Familial factors in the association between preeclampsia and later ESRD.
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ABSTRACT: 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.
SUBMITTER: Vikse BE
PROVIDER: S-EPMC3488941 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundSeveral registry-based studies, using diagnostic codes, have suggested that preeclampsia is a risk factor for end-stage renal disease (ESRD). However, because the 2 diseases share risk factors, the true nature of their association remains uncertain. Our goals were to conduct a population-based study to determine the magnitude of the association between preeclampsia and ESRD and evaluate the role of shared risk factors.Study designPopulation-based nested case-control study.Setting & participantsThe US Renal Data System was used to identify women with ESRD from a cohort of 34,581 women who gave birth in 1976 to 2010 in Olmsted County, MN. 44 cases of ESRD were identified and each one was matched to 2 controls based on year of birth (±1 year), age at first pregnancy (±2 years), and parity (±1 or ≥4).PredictorPreeclamptic pregnancy, confirmed by medical record review.OutcomeESRD.MeasurementsPrepregnancy serum creatinine and urine protein measurements were recorded. Comorbid conditions existing prior to pregnancy were abstracted from medical records and included kidney disease, obesity, diabetes, and hypertension.ResultsThere was evidence of kidney disease prior to the first pregnancy in 9 of 44 (21%) cases and 1 of 88 (<1%) controls. Per chart review, 8 of 44 (18%) cases versus 4 of 88 (5%) controls had preeclamptic pregnancies (unadjusted OR, 4.0; 95% CI, 1.21-13.28). Results were similar after independent adjustment for race, education, diabetes, and hypertension prior to pregnancy. However, the association was attenuated and no longer significant after adjustment for obesity (OR, 3.25; 95% CI, 0.93-11.37).LimitationsThe limited number of ESRD cases and missing data for prepregnancy kidney function.ConclusionsOur findings confirm that there is a sizable association between preeclampsia and ESRD; however, obesity is a previously unexplored confounder. Pre-existing kidney disease was common, but not consistently coded or diagnosed.
| S-EPMC5366077 | biostudies-literature
Project description:Association between preeclampsia and gut microbiota
| PRJEB31042 | ENA
Project description:It has not been established how history of hypertension in the father or mother of pregnant women, combined with obesity or smoking, affects the risk of main forms of pregnancy-induced hypertension. A cohort of 912 pregnant women, recruited in the first trimester, was assessed; 113 (12.4%) women developed gestational hypertension (GH), 24 (2.6%) developed preeclampsia (PE) and 775 women remained normotensive (a control group). Multiple logistic regression was used to calculate adjusted odds ratios (AOR) (and 95% confidence intervals) of GH and PE for chronic hypertension in the father or mother of pregnant women. Some differences were discovered. (1) Paternal hypertension (vs. absence of hypertension in the family) was an independent risk factor for GH (AOR-a = 1.98 (1.2-3.28), p = 0.008). This odds ratio increased in pregnant women who smoked in the first trimester (AOR-a = 4.71 (1.01-21.96); p = 0.048) or smoked before pregnancy (AOR-a = 3.15 (1.16-8.54); p = 0.024), or had pre-pregnancy overweight (AOR-a = 2.67 (1.02-7.02); p = 0.046). (2) Maternal hypertension (vs. absence of hypertension in the family) was an independent risk factor for preeclampsia (PE) (AOR-a = 3.26 (1.3-8.16); p = 0.012). This odds ratio increased in the obese women (AOR-a = 6.51 (1.05-40.25); p = 0.044) and (paradoxically) in women who had never smoked (AOR-a = 5.31 (1.91-14.8); p = 0.001). Conclusions: Chronic hypertension in the father or mother affected the risk of preeclampsia and gestational hypertension in different ways. Modifiable factors (overweight/obesity and smoking) may exacerbate the relationships in question, however, paradoxically, beneficial effects of smoking for preeclampsia risk are also possible. Importantly, paternal and maternal hypertension were not independent risk factors for GH/PE in a subgroup of women with normal body mass index (BMI).
