Idiopathic nephrotic syndrome and atopy: is there a common link? - PubMed (original) (raw)

Review

Maher Abdel-Hafez et al. Am J Kidney Dis. 2009 Nov.

Abstract

Numerous reports during the last 60 years have reported a strong association between idiopathic nephrotic syndrome and atopic disorders. Idiopathic nephrotic syndrome can be precipitated by allergic reactions and has been associated with both aeroallergens (pollens, mold, and dust) and food allergies. Patients with idiopathic nephrotic syndrome also may show increased serum immunoglobulin E (IgE) levels. A review of the literature suggests that although some idiopathic nephrotic syndrome cases may be associated with allergies, evidence that it is a type of allergic disorder or can be induced by a specific allergen is weak. Rather, it is likely that the proteinuria and increased IgE levels in patients with idiopathic nephrotic syndrome are caused by increased levels of interleukin 13 observed in these patients. Recent studies suggest that interleukin 13, a known stimulator of IgE response, may mediate proteinuria in patients with minimal change disease because of its ability to directly induce CD80 expression on the podocyte.

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Figures

Figure 1

Figure 1

(A) (1) Antigen-presenting cells (APCs) and activated B cells express CD80, which binds to CD28 on the (2) T effector (Teff) cellular membrane. In the absence of suppression by (3) T regulatory (Treg) cells, T effector cells release interleukin 4 (IL-4) and IL-13. These 2 cytokines trigger (4) the switch from immunoglobulin M (IgM) to IgE in the B cell. (B) T effector cells express cytotoxic T-lymphocyte antigen-4 (CTLA-4), which will compete with CD28 for CD80, resulting in (1) decreased activation of T effector cells. In addition, (2) T regulatory cells suppress T effector activation by releasing IL-10 and soluble CTLA-4. These combined events result in decreased production of IL-4, IL-13, and (3) IgE.

Figure 2

Figure 2

In patients with minimal change disease, activation of T effector (T eff) cells is by (1) antigen-presenting cells (APCs) after exposure to microbial pathogen-associated molecular patterns (PAMP). It is unknown whether activated B cells have a role (?). (2) Activated T effector cells release cytokines, including interleukin 13 (IL-13). IL-13 will induce the switch from immunoglobulin M (IgM) to IgE in B cells and expression of (3) CD80 by podocytes. A postulated defect in (4) T regulatory (T reg) cell function will allow T effector cells to continue secreting the pathogenetic cytokine.

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