HTN in pregnancy
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"hypertension" AND "pregnancy" AND "preeclampsia"
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Hypertension in Pregnancy
Classification
Hypertension in pregnancy is defined as BP ≥ 140/90 mmHg. The normal physiologic trend shows a nadir at ~18-22 weeks (median 113/69 mmHg), rising back to term levels. The upper reference limit is 144/95 mmHg at term.
There are five main categories:
| Category | Definition | Key Risk |
|---|---|---|
| Transient HTN | BP normalizes on subsequent testing without treatment | 40% risk of gestational HTN/preeclampsia |
| White-coat HTN | Clinic BP ≥140/90 but home BP <135/85 | 8% risk of preeclampsia (double baseline) |
| Gestational HTN | New HTN after 20 weeks, no features of preeclampsia | 25% progress to preeclampsia |
| Preeclampsia | HTN after 20 weeks + maternal/uteroplacental organ dysfunction | Risk of chronic HTN, CVD, CKD later |
| Chronic HTN | BP ≥140/90 pre-pregnancy or before 20 weeks, persists >12 wks postpartum | 25% risk of superimposed preeclampsia |
- Comprehensive Clinical Nephrology, 7th Edition
Epidemiology
- HTN affects 10-12% of all pregnancies
- Global preeclampsia incidence: 4.6% of all pregnancies
- Eclampsia: 1.4% globally (lower in high-income countries - ~0.3% of hypertensive pregnancies)
- Comprehensive Clinical Nephrology, 7th Edition
Preeclampsia
Diagnostic Criteria
Preeclampsia = new hypertension after 20 weeks + any one of the following:
- Proteinuria: uPCR >30 mg/mmol or uACR >8 mg/mmol (note: proteinuria is not essential if other criteria exist)
- AKI
- Elevated transaminases (liver dysfunction)
- Neurological features (headache, visual disturbance, altered consciousness, seizures)
- Thrombocytopenia (platelets <100,000/mm³)
- Uteroplacental dysfunction: fetal growth restriction, abnormal umbilical artery Doppler, or stillbirth
Severe features include: SBP ≥160 or DBP ≥110 mmHg, pulmonary edema, thrombocytopenia, marked renal/hepatic dysfunction, and CNS manifestations.
Risk Factors
Obstetric: Nulliparity, previous preeclampsia, multiple gestation, new partner, IVF conception
Medical: Chronic HTN, CKD, pre-gestational diabetes, obesity (BMI >30), antiphospholipid syndrome, SLE, polycystic ovarian syndrome
Genetic/Other: Thrombophilia, first-degree relative with preeclampsia, age >40, born SGA
Pathogenesis
The mechanism follows a two-stage model:
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Stage 1 - Abnormal placentation (early pregnancy): Failed trophoblastic invasion of spiral arteries. Normally, trophoblasts remodel spiral arteries into low-resistance, high-capacitance vessels. In preeclampsia, this remodeling fails, causing uteroplacental ischemia and oxidative stress in the placenta.
-
Stage 2 - Systemic maternal disease: Hypoxic placenta releases factors causing:
- Decreased circulating PlGF (placental growth factor - proangiogenic)
- Increased sFlt-1 (soluble fms-like tyrosine kinase-1 - antiangiogenic)
- Systemic endothelial dysfunction → hypertension, proteinuria, multiorgan involvement
- Comprehensive Clinical Nephrology, 7th Edition
HELLP Syndrome
HELLP = Hemolysis, Elevated Liver enzymes, Low Platelets
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Considered a variant of severe preeclampsia, though may be a separate entity
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Women with HELLP tend to be older, White, and multiparous compared to preeclampsia
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Characteristic renin-angiotensin changes of preeclampsia do not occur in HELLP
-
AKI occurs in 10-25% of preeclampsia/HELLP cases (vs ~1% in preeclampsia alone)
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Management is similar to severe preeclampsia - delivery is the definitive treatment
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Key distinction from TTP: preceding HTN/proteinuria/liver injury favor HELLP; severe hemolysis/renal failure without liver injury favors TTP. Plasma exchange benefits TTP but not HELLP.