| S-EPMC8296897 | biostudies-literature
Project description:IntroductionFamilial IgA nephropathy (IgAN) has been widely reported. However, its clinicohistologic characteristics and long-term prognosis are not clear.MethodsA total of 348 familial IgAN cases from 167 independent families were recruited and their clinicohistologic characteristics as well as lifetime risk of end-stage renal disease (ESRD) were compared to 1116 sporadic IgAN patients from the same geographic region.ResultsOf all familial IgAN patients, 60 (17%) came from 32 single-generation (SG; all affected individuals are siblings) families, whereas 286 (82%) came from 134 multiple-generation (MG; affected individuals were present in at least 2 consecutive generations) families. The lifetime ESRD risk was significantly higher in familial patients than sporadic ones after adjusting by gender (hazard ratio [HR]=1.40, 95% confidence interval [CI]: 1.12-1.74, P = 0.004), with 5 years younger in median ESRD age (60 years vs. 65 years in familial and sporadic cases separately). Interestingly, among familial patients, we found cases from SG families (vs. MG families: HR = 2.62, 95% CI: 1.59-4.31, P < 0.001) or with early onset (onset age <30 years) (vs. late onset: HR = 4.79, 95% CI: 3.16-7.26, P < 0.001) had higher lifetime ESRD risk. Furthermore, among sporadic patients, men had lower estimated glomerular filtration rate (eGFR), higher urine protein, higher Oxford T score, and higher risk for life span ESRD compared with women (male vs. female, 25% vs. 17%, P = 0.003) whereas these gender differences were not seen in familial patients.ConclusionFamilial IgAN cases had poorer renal outcomes and less gender differences compared with sporadic cases. These findings provide evidence that familial disease represent a distinct subtype of more progressive IgAN. Early diagnosis could improve the prognosis of cases with familial IgAN.
| S-EPMC7783566 | biostudies-literature
Project description:Background and objectivesA recent meta-analysis found that about 30% of women with a previous preeclamptic pregnancy had persistent microalbuminuria at follow-up. The analysis was, however, based on small studies, and more data are needed.Design, setting, participants, & measurementsUsing data from the Medical Birth Registry in Norway, this study identified women with or without preeclampsia in their first pregnancy 9-11 years previously (1998-2000). Women with diabetes, rheumatic disease, essential hypertension, or renal disease before first pregnancy and/or preeclampsia in later pregnancies were excluded. Eighty-nine women with and 69 women without preeclampsia participated in the study. Urinary albumin-to-creatinine ratio (ACR) was measured in three morning urine samples. Estimated GFR (eGFR) was calculated using the CKD-Epidemiology Collaboration formula.ResultsMedian urinary ACR in follow-up urine samples was 0.53 mg/mmol for women with and 0.50 mg/mmol for women without preeclampsia (P=0.54). Only one woman (1%) with previous preeclampsia had urinary ACR >2.5 mg/mmol in two of three urine samples. Preeclampsia was not associated with urinary ACR above the 75th percentile. Women with preeclampsia did not have significantly higher eGFR than women without preeclampsia (107.9 versus 104.9 ml/min per 1.73 m(2); P=0.12), but preterm preeclampsia was significantly associated with eGFR above the 75th percentile (P=0.03).ConclusionsIn this population-based study of otherwise healthy women, preeclampsia 10 years earlier was not associated with increased risk of persisting microalbuminuria. Estimated GFR was not significantly different between women with and those without preeclampsia, but preterm preeclampsia was associated with high normal eGFR.
