Hodgkin's Disease and Lipoid Nephrosis

Couser, William G.; Badger, Alison M.; Cooperband, S R; Stilmant, Magda M.; Jermanovich, Nancy B.; Aurora, Sheena K.; Döner, Davut; Schmitt, Gabriela Cristina

doi:10.1016/s0140-6736(77)91246-6

Cited by 24 publications

(5 citation statements)

References 9 publications

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“…In MCNS, the hypothesis of a pathogenic circulating factor is based merely on experimental data showing the induction of albuminuria in rats upon injection of culture supernatants of stimulated PBMC (peripheral blood mononuclear cells) from patients with MCNS [80][81][82] or of a factor produced by human T-cell hybridomas derived from an MCNS patient in relapse [83]. Also, the association of MCNS with lymphoproliferative disease, in particular Hodgkin's disease [84,85], T-cell lymphoma [86] and thymoma [87], and the induction of remission by removal of the tumour suggested that circulating factors might play a causal role in the mechanism of proteinuria.…”

Section: Circulating Permeability Factorsmentioning

confidence: 99%

Role of the immune system in the pathogenesis of idiopathic nephrotic syndrome

2004

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Idiopathic NS (nephrotic syndrome) is characterized by massive proteinuria, due to a leak in the glomerular barrier to proteins. Genetic defects that affect the function and the composition of the glomerular capillary wall, in particular of the visceral epithelial cells, have recently been recognized as the cause of familial forms of NS. MCNS (minimal change NS) and FSGS (focal and segmental glomerulosclerosis) are common non-familial forms of NS in which the causative defect has not yet been identified. Several studies have shown that non-familial NS is associated with the presence of circulating permeability factors and with complex disturbances in the immune system. Thus far, there is no direct evidence that these factors directly alter glomerular permeability to proteins, and some of these factors may be a consequence, rather than a cause, of NS. In this review, we will briefly highlight the mechanisms that underlie proteinuria in general and focus on the immunological disturbances associated with idiopathic NS, with attention to potential mechanisms whereby the immune system may directly act on the glomerular capillary filter.

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Section: Circulating Permeability Factorsmentioning

confidence: 99%

Role of the immune system in the pathogenesis of idiopathic nephrotic syndrome

2004

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“…The involvement of such a factor in MCNS is less conclusive, but culture supernatants from peripheral blood mononuclear cells (PBMCs) of patients with MCNS can induce proteinuria in rats [3], as can a factor derived from a Tcell hybridoma derived from an MCNS patient in relapse [4]. There is also an association of MCNS with a number of lymphoproliferative diseases, including Hodgkin's disease [5], T-cell lymphoma [6] and thymoma [7], with remission occurring following tumour removal.…”

Section: Introductionmentioning

confidence: 99%

Is there a role for rituximab in the treatment of idiopathic childhood nephrotic syndrome?

Smith

2007

Pediatr Nephrol

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We each have nephrotic patients who become steroid dependent and in whom multiple immunosuppressive agents are employed. There is a need to balance possible therapeutic benefits with drug toxicity. This case report describes such a patient, who has suffered from nephrotic syndrome for over 11 years and had become resistant to the usual therapies. He was therefore given a single dose of the anti-CD20 drug rituximab, to which he showed a prompt response, leaving him free of proteinuria for the past 10 months.

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“…The enhanced vascular permeability fac tors released by abnormal T cells are suggest ed to cause nephrotic syndrome [3,4]. Symp toms observed in our case such as eruption, edema and pleural effusion seem to be de rived from factors which enhance vascular permeability.…”

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confidence: 54%