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Published on: June 23, 2015
Pregnancy and Kidney Disease Progression in Autosomal Dominant Polycystic Kidney Disease
Stephanie Lapierre-Nguyen1, Zhiying You1, Berenice Gitomer1
1Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado Anschutz, Aurora, Colorado.
Key Points:
In an observational cohort of mostly non-Hispanic White women, pregnancy was not associated with later-life accelerated kidney function decline. Pregnancy occurring during the HALT Progression of Polycystic Kidney Disease (HALT-PKD) trial was not associated with kidney disease progression relative to women who did not become pregnant. Prior evidence indicates that adverse pregnancy outcomes may be involved in autosomal dominant polycystic kidney disease progression; pregnant women should be closely monitored.
Background:
Data are conflicting regarding whether pregnancy influences disease progression in women with autosomal dominant polycystic kidney disease (ADPKD). This study examined whether pregnancy or number of pregnancies was associated with kidney disease progression in women with ADPKD.
Methods:
Women with early- (study A) and late-stage (study B) ADPKD from the HALT Progression of Polycystic Kidney Disease (HALT-PKD) trial were included to examine the association between self-reported number of pregnancies (categorical predictor: no pregnancy versus 1-2 pregnancies and ≥3 pregnancies), annual slope of eGFR, annual percent change in total kidney volume (%ΔTKV), and a composite outcome (kidney failure, 50% decline in eGFR, or death) using multivariable linear regression and Cox proportional hazard models. In addition, women who became pregnant, had full-term pregnancies, and available data during study participation ( n =13) were propensity matched (1:4) to women who were not pregnant during study participation, and a mixed model was applied to determine the association of pregnancy with eGFR slope and %ΔTKV.
Results:
Across all analyses, 455 women with a median age of 45 (interquartile range, 38-50) years and eGFR of 69±25 ml/min per 1.73 m 2 at baseline were included. One hundred ninety-nine women had 1-2 pregnancies, and 165 women had ≥3 pregnancies. There was no association of 1-2 pregnancies or ≥3 pregnancies (versus no pregnancies) with eGFR slope ( β -estimate [95% confidence interval (CI)]; 1-2 pregnancies: 0.22 [-0.44 to 0.89]; ≥3 pregnancies: -0.46 [-1.16 to 0.25]), %ΔTKV ( β -estimate [95% CI]; 1-2 pregnancies: 0.92 [-0.34 to 2.17]; ≥3 pregnancies: 0.69 [-0.67 to 2.04]), or time to composite outcome (hazard ratio [95% CI]; 1-2 pregnancies: 1.04 [0.56 to 1.93]; ≥3 pregnancies: 1.48 [0.78 to 2.77]) in adjusted models. Moreover, there was no difference in annual eGFR slope ( β -estimate: -0.14 [95% CI, -2.72 to 2.44]) and %ΔTKV ( β -estimate: 0.04 [95% CI, -3.74 to 3.82]) in women who became pregnant matched to women who did not became pregnant during their participation in the study.
Conclusions:
Pregnancy was not associated with ADPKD progression among women with early- and late-stage ADPKD enrolled in the HALT-PKD trial.
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