| S-EPMC3700700 | biostudies-literature
Project description:BACKGROUND:Preeclampsia is a serious pregnancy-specific syndrome with incompletely understood pathogenesis. Previous study has demonstrated that the decreased CXCR2 in preeclamptic placentas may contribute to the development of preeclampsia. The role of single nucleotide polymorphisms (SNPs) of CXCR2 gene in the pathogenesis of preeclampsia remains largely unexplored. Thus, we aimed to investigate the association between polymorphisms of CXCR2 gene and preeclampsia in Han Chinese women. METHODS:Totally 481 pregnant women, including 243 controls and 238 patients with preeclampsia were recruited. The rs1126579 and rs2230054 polymorphisms in CXCR2 gene were tested using polymerase chain reaction-restriction fragment length polymorphism method. RESULTS:Significantly increased risk of preeclampsia was observed in the rs1126579 CC or TC/CC genotypes when compared with TT genotype (CC vs. TT: odss ratio [OR] = 2.11, 95% confidence interval [CI] = 1.18-3.76, p = 0.039; TC/CC vs. TT: OR = 1.89, 95% CI = 1.29-2.78, p = 0.001). Markedly higher risk of preeclampsia was found to be associated with rs1126579 TC genotype (TC vs. TT/CC: OR = 1.48, 95% CI = 1.04-2.12, p = 0.031). After stratification analysis, the different distribution of TC/CC genotypes was particularly significant in the severe preeclampsia group (OR = 2.15, 95% CI = 1.42-3.24, p < 0.01), the early-onset severe preeclampsia group (OR = 1.97, 95% CI = 1.14-3.42, p = 0.013), and the late-onset severe preeclampsia group (OR = 2.29, 95% CI = 1.39-3.78, p < 0.01). Besides, TC genotype carriers had a 1.55 fold increased risk of severe preeclampsia (95% CI = 1.06-2.27, p = 0.022) and a 1.80 fold increased risk of late onset severe preeclampsia (95% CI = 1.14-2.83, p = 0.01) than those of TT/CC genotype carriers. CONCLUSIONS:Our study suggests a genetic association between rs1126579 polymorphism in CXCR2 gene and increased risk of preeclampsia. These data provide a new clue for future investigation.
| S-EPMC6465673 | biostudies-literature
Project description:ObjectivesTo investigate the relationship between a prostasin gene variations and the development of preeclampsia in a Pakistani female population. Methods: This was a case-control study carried out at University of Karachi, Karachi, Pakistan between May 2018 and 2019. A single nucleotide polymorphism (SNP) at rs12597511 locus was examined with polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analyses in 76 preeclamptic and 74 normotensive expecting mothers.ResultsWe observed significantly increased risk of preeclampsia associated with the CC genotype of rs12597511 polymorphism as compared to TT (p less than 0.001, OR=8.08, 95% CI: 1.28-31.19) and TT/TC (p less than 0.001, OR=14.66 and 95% CI: 3.31-65.07) genotypes carriers. Calculation of the allelic distribution revealed a higher frequency of the T allele (82%) among controls; however, the C allele was more prevalent in the preeclamptic group (36%) significantly.ConclusionThe significantly higher C allele frequency in the prostasin gene at the rs12597511 locus in the preeclamptic group indicates that the distribution of the C allele of the prostasin gene is a potential risk factor contributing to the development of preeclampsia.
