What is the global prevalence of immunoglobulin A (IgA) nephropathy?

Updated: May 19, 2020
  • Author: Sohail Abdul Salim, MD, FASN, FACP; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Distribution of IgA nephropathy varies in different geographic regions throughout the world. IgA nephropathy is observed in up to 40% of all biopsies performed for glomerular disease in Asia, compared with 20% in Europe and 10% in North America. High prevalence rates are observed in Singapore, Japan, Australia, Hong Kong, Finland, and southern Europe, whereas low prevalence rates are the rule in the United Kingdom, Canada, and the United States.

A study from Scotland found a significant twofold increase in the diagnosis of IgA nephropathy in the patients residing in the most socioeconomically deprived areas compared with the least deprived ones. The variation was not explained by the demographics of the underlying population. [8] .

In a study by Zhou from east China utilizing renal biopsies from 2001-2017, IgA nephropathy was the most common type of primary glomerulonephritis, accounting for 50% of cases. The diagnosis rate of IgA nephropathy remained steady over that 15-year period; however, the prevalence of membranous nephropathy increased, becoming the second most common type. [9]

In Asia, routine urinalyses are performed for schoolchildren, and kidney biopsies are performed for patients with asymptomatic hematuria, thus raising the reported prevalence of the disease. The estimated annual incidence in Japan is 3.9–4.5 per 100,000 population. [10]  

The prevalence of IgA nephropathy is highest in geographic areas with large numbers of endemic helminthic species that infest humans, and most of the IgA nephropathy susceptibility loci identified by genome-wide association studies include genes involved in the maintenance of the intestinal epithelial barrier and response to mucosal pathogens, which would confer protection against helminthic infestation. Thus, the increased risk of IgA nephropathy in these populations may be an untoward consequence of a protective adaptation to helminthic infections. It would also explain the association of mucosal infections as a frequent trigger for IgA nephropathy. [11]

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