Hydroureteronephrosis is the most significant renal alteration during pregnancy.

Physiologic
dilatation of the collecting system begins in the first trimester at 6-10 weeks' gestation and
persists until 4-6 weeks following delivery.[5] Early theories suggest that hydronephrosis of
pregnancy may be a hormonally induced phenomenon whereby ureteral smooth muscles
relax in response to high levels of circulating progesterone. In early pregnancy, increased
progesterone secretion dilates the ureters and reduces ureteral peristalsis, causing
hydronephrosis. Alternatively, the predominant theory ascribes ureteric dilatation to
compression of the ureter by the enlarging gravid uterus at the level of the pelvic brim, where
the ureter crosses the iliac vessels.
Dilatation is greater on the right side than on the left because of pressure due to physiologic
engorgement of the right ovarian vein and dextrorotation of the uterus.[4] Swanson and
associates (1995) observed that hydroureteronephrosis was not routinely found below the
pelvic brim and was altogether absent in patients who had undergone urinary diversion.[5]

Volume changes during pregnancy

Glomerular filtration rate (GFR) and renal plasma flow (RPF) increase by as much as 25-50%
during pregnancy. Both of these changes are attributable to increases in cardiac output,
decreases in renal vascular resistance, and increases in serum levels of progesterone,
aldosterone, deoxycorticosterone, placental lactogen, and chorionic gonadotropin. GFR and
RPF enhancements also contribute to the increase in glucose, amino acid, protein, and
vitamin secretion. As a result of the GFR and RPF modulations, which peak at 9-11 weeks'
gestation, renal volume increases during pregnancy by as much as 30% above the reference
range. The sustained elevation of prolactin levels in the pregnant patient has a growth
hormonetype effect by increasing the glomerular surface area, which also contributes to an
increase in renal volume.
Along with increases in GFR and RPF, the filtered load of sodium, calcium, and urate
increases. Although calcium and urate excretion increases, sodium excretion remains
unchanged. The urinary excretion rate of calcium stone inhibitors, such as citrate and
magnesium, also increases in the pregnant patient; likewise, increased glycosaminoglycans
and acidic glycoproteins inhibit oxalate stone formation (eg, nephrocalcin). This explains
why pregnancy is not associated with a net increase in the rate of stone formation relative to
nonpregnant patients. The net effect of these physiologic changes is a stable relative
supersaturation of important ions such as calcium oxalate, urate, and phosphate.

Uric acid stone formation

The formation of uric acid stones requires continued and excessive oversaturation of urine
with uric acid or extreme aciduria. Dehydration, hyperuricosuria, and significantly acidic
urine contribute to uric acid supersaturation and stone formation. However, during gestation,
urine tends to be more alkaline, probably because of greater intrinsic purine use and increased
urinary citrate excretion. Thus, renal units are generally protected against uric acid stone
formation during pregnancy.

Calcium oxalate and calcium phosphate stone formation

Although pathologic calcium oxalate supersaturation has been identified in the urine of
pregnant women, the incidence of crystalluria is no higher than in women who are not

pregnant. In the pregnant patient, physiologic absorptive hypercalciuria is due to elevated

levