BACKGROUND AND OBJECTIVES: Women with preeclampsia have increased risk of developing ESRD. This study assessed whether this can be explained by preeclampsia itself or by familial aggregation of common risk factors. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Since 1967, the Medical Birth Registry of Norway has registered data on all births in the country. By linkage with the Norwegian Population Registry, different, but overlapping, cohorts were defined: the first and second cohorts included women and a sibling (first cohort) or child (second cohort) with a registered first birth between 1967 and 2008. Similar cohorts were defined for men. The Norwegian Renal Registry provided data on ESRD from 1980 to June 2009. RESULTS: Cohort 1 was used for the main analyses and included 570,675 women, 291 of whom developed ESRD after a median 18.2 years. Compared with women without preeclampsia and no siblings with preeclampsia, women without preeclampsia but a sibling with preeclampsia had a relative risk (RR) of ESRD of 0.96 (95% confidence interval, 0.59-1.6), women with preeclampsia but no siblings with preeclampsia had a RR of 6.0 (4.4-8.1), and women with preeclampsia and a sibling with preeclampsia had a RR of 2.8 (0.88-8.6). Further analyses of women showed no increased risk of ESRD if a child had preeclampsia in first pregnancy. CONCLUSIONS: Familial aggregation of risk factors does not seem to explain increased ESRD risk after preeclampsia. These findings support the hypothesis that preeclampsia per se may lead to kidney damage.
BACKGROUND AND OBJECTIVES:Women with preeclampsia have increased risk of developing ESRD. This study assessed whether this can be explained by preeclampsia itself or by familial aggregation of common risk factors. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Since 1967, the Medical Birth Registry of Norway has registered data on all births in the country. By linkage with the Norwegian Population Registry, different, but overlapping, cohorts were defined: the first and second cohorts included women and a sibling (first cohort) or child (second cohort) with a registered first birth between 1967 and 2008. Similar cohorts were defined for men. The Norwegian Renal Registry provided data on ESRD from 1980 to June 2009. RESULTS: Cohort 1 was used for the main analyses and included 570,675 women, 291 of whom developed ESRD after a median 18.2 years. Compared with women without preeclampsia and no siblings with preeclampsia, women without preeclampsia but a sibling with preeclampsia had a relative risk (RR) of ESRD of 0.96 (95% confidence interval, 0.59-1.6), women with preeclampsia but no siblings with preeclampsia had a RR of 6.0 (4.4-8.1), and women with preeclampsia and a sibling with preeclampsia had a RR of 2.8 (0.88-8.6). Further analyses of women showed no increased risk of ESRD if a child had preeclampsia in first pregnancy. CONCLUSIONS: Familial aggregation of risk factors does not seem to explain increased ESRD risk after preeclampsia. These findings support the hypothesis that preeclampsia per se may lead to kidney damage.
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