Table 1.

Human pregnancy complications.

Pregnancy complication	Percent impact	Current means of identification	Underlying pathology
PE	• 3–5% of pregnancies [177] • Accounts for 14% of pregnancy-associated maternal deaths [177, 178]	• High blood pressure [354] • Proteinuria [354] • Possible renal, liver, pulmonary, and neurological sequelae [177] • PE is sometimes split into two categories with separate pathologies: early onset PE (EPE), <34 weeks gestation and late onset PE (LPE), ≥34 weeks gestation	• Abnormal trophoblast invasion of the maternal decidua and incomplete remodeling of maternal spiral arteries leads to placental ischemia and a pro-inflammatory environment [179] • Often associated with IUGR [177] • EPE: considered a fetal disease with associated placental dysfunction • LPE: a maternal disorder; placenta usually functions properly and is associated with better maternal and fetal outcomes, at least in part based on later delivery (obviating prematurity as a contributor to pathology) [180]
EPL	• 15–25% of all clinical pregnancies [181–183]		• Fetal chromosomal abnormalities are the major cause [184, 185]; however, in cases of normal fetal karyotype, the cause is typically unknown [186–189]
RPL	• ~1% of all women [190]	• RPL is identified by two or more clinical EPLs (pregnancy diagnosis based on ultrasound or tissue/pathology, not chorionic gonadotropin detection alone) [181, 191]	• When uterine anatomical anomalies, genetic factors, antiphospholipid syndrome, or hormonal pathologies are ruled out, more than 50% of patients suffer from unexplained RPL [181, 182, 192]
FGR/IUGR	• 10% of pregnancies [193]	• Ultrasound-estimated fetal weight less than the 10th percentile for that gestational age or a fetus at <10th percentile at birth [193]	• Origins stem from errors in early placental development [194] • Caused by placental insufficiency, genetic syndromes, maternal malnutrition, multiple gestation, teratogens, and oxygen deprivation [134, 195]
			• Maternal vascular malperfusion is considered the leading cause of pathology in FGR placentas and can be accompanied with placental hypoplasia, infarction, and hemorrhage [196]
			• Often associated with PE [177]
Pre-GD	• ~7% of all pregnancies [11] • High risk of maternal morbidity [197]	• Having type 1 or type 2 diabetes prior to start of pregnancy	• Hyperglycemia can impair and disrupt fetal organ development [8] • Placentas from women with diabetes generally have greater surface area, Hofbauer cells, vasculature, and diffusion distance [199]
GDM	• Leading cause of fetal macrosomia [198]	• Glucose intolerance and insulin resistance development during pregnancy	• Placental pathologies include chorionic villus immaturity, high villus density, stromal edema, thicker than average collagen fibers, and diffuse villous stromal calcifications [17], potentially impacting function
PTB	• ~11% of all pregnancies [170] • 75% of perinatal mortality is due to PTB [200]	• Birth before 37 weeks of gestation [170]	• Oxidative stress and inflammation leading to early rupture of membranes are known to be leading causes of PTB, in addition to retroplacental abruption, chronic villitis, and twin gestations [201] • Other causes hypothesized to be involved include vertically transmitted infections, maternal environmental stress, and intra-amniotic inflammation [170, 200]