Abstract

Objective IgA nephropathy (IgAN) is a common progressive primary kidney disease, and affects women in childbearing ages. Most of the women with IgAN reportedly have few problems with pregnancy, if they are normotensive and their preconception GFR exceeds 70ml/min. However, much of the relationship between pregnancy and IgAN remains to be investigated. The aim of the present study is to clarify whether IgAN and pregnancy have mutually adverse influence on the other. Design and methods Pregnant grouped ddY (gddY) mice, a model of IgAN, and pregnant Slc:ddY mice (control) were divided into four groups (1. control, 2. control+sFlt-1, 3. gddY, 4. gddY+sFlt-1). PE-like phenotype was induced by overexpressing sFlt-1 using adenovirus administered at 14.5dpc. Results gddY mice showed significantly higher BP before mating and stay hypertensive until the end of experiments. Compared with control and control+sFlt-1 mice, gddY mice showed higher SBP and urinary albumin creatinine ratio. Compared with control mice, gddY mice showed small litter size, small fetal weights and high resorption rate. Moreover, gddY+sFlt-1 mice showed severe endotheliosis and foot process effacement. gddY+sFlt-1 mice showed much poorer pregnancy outcomes. Conclusions Pregnant gddY mice show PE-like phenotype and adverse pregnancy outcome, suggesting that IgAN aggravates PE. Pregnancy is a risk factor of progressing IgAN.

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