Background/Aim: In idiopathic nephrotic syndrome (INS), ciclosporin A (CsA) was shown to decrease proteinuria, an effect explained by its immunologic and hemodynamic actions. In order to determine whether CsA could have a direct action on glomerular cells, we studied the effect of CsA on glomerular cells in vitro, particularly on glycosaminoglcycans (GAG) and heparan sulfates (HS) which are decreased in INS patients. Methods: Human glomerular epithelial cells and rat mesangial cells were cultured at various concentrations of CsA. HS were quantified using a cationic membrane after metabolic labeling. Results: Mesangial cell GAG and HS and epithelial cell HS increased significantly when cells were cultured with CsA. For both cell types this increase was prevailing on the secreted fraction of HS in comparison with the cellular fraction. CsA induced also an increase in cellular cAMP levels, but the effect of CsA was not transduced via a cAMP pathway. Conclusions: CsA is able to increase glomerular GAG and HS in vitro. As this effect of CsA was the opposite effect on glomerular cells to the effect of plasma from INS patients, we conclude that this direct action of CsA on glomerular cells could explain in part the effect of this drug in decreasing proteinuria in INS.

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Studies of Vascular Permeability Factor derived from T Lymphocytes and Inhibitory Effect of Plasma on Its Production in Minimal Change Nephrotic Syndrome

Cited by 47 publications

References 4 publications

Minimal Change Nephrotic Syndrome Revealing Solid Tumors

Minimal Change Nephrotic Syndrome Revealing Solid Tumors

Polymorphism of the Interleukin-4, Interleukin-13, and Signal Transducer and Activator of Transcription 6 Genes in Indonesian Children with Minimal Change Nephrotic Syndrome

Increased Glomerular Cell Heparan Sulfates in vitro by Ciclosporin A: A Possible Explanation of Its Beneficial Effect in Idiopathic Nephrotic Syndrome

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