Nina D Paauw1, Anne Marijn van der Graaf2, Rita Bozoglan3, David P van der Ham4, Gerjan Navis5, Ron T Gansevoort5, Henk Groen6, A Titia Lely7. 1. Department of Obstetrics, Wilhelmina Children's Hospital Birth Center, University Medical Center Utrecht, Utrecht, the Netherlands. 2. Department of Pathology, University Medical Centre Groningen, Groningen, the Netherlands; Department of Medical Biology, University Medical Centre Groningen, Groningen, the Netherlands; Department of Obstetrics and Gynaecology, University Medical Centre Groningen, Groningen, the Netherlands. 3. Department of Obstetrics and Gynaecology, University Medical Centre Groningen, Groningen, the Netherlands. 4. Department of Obstetrics and Gynaecology, Martini Hospital, Groningen, the Netherlands. 5. Department of Nephrology, University Medical Centre Groningen, Groningen, the Netherlands. 6. Department of Epidemiology, University of Groningen, Groningen, the Netherlands. 7. Department of Obstetrics, Wilhelmina Children's Hospital Birth Center, University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address: a.t.lely@umcutrecht.nl.
Abstract
BACKGROUND: Registry-based studies report an increased risk for end-stage kidney disease after hypertensive disorders of pregnancy (HDPs). It is unclear whether HDPs lead to an increased incidence of chronic kidney disease (CKD) and/or progression of kidney function decline. STUDY DESIGN: Subanalysis of the Prevention of Renal and Vascular Endstage Disease (PREVEND) Study, a Dutch population-based cohort with follow-up of 5 visits approximately 3 years apart. SETTING & PARTICIPANTS: Women without and with patient-reported HDPs (non-HDP, n=1,805; HDP, n=977) were identified. Mean age was 50 years at baseline and median follow-up was 11 years. FACTOR: An HDP. OUTCOMES: (1) The incidence of CKD using Cox regression and (2) the course of kidney function (estimated glomerular filtration rate [eGFR] and 24-hour albuminuria) over 5 visits using generalized estimating equation analysis adjusted for age, mean arterial pressure, and renin-angiotensin system (RAS) blockade. CKD was defined as eGFR<60mL/min/1.73m2 and/or 24-hour albuminuria with albumin excretion > 30mg, and end-stage kidney disease was defined as receiving dialysis or kidney transplantation. RESULTS: During follow-up, none of the women developed end-stage renal disease and the incidence of CKD during follow-up was similar across HDP groups (HR, 1.04; 95% CI, 0.79-1.37; P=0.8). Use of RAS blockade was higher after HDP at all visits. During a median of 11 years, we observed a decrease in eGFR in both groups, with a slightly steeper decline in the HDP group (98±15 to 88±16 vs 99±17 to 91±15mL/min/1.73m2; Pgroup<0.01, Pgroup*visit<0.05). The group effect remained significant after adjusting for mean arterial pressure, but disappeared after adjusting for RAS blockade. The 24-hour albuminuria did not differ between groups. LIMITATIONS: No obstetric records available. HDPs defined by patient report rather than health records. CONCLUSIONS: HDPs did not detectably increase the incidence of CKD. During follow-up, we observed no differences in albuminuria, but observed a marginally lower eGFR after HDP that was no longer statistically significant after adjusting for the use of RAS blockers. In this population, we were unable to identify a significant risk for kidney function decline after patient-reported HDP.
BACKGROUND: Registry-based studies report an increased risk for end-stage kidney disease after hypertensive disorders of pregnancy (HDPs). It is unclear whether HDPs lead to an increased incidence of chronic kidney disease (CKD) and/or progression of kidney function decline. STUDY DESIGN: Subanalysis of the Prevention of Renal and Vascular Endstage Disease (PREVEND) Study, a Dutch population-based cohort with follow-up of 5 visits approximately 3 years apart. SETTING & PARTICIPANTS: Women without and with patient-reported HDPs (non-HDP, n=1,805; HDP, n=977) were identified. Mean age was 50 years at baseline and median follow-up was 11 years. FACTOR: An HDP. OUTCOMES: (1) The incidence of CKD using Cox regression and (2) the course of kidney function (estimated glomerular filtration rate [eGFR] and 24-hour albuminuria) over 5 visits using generalized estimating equation analysis adjusted for age, mean arterial pressure, and renin-angiotensin system (RAS) blockade. CKD was defined as eGFR<60mL/min/1.73m2 and/or 24-hour albuminuria with albumin excretion > 30mg, and end-stage kidney disease was defined as receiving dialysis or kidney transplantation. RESULTS: During follow-up, none of the women developed end-stage renal disease and the incidence of CKD during follow-up was similar across HDP groups (HR, 1.04; 95% CI, 0.79-1.37; P=0.8). Use of RAS blockade was higher after HDP at all visits. During a median of 11 years, we observed a decrease in eGFR in both groups, with a slightly steeper decline in the HDP group (98±15 to 88±16 vs 99±17 to 91±15mL/min/1.73m2; Pgroup<0.01, Pgroup*visit<0.05). The group effect remained significant after adjusting for mean arterial pressure, but disappeared after adjusting for RAS blockade. The 24-hour albuminuria did not differ between groups. LIMITATIONS: No obstetric records available. HDPs defined by patient report rather than health records. CONCLUSIONS: HDPs did not detectably increase the incidence of CKD. During follow-up, we observed no differences in albuminuria, but observed a marginally lower eGFR after HDP that was no longer statistically significant after adjusting for the use of RAS blockers. In this population, we were unable to identify a significant risk for kidney function decline after patient-reported HDP.
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