Renal size enlarges: by 1cm, secondary to increased interstitial volume and distended renal vasculature, with renal volume increasing up to 30%.

Dilatation of the collecting systems: producing physiological hydronephrosis and hydroureters (right ” class=LK href=”javascript:void(0)” target=right xpath=”/CT{06b9ee1beed594192fe83c602fef4af9a59e63f847d6df62927a64e26327cf0c39fb29f2319efbd87dee7ad2290c3617}/ID(AB2-M1)”>> left side), which starts in the second month of pregnancy and is maximal by the middle of the second trimester. It is caused by mechanical obstruction by the growing uterus and ovarian venous plexus and smooth muscle relaxation due to progesterone.

Renal plasma flow (RPF) rate: goes up early in the first trimester, reaching an increase of ˜75% by 16 weeks’ gestation. This is maintained until 34 weeks’ gestation, followed by a decline of ˜25% towards term.

GFR: increases by 50% by the end of the first trimester, which is maintained until term. GFR has returned to normal levels by 3 months after delivery.

Renal function and biochemical parameters: are affected by changes in RPF and GFR. Creatinine clearance increases and serum levels of creatinine, urea, and urate fall in normal pregnancy due to glomerular hyperfiltration (Table 15.1). Raised GFR causes an increased glucose load at the renal tubules and results in glucose excretion (physiological glycosuria of pregnancy which tends to be intermittent). Of note, patients with persistent glycosuria should be screened for diabetes mellitus. Proteinuria is only increased in women with pre-existing proteinuria before pregnancy. Urine output is increased.

Salt and water handling: a reduction in serum sodium causes reduced plasma osmolality. The kidney compensates by increasing renal tubular reabsorption of sodium. Plasma renin activity is increased 10-fold and levels of angiotensinogen and angiotensin are increased 5-fold. Osmotic thresholds for ADH and thirst decrease.

Acid-base metabolism: serum bicarbonate is reduced. Increased progesterone stimulates the respiratory centre, resulting in reduced PCO₂.

Bladder: displacement occurs (superiorly and anteriorly) due to the enlarging uterus. The bladder becomes hyperaemic and raised oestrogen levels cause hyperplasia of muscle and connective tissues. Bladder pressures can increase over pregnancy (from 9 to 20cmH₂O), with associated rises in absolute and functional urethral length and pressures.

Haematuria: there is an increased risk of non-visible haematuria due to elevation of the trigone and increased bladder vascularity. Persistent non-visible haematuria, patients with associated risk factors (i.e. smoking), or visible haematuria will need further investigation
similar to non-gravid patients. Placenta precreta (placenta invades the bladder) can cause haematuria and should be excluded as a cause.

LUTS: urinary frequency (>7 voids during the day) and nocturia (≥1 void at night) increase over the duration of gestation (incidence of 80-90% in third trimester). Urgency is reported in up to 60% and urge incontinence may develop in 10-20%, predominantly in the third trimester. These effects are contributed to by pressure on the bladder from the enlarging uterus, causing reduced functional capacity. Nocturia is also exacerbated due to the increased excretion of water (whilst lying down) that tends to be retained during the day. Normal bladder function returns in the majority soon after delivery.

Acute urinary retention: is uncommon during pregnancy, but may occur at 12-14 weeks’ gestation in association with a retroverted uterus, which resolves by 16 weeks. Fibroids and other uterine anomalies may predispose to retention. Post-partum urinary retention occurs in up to 18%, associated with epidural use, assisted or first delivery, and long duration of labour.

Stress urinary incontinence: occurs in around 22% and increases with parity. It is partly caused by the placental production of peptide hormones (relaxin), which induces collagen remodelling and consequent softening of tissues of the birth canal. Infant weight, duration of first and second stages of labour (vaginal delivery), and instrumental delivery (ventouse extraction or forceps delivery) increase risks of post-partum stress incontinence.