Hypertensive disorders of pregnancy, which include gestational hypertension; preeclampsia; eclampsia; and hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome, are the leading contributors to maternal and perinatal morbidity and mortality worldwide (1). Women with underlying kidney diseases have an increased probability of developing preeclampsia during their pregnancy. Once diagnosed, delivery timing is a delicate balance between the risks of prematurity for the newborn and risks of worsening disease for the mother.
In most cases of preeclampsia, women will develop proteinuria due to a capillary leak and decreased colloid oncotic pressure. However, there are recent publications that support widening the definition of preeclampsia to include cases that manifest as hypertension without proteinuria and vice versa (2). Current practice guidelines state that once proteinuria meets diagnostic criteria for preeclampsia, repeated quantifications of proteinuria are not necessary, as the change in proteinuria (massive, marked, modest, or none) does not correlate with differences in maternal or fetal outcome (1, 3, 4). Thus, urine protein levels are not routinely followed once the diagnosis of preeclampsia is made. The diagnosis of preeclampsia in women with preexisting proteinuria due to underlying kidney diseases is particularly challenging, as there are not well-established clinical criteria to differentiate preeclampsia from worsening kidney diseases using proteinuria alone. Instead, the clinician must rely on other laboratory evaluations and symptoms.
Due to the physiology of preeclampsia, women affected with preeclampsia lack the hypervolemia associated with normal pregnancy. During the delivery admission, a clinician should use caution with fluid management to correct the intravascular depletion and oliguria. For example, vigorous intravenous fluid therapy can lead to increased pulmonary wedge pressure, causing pulmonary edema and subsequent respiratory compromise, especially in the setting of preeclampsia with severe features (5). Additionally, with severe disease, intense vasospasm leads to further contraction of the intravascular space as kidney blood flow and the glomerular filtration rate decrease. These intrarenal changes often manifest as oliguria during labor and the first 24 hours postpartum (1).
Women who are diagnosed with a hypertensive disorder of pregnancy are closely surveilled for signs of uteroplacental insufficiency with fetal growth and amniotic fluid assessments on ultrasound and at least weekly antenatal testing to assess fetal well-being. Fetal growth restriction, oligohydramnios (low amniotic fluid), and/or non-reassuring fetal status may necessitate preterm delivery. However, most preterm deliveries occur due to worsening maternal disease prior to 37 weeks, usually due to severe-range blood pressures (>160 mm Hg systolic or >110 mm Hg diastolic) and/or significant serum laboratory changes (platelets <100 x 109 L, liver enzymes more than twice the upper limit of normal concentrations, or creatinine >1.1 mg/dL or doubling). Serum uric acid levels are not used clinically to make the diagnosis of preeclampsia or to determine disease severity (1).
The current standard of care is to offer delivery at 37 weeks (full term) to those patients with mild hypertensive disease (gestational hypertension or preeclampsia without severe features). This recommendation is based largely on the results of the Induction of Labour Versus Expectant Monitoring for Gestational Hypertension or Mild Pre-eclampsia After 36 Weeks' Gestation (HYPITAT) trial, which showed a significant reduction in a composite of adverse maternal outcome, including new-onset severe preeclampsia, HELLP syndrome, eclampsia, pulmonary edema, or placental abruption in women who underwent induction of labor after 36 weeks compared with expectant management (6). For those women with severe hypertensive disease (HELLP, eclampsia, or preeclampsia with severe features), delivery is typically recommended at 34 weeks or at the time of diagnosis if after 34 weeks. However, delivery timing often requires individualization for these patients. For those patients with pre-existing kidney diseases or cases that fall outside of prescribed guidelines, collaboration and communication between maternal fetal medicine specialists and nephrologists will ensure the best outcomes for both the mother and newborn.
Collaboration and communication between maternal fetal medicine specialists and nephrologists will ensure the best outcomes for both the mother and newborn.
Footnotes
References
- 1.↑
Gestational hypertension and preeclampsia: ACOG Practice Bulletin Summary, Number 222. Obstet Gynecol 2020; 135:1492–1495. doi: 10.1097/AOG.0000000000003892
- 2.↑
Sibai BM, Stella CL. Diagnosis and management of atypical preeclampsia-eclampsia. Am J Obstet Gynecol 2009; 200:481.e1–481.e7. doi: 10.1016/j.ajog.2008.07.048
- 3.↑
Schiff E, et al. The importance of urinary protein excretion during conservative management of severe preeclampsia. Am J Obstet Gynecol 1996; 175:1313–1316. doi: 10.1016/s0002-9378(96)70047-9
- 4.↑
Newman MG, et al. Perinatal outcomes in pre-eclampsia that is complicated by massive proteinuria. Am J Obstet Gynecol 2003; 188:264–268. doi: 10.1067/mob.2003.84
- 5.↑
Hankins GD, et al. Longitudinal evaluation of hemodynamic changes in eclampsia. Am J Obstet Gynecol 1984; 150:506–512. doi: 10.1016/s00002-9378(84)90429-0
- 6.↑
Koopmans CM, et al.; HYPITAT Study Group. Induction of Labour Versus Expectant Monitoring for Gestational Hypertension or Mild Pre-eclampsia After 36 Weeks' Gestation (HYPITAT): A multicentre, open-label randomised controlled trial. Lancet 2009; 374:979–988. doi: 10.1016/S0140-6736(09)60736-4