We propose that excessive fructose intake (>50 g/d) may be one of the underlying etiologies of metabolic syndrome and type 2 diabetes. The primary sources of fructose are sugar (sucrose) and high fructose corn syrup. First, fructose intake correlates closely with the rate of diabetes worldwide. Second, unlike other sugars, the ingestion of excessive fructose induces features of metabolic syndrome in both laboratory animals and humans. Third, fructose appears to mediate the metabolic syndrome in part by raising uric acid, and there are now extensive experimental and clinical data supporting uric acid in the pathogenesis of metabolic syndrome. Fourth, environmental and genetic considerations provide a potential explanation of why certain groups might be more susceptible to developing diabetes. Finally, we discuss the counterarguments associated with the hypothesis and a potential explanation for these findings. If diabetes might result from excessive intake of fructose, then simple public health measures could have a major impact on improving the overall health of our populace.

Controversy exists as to whether minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) represent different diseases or are manifestations within the same disease spectrum. Urinary excretion of CD80 (also known as B7.1) is elevated in patients with MCD and hence we tested whether urinary CD80 excretion might distinguish between patients with MCD from those with FSGS. Urinary CD80 was measured in 17 patients with biopsy-proven MCD and 22 with proven FSGS using a commercially available enzyme-linked immunosorbent assay and its molecular size determined by western blot analysis. A significant increase in urinary CD80, normalized to urinary creatinine, was found in patients with MCD in relapse compared to those in remission or those with FSGS. No significant differences were seen when CD80 urinary excretion from MCD patients in remission were compared to those with FSGS. In seven of eight MCD patients in relapse, CD80 was found in glomeruli by immunohistochemical analysis of their biopsy specimen. No CD80 was found in glomeruli of two patients with FSGS and another MCD patient in remission. Thus, our study supports the hypothesis that MCD and FSGS represent two different diseases rather than a continuum of one disease. Urinary CD80 excretion may be a useful marker to differentiate between MCD and FSGS.

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. KeywordsAtopy; nephrotic syndrome; minimal change disease Idiopathic nephrotic syndrome in children is a clinical syndrome associated with a variety of glomerular lesions. Minimal change disease (MCD) is the most common cause of idiopathic nephrotic syndrome. MCD is often abrupt in onset. It can be dramatic in presentation, yet is one of the most rewarding diseases for a physician to manage because response to corticosteroids often is rapid and complete. Because kidney biopsy usually is not performed when the disease responds to corticosteroid therapy, the term MCD has become synonymous with steroid-sensitive nephrotic syndrome. The mechanism(s) underlying the MCD pathogenesis are unknown, although it is believed to be immunologically mediated. 1 Strong evidence suggests that it may be caused by a circulating factor, possibly T-cell related, that causes podocyte dysfunction resulting in massive proteinuria. 2 However, there also have been numerous reports linking MCD with atopic disorders and increases in serum immunoglobulin E (IgE) levels. In this review, we discuss the evidence supporting the association of atopy and whether there may be a common underlying immune disorder that may predispose patients to both conditions. ATOPYAtopy is a term used to describe IgE-mediated diseases. Persons with atopy have a hereditary predisposition to produce IgE antibodies to common allergens and often manifest with 1 or more atopic diseases (asthma, allergic rhinitis, and atopic eczema). Atopic patients mount an exaggerated immunologic response characterized by production of allergen-specific IgE antibodies and positive reactions to extracts of common aeroallergens on skin-prick tests. Type 2 helper T cells (T H 2) from patients with atopy respond to allergens in vitro by expressing such cytokines as interleukin 4 (IL-4) and IL-13 3 (Fig 1A and B). Early Reports of Atopy With MCDIn 1951, Fanconi et al 4 were among of the first to associate atopy and nephrotic syndrome. Forty-three percent of th...

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