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Kidney Int. 2004 Sep;66(3):905-8.

Epidemiologic data of primary glomerular diseases in western France.

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1
Laboratoire d'Anatomie Pathologique, Centre Hospitalier et Universitaire, Rennes, France. pierre.simon@ch-stbrieuc.fr

Abstract

Between January 1, 1976, and December 31, 2002, histologic diagnosis of primary glomerular diseases (PGD) was made in 898 patients born and living at the time of diagnosis in a region of France, comprising 412,735 inhabitants, of whom 391,265 were aged from 10 to 85 years. The prevalence of PGD during a 75-year exposure to risk (10 to 85 years of age) was evaluated to 6.9 in 1000 (8.2 in 1000 males and 5.1 in 1000 females) during the 27-year period. The most common PGD was IgA nephropathy (IgAN) with a prevalence of 2.4 in 1000 (3.6 in 1000 males and 1.3 in 1000 females). The annual incidence of PGD was evaluated separately for two consecutive 10-years periods: period A (1976 to 1985), period B (1986 to 1995) and for one 7-year period: period C (1996 to 2002). Within each of these three periods, annual incidence of PGD was 89, 76, and 65 per million inhabitants. During this 27-year period, the annual incidences of membranoproliferative glomerulonephritis (GN) and membranous nephropathy were declining and the incidence of crescentic proliferative GN was strongly progressing, whereas annual incidence of nephrosis remained stable. The incidence of IgAN remained the same throughout the three periods: 28, 28, and 26 per million inhabitants. Whereas the incidence of IgAN was three- to fourfold higher in the adult aged from 20 to 59 years than in the elderly during the periods A (38 vs. 11 per million inhabitants) and B (37 vs. 12 per million inhabitants), the incidence became similar whatever age groups during the last period C (20 to 59 years, 25 per million inhabitants; 60 to 79 years, 27 per million inhabitants; and 80 years and over, 28 per million inhabitants. The stability of annual incidence according to period and age, which is demonstrated for the first time during the last period, provides a new evidence of a role for genetic factors in the pathogenesis of IgAN.

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