Interleukin-4 and interleukin-4 receptor polymorphisms in minimal change nephropathy

Parry, R. G.; Gillespie, K. M.; Parnham, A.; Clark, A. G. B.; Mathieson, Peter W.

doi:10.1042/cs0960665

Cited by 14 publications

(12 citation statements)

References 11 publications

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“…These findings seem to be at variance with previous reports showing that serum IL-4 levels decreased during relapse but increased in nephrotic patients with long-term remission [15]. However, genetic study also showed no evidence of association between polymorphism of IL-4 or IL-4R and childhood NS [23]. The reason for the unchanged serum IL-4 levels pre and post treatment in this study is unknown.…”

Section: Discussioncontrasting

confidence: 84%

Implication of serum IgE in childhood nephrotic syndrome

Tain

Chen

Yang

2003

Pediatric Nephrology

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Elevated serum IgE levels have been related to glomerular diseases. We investigated the relationship between serum total and specific IgE levels and their modulating factors [interleukin-4 (IL-4) and sCD23] and the outcome of childhood nephrotic syndrome (NS) after steroid treatment. We found that children with NS had significantly higher serum IgE levels than age-matched allergic patients and normal controls. Patients with steroid-resistant nephrotic syndrome (SRNS) had higher serum IgE levels than patients with steroid-sensitive nephrotic syndrome (SSNS) both pre and post treatment. Elevated initial serum IgE levels appeared to be associated with poor outcome. Although one-half of nephrotic children had detectable specific IgE to common allergens (dust mites or milk), the presence of specific IgE was not correlated with disease outcome. Serum IL-4 levels were not different among normal controls and patients with SRNS or SSNS. However, serum sCD23 levels in NS patients were significantly higher than in normal controls both pre and post treatment. Serum sCD23, but not IL-4, levels were correlated with serum total IgE levels. Our results suggest that regulation of total IgE production correlates with the disease activity and outcome of NS, although the presence of common specific IgE may not be linked to the pathogenesis.

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Section: Discussioncontrasting

confidence: 84%

Implication of serum IgE in childhood nephrotic syndrome

Tain

Chen

Yang

2003

Pediatric Nephrology

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“…An elevated expression of IL-13 mRNA was shown by Yap et al [137] using a semi-quantitative RT (reverse transcriptase)-PCR technique; this was associated with decreased expression of TNF-α and CD14 in monocytes [138]. It has been shown that the increased expression of IL-13 was not related to known polymorphisms in the IL-13 gene [139] or in the genes encoding the transmembrane receptors for IL-4 and IL-13 [140,141].…”

Section: Role Of T-cells and Cytokinesmentioning

confidence: 90%

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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“…These efforts have focused on the analysis of polymorphisms in a number of genes, including those coding for angiotensin-converting enzyme (ACE) [1][2][3][4][5][6], cytokines or growth factors [7][8][9][10][11][12][13][14][15][16][17][18], apolipoprotein E (APOE) [19][20][21], paraoxonase 1 (PON1) [22], multiple drug resistance 1 (MDR1, also known as ABCB1, ATP-binding cassette, sub-family B member 1) [23], and glucocorticoid receptor (NR3C1) [24,25]. However, the results of these studies have not been consistent.…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms of the MDR1 and MIF genes in children with nephrotic syndrome

Choi

Cho

et al. 2011

Pediatr Nephrol

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Oral steroid treatment is the first line of therapy for childhood nephrotic syndrome (NS). Nonetheless, some patients are resistant to this treatment. Many efforts have been made to explain the differences in the response to steroid treatment in patients with NS based on the genetic background. We have investigated single nucleotide polymorphisms of the MDR1 [C1236T (rs1128503), G2677T/A (rs2032582), and C3435T (rs1045642)] and MIF (G-173C, rs755622) genes in 170 children with NS. Of these children, 69 (40.6%) were initial steroid non-responders, and 23 (13.5% of total) developed chronic kidney disease. Renal biopsy findings, which were available for 101 patients, showed that 35 patients had minimal change lesion and 66 had focal segmental glomerulosclerosis. The frequencies of the MDR1 1236 CC (18.8 vs 7.2%) or TC (53.5 vs 43.5%) genotype and C allele (45.5 vs 29.0%) were significantly higher in the initial steroid responders than in the non-responders. Analysis of MDR1 three-marker haplotypes revealed that the frequency of the TGC haplotype was significantly lower in the initial steroid responders than in the non-responders (15.8 vs 29.0%). There was no association between the MIF G-173C polymorphism and clinical parameters, renal histological findings, and steroid responsiveness. These data suggest that the initial steroid response in children with NS may be influenced by genetic variations in the MDR1 gene.

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Interleukin-4 and interleukin-4 receptor polymorphisms in minimal change nephropathy

Cited by 14 publications

References 11 publications

Implication of serum IgE in childhood nephrotic syndrome

Implication of serum IgE in childhood nephrotic syndrome

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

Polymorphisms of the MDR1 and MIF genes in children with nephrotic syndrome

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