| S-EPMC7804221 | biostudies-literature
Project description:Background and objectivesExperimental evidence suggests a role for monocytes in the biology of kidney disease progression; however, whether monocyte count is associated with risk of incident CKD, CKD progression, and ESRD has not been examined in large epidemiologic studies.Design, settings, participants, & measurementsWe built a longitudinal observational cohort of 1,594,700 United States veterans with at least one eGFR during fiscal year 2004 (date of last eGFR during this period designated time zero) and no prior history of ESRD, dialysis, or kidney transplant. Cohort participants were followed until September 30, 2013 or death. Monocyte count closest to and before time zero was categorized in quartiles: quartile 1, >0.00 to ≤0.40 thousand cells per cubic millimeter (k/cmm); quartile 2, >0.40 to ≤0.55 k/cmm; quartile 3, >0.55 to ≤0.70 k/cmm; and quartile 4, >0.70 k/cmm. Survival models were built to examine the association between monocyte count and risk of incident eGFR<60 ml/min per 1.73 m2, risk of incident CKD, and risk of CKD progression defined as doubling of serum creatinine, eGFR decline ≥30%, or the composite outcome of ESRD, dialysis, or renal transplantation.ResultsOver a median follow-up of 9.2 years (interquartile range, 8.3-9.4); in adjusted survival models, there was a graded association between monocyte counts and risk of renal outcomes. Compared with quartile 1, quartile 4 was associated with higher risk of incident eGFR<60 ml/min per 1.73 m2 (hazard ratio, 1.13; 95% confidence interval, 1.12 to 1.14) and risk of incident CKD (hazard ratio, 1.15; 95% confidence interval, 1.13 to 1.16). Quartile 4 was associated with higher risk of doubling of serum creatinine (hazard ratio, 1.22; 95% confidence interval, 1.20 to 1.24), ≥30% eGFR decline (hazard ratio, 1.18; 95% confidence interval, 1.17 to 1.19), and the composite renal end point (hazard ratio, 1.19; 95% confidence interval, 1.16 to 1.22). Cubic spline analyses of the relationship between monocyte count levels and renal outcomes showed a linear relationship, in which risk was higher with higher monocyte count. Results were robust to changes in sensitivity analyses.ConclusionsOur results show a significant association between higher monocyte count and risks of incident CKD and CKD progression to ESRD.
| S-EPMC5383390 | biostudies-literature
Project description:ObjectiveTo estimate the relationship between the risk of preeclampsia and two thrombophilia gene single-nucleotide polymorphisms (SNPs), the factor V G1691A SNP and the prothrombin G20210A SNP.Date sourcesA systematic search of the English-language literature up to November 2012 was performed using Medline and EMBASE. Search terms included "preeclampsia," "thrombophilia," "factor V Leiden," "prothrombin gene 20210," and their combinations.Result(s)Thirty-seven studies with 5048 preeclampsia patients and 6796 controls were included in the meta-analysis. We found that the prothrombin G20210A polymorphism was associated with an increased risk of all preeclampsia (pooled odds ratio (OR)?=?1.81, 95% confidence interval (CI) 1.25-2.63) and severe preeclampsia (pooled OR?=?3.02, 95%CI 2.06-4.45). Meanwhile, the pooled OR for the association between factor V Leiden and all preeclampsia was 1.60 (95%CI 1.28-2.00) and 2.45 (95%CI 1.63-3.69) for the cases of severe preeclampsia.Conclusion(s)This meta-analysis supports that the factor V G1691A SNP and the prothrombin G20210A SNP are associated with an increased risk for both preeclampsia overall and severe preeclampsia.
| S-EPMC4072713 | biostudies-literature
Project description:Lower self-control is a significant correlate or predictor of a wide range of adult outcomes, and this association may be due to more general tendencies toward childhood externalizing problems. The present study examined the association between toddlerhood self-control expressed within a "don't" compliance task (at 14-36 months) and later externalizing problems (parent-reported externalizing problems from age 4 to 12 years, teacher-reported externalizing problems from age 7 to 12 years, and self-reported conduct disorder symptoms at age 17 years) in a longitudinal, genetically informative study. The slope of self-control, but not its intercept, predicted later teacher-reported, but not parent- or self-reported, externalizing problems. That is, increase in self-control during toddlerhood was associated with lower levels of later teacher-reported externalizing problems. The slope of self-control was no longer a significant predictor of teacher-reported externalizing problems after controlling for observed disregard for others, a robust predictor of externalizing problems. Thus, the hypothesis that self-control is the primary predictor of externalizing problems was not supported. Results from genetic analyses suggested that the covariance between the slope of self-control and teacher-reported externalizing problems is due to both genetic and shared environmental influences.
| S-EPMC5834389 | biostudies-literature