-
Brenner and Rector's The Kidney, 2-Volume Set; Creasy & Resnik's Maternal-Fetal Medicine
Eclampsia
- Seizures in a woman with preeclampsia that cannot be attributed to other causes
- ~20% of eclamptic episodes occur >48 hours postpartum - vigilance must continue after delivery
- Magnesium sulfate is the treatment of choice for seizure prevention and treatment (superior to phenytoin/diazepam)
Management
Treatment Thresholds
- Severe HTN (SBP ≥160 or DBP ≥105-110 mmHg): Immediate antihypertensive therapy is indicated - untreated severe HTN carries risk of maternal stroke and placental abruption
- Mild-moderate HTN (140-159/90-109 mmHg): Treat to reduce risk of progression; target BP typically 130-150/80-100 mmHg
Antihypertensive Drug Safety in Pregnancy
| Drug | Class | Notes |
|---|---|---|
| Methyldopa | Central α2-agonist | First-line; most extensive safety data; sedation, short duration |
| Labetalol (oral/IV) | α+β blocker | Preferred β-blocker; theoretical benefit on uteroplacental flow; avoid in asthma |
| Nifedipine (long-acting) | CCB | Once-daily dosing; may cause edema |
| Nicardipine (IV) | CCB | Extensive data as tocolytic; effective for acute control |
| Hydralazine (IV/IM) | Direct vasodilator | Second-line acute; risk of maternal hypotension and placental abruption |
| Metoprolol | β-blocker | Less safety data than labetalol |
| Verapamil/Diltiazem | CCB | Limited data; no known adverse fetal effects |
| Diuretics | - | Generally avoided - may impair plasma volume expansion |
| Atenolol | β-blocker | Avoid - associated with fetal growth restriction |
| Nitroprusside | Vasodilator | Avoid if >4 hours - fetal cyanide poisoning risk |
| ACE inhibitors | RAAS | Contraindicated - fetal renal agenesis, oligohydramnios, skull defects |
| ARBs | RAAS | Contraindicated - same risks as ACEi |
- Brenner and Rector's The Kidney; Goodman & Gilman's Pharmacological Basis of Therapeutics
Acute Severe HTN Protocol
- Labetalol IV: 20 mg IV, escalate to 40 mg at 10 min if inadequate
- Hydralazine IV/IM: 5-10 mg, repeat at 20-min intervals
- Add magnesium sulfate for CNS manifestations or severe preeclampsia (seizure prophylaxis)
Definitive Treatment
Delivery is the only cure for preeclampsia. If severe preeclampsia with end-organ damage and a mature fetus - deliver promptly. If very preterm, temporizing with hospitalization and pharmacotherapy may allow further fetal maturation.
Prevention
Low-dose aspirin (75-150 mg/day) initiated before 16 weeks in high-risk women reduces preeclampsia incidence. Meta-analyses support its use; a Cochrane review confirms benefit. Some guidelines (e.g., USPSTF) recommend universal aspirin for moderate-high risk women. Long-term follow-up data on children exposed to low-dose aspirin in utero are reassuring.
- Brenner and Rector's The Kidney; NKF Primer on Kidney Diseases, 8e
Calcium supplementation (in populations with low calcium intake) also reduces BP disorders of pregnancy.
Secondary Causes of HTN in Pregnancy
At least 10% of chronic HTN in pregnancy has a secondary cause. Screen for:
- Renal artery stenosis (fibromuscular dysplasia) - suspect with severe resistant HTN; MR angiography is safe
- Pheochromocytoma - catastrophic if missed; can trigger fatal crisis during labor
- Primary hyperaldosteronism - may worsen in pregnancy (progesterone partially antagonizes aldosterone but not universally); spironolactone has theoretical risks (antiandrogenic) - eplerenone preferred if needed
- Obstructive sleep apnea - 40% of women with HTN in pregnancy may have OSA
Long-term Implications
Women who have had preeclampsia carry significantly elevated long-term risks of:
- Chronic hypertension
- Cardiovascular disease
- Chronic kidney disease
These women warrant cardiovascular risk factor surveillance postpartum.
Recent evidence (2025): A network meta-analysis in AJOG (PMID 40216176) compared oral antihypertensives in pregnancy and may update relative preferences among labetalol, nifedipine, and methyldopa - worth reviewing if making clinical decisions.
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