Obstetric Topic 07. Physiologic changes in pregnancy (renal system, hormonal changes)

I. Renal System

Anatomic Changes

• Kidney size increases during pregnancy.
• Ureteral dilatation / physiologic hydroureter: progesterone smooth muscle relaxation + uterine compression.
• Right side is usually more affected.
• Urinary stasis → higher risk of UTI, pyelonephritis and kidney stones.

Renal Blood Flow and GFR

• Renal blood flow (RBF) increases early in pregnancy.
• GFR increases by about 50% → renal hyperfiltration.
• Consequences:

• Fluid retention and plasma volume expansion.
• Serum creatinine and BUN/urea decrease.
• Glycosuria may occur despite normal blood glucose.
• Mild proteinuria/protein excretion may occur; significant proteinuria is abnormal.

Water, Electrolytes and Bladder

• RAAS activity increases → sodium/water retention → plasma volume expansion.
• Respiratory alkalosis compensation: kidneys excrete more HCO3- → serum bicarbonate decreases.
• Clinical point: pregnancy creatinine is low; a normal nonpregnant creatinine may be abnormal in pregnancy.
• Bladder capacity increases by progesterone effect.
• Frequent urination: GFR ↑ + bladder compression by uterus.
• Late pregnancy/labor: overdistended bladder can impair fetal descent and postpartum uterine contraction → regular voiding.

II. Placental and Pregnancy Hormones

Human Chorionic Gonadotropin

• Human chorionic gonadotropin (hCG): from syncytiotrophoblast of placenta.
• Function: maintains corpus luteum → progesterone/estrogen production until placental takeover.
• Peak: around GW10, then declines/plateaus.
• Pregnancy detection:

• Serum hCG: about 1 week after conception/fertilization.
• Urine hCG: about 2 weeks after conception, around missed period.

• High hCG: multiple pregnancy, molar pregnancy, choriocarcinoma, trisomy 21 screening context or wrong dating.
• Low/abnormal rise: ectopic pregnancy, failing pregnancy/abortion or wrong dating.
• High hCG can stimulate TSH receptor → transient lower TSH / gestational thyrotoxicosis in severe cases.

Estrogens

• Source: corpus luteum early → placenta after luteoplacental shift.
• Main pregnancy estrogen: estriol (E3); fetal adrenal/liver precursors contribute.
• Functions:

• Increases uterine growth and uteroplacental blood flow.
• Breast ductal growth.
• Increases hepatic binding proteins: TBG, CBG and SHBG.
• Enhances RAAS activity → plasma volume increases.

• Low estrogen/estriol can be associated with fetal death or fetal/placental compromise.

Progesterone

• Source: corpus luteum until about GW10 → placenta.
• Main role: maintains pregnancy.
• Functions:

• Supports implantation and decidualization.
• Smooth muscle relaxation → vascular tone ↓, GI motility ↓, ureteral dilatation, uterine contractility ↓.
• Increases basal body temperature.
• Stimulates breast alveolar growth, but inhibits prolactin-mediated milk secretion during pregnancy.

Human Placental Lactogen

• Human placental lactogen (hPL) / human chorionic somatomammotropin (hCS): from syncytiotrophoblast/placenta.
• Purpose: ensure nutrient supply to fetus.
• Functions:

• Lipolysis ↑ → free fatty acids for maternal energy.
• Maternal insulin resistance ↑ → maternal glucose use ↓ → glucose supply to fetus maintained.
• Diabetogenic effect → contributes to GDM in susceptible patients.

Prolactin and Oxytocin

• Prolactin: from anterior pituitary; increases throughout pregnancy.
• Function: breast development and milk production; action is inhibited by estrogen/progesterone during pregnancy.
• Oxytocin: released from posterior pituitary; increases near term and peaks during labor.

• Labor → uterine contractions.
• Nipple stimulation → milk letdown.

Relaxin and Cortisol

• Relaxin: from corpus luteum and placenta; peaks in 1st trimester.
• Functions: promotes implantation, decreases uterine contractility, softens cervix, relaxes pelvic ligaments.
• Cortisol: maternal cortisol increases throughout pregnancy.
• Cortisol functions:

• Promotes insulin resistance.
• Fetal organ maturation, especially lung type II pneumocytes and surfactant production.
• Participates in onset of labor.

III. Maternal Endocrine Glands

Thyroid

• hCG has weak TSH-like activity → mild thyroid stimulation, especially in 1st trimester.
• Estrogen → TBG ↑ → total T4/T3 increase.
• Free T3/T4 and TSH: usually minimal change within pregnancy-specific ranges.
• BMR increases.
• Placental transfer:

• Maternal TSH does not cross the placenta.
• Maternal free T4 crosses placenta → important for fetal brain development, especially early.
• TSH receptor antibodies and antithyroid drugs can cross placenta.

Other Endocrine Changes

• Parathyroid/calcium: total calcium decreases from lower albumin; ionized calcium usually remains normal.
• Vitamin D activation ↑ → intestinal calcium absorption ↑ for fetal skeleton.
• Pituitary size increases from lactotroph hyperplasia; prolactin rises markedly.
• Severe postpartum hemorrhage can cause pituitary ischemia → Sheehan syndrome.
• Adrenal: cortisol, aldosterone and CBG increase.
• Pancreas: beta-cells increase insulin secretion to compensate for insulin resistance; failure → GDM.