Ivan D. Maya, MD, FACP
INDEX WORDS: Preeclampsia; endotheliosis; proteinuria; vascular endothelial growth factor.
reeclampsia usually develops during the third trimester of pregnancy and resolves after delivery. The hallmarks are new onset of proteinuria and hypertension during the last trimesterof pregnancy associated with edema and hyperuricemia1 (Table 1). The amount of proteinuria probably is related to the endothelial damage in glomeruli.2 The increase in blood pressure probably is secondary to the high vascular resistance, which decreases arterial compliance and causes endothelial dysfunction.3-5 Although the cause of preeclampsia is not clear, there is evidence that theendothelial alteration in patients with preeclampsia is the result of decreased levels of 1 or more circulating factors, including vascular endothelial growth factor (VEGF)6 and placental growth factor (PlGF).7 Both are angiogenic substances that have an important role in keeping the endothelial cells healthy. The decrease in plasma levels of these angiogenic factors causes endothelial dysfunction andmicroangiopathy targeting different organs, including the brain, liver, and kidney.8 It is very unusual to develop preeclampsia before 20 weeks of gestation, and if present, it is associated most commonly with trophoblastic disease (hydatidiform mole), hydrops fetalis, and genetic malformations.9-11 Case reports of preeclampsia before 20 weeks of gestation were reported from Japan12 and the UnitedKingdom.13 This case report is a rare presentation of preeclampsia before 20 weeks of gestation in a 17-year-old African-American primigravida.
CASE REPORT Clinical History
A 17-year-old African-American woman at 19 weeks’ gestation in her ﬁrst pregnancy (dated by means of an 8-week ultrasound) presented for her routine monthly prenatal visit. Up to that time, her pregnancy had been uneventful. Herblood pressure and urinalysis results were normal until her ofﬁce visit, when blood pressure was recorded at 148/90 mm Hg and she had 4 proteinuria by means of dipstick urinalysis. She was admitted to the hospital for further testing. Her medical, surgical, and social history was negative. Current medications included only prenatal vitamins.
She had no allergies, and review of systemsshowed negative results. Physical examination showed a blood pressure of 148/87 mm Hg, pulse of 74 beats/min, height of 5 feet, weight of 164 pounds, and body mass index of 32 kg/m2. She was afebrile. Physical examination results were unremarkable, except for a gravid uterus. Her initial laboratory studies showed a normal cell blood count, and chemistry proﬁle showed the following values: creatinine,0.8 mg/dL (70.7 mmol/L); blood urea nitrogen, 9 mg/dL (3.21 mmol/L); glucose, 77 mg/dL (4.3 mmol/L); albumin, 2.4 g/dL (24 g/L); and aspartate transaminase, 49 U/L. Glomerular ﬁltration rate calculated using the Modiﬁcation of Diet in Renal Disease Study equation was 94 mL/min/1.73 m2 (1.57 mL/s/1.73 m2). Antinuclear antibody titer was 1:80, and antistreptolysin O titer was negative.Anticardiolipin antibodies to immunoglobulin G and immunoglobulin M were negative. Group A streptococcus test was negative, as was a rapid plasma reagin test. Protime was normal, with an international normalized ratio of 0.94 and a partial thromboplastin time of 26 seconds. Urinalysis showed 3 protein, but otherwise was unremarkable. A 24-hour urine sample showed 1,789 mg of protein. PlGF and VEGF plasmalevels were not measured. Ultrasound of the kidneys showed a right kidney measuring 10.7 cm and a left kidney measuring 11.2 cm. Both kidneys were mildly echogenic, but otherwise unremarkable. Renal Doppler showed normal velocity at 1.0 and 0.76 m/s, respectively. A real-time ultrasound-guided percutaneous kidney biopsy was performed using an 18 G automated biopsy gun (BioPince; Medical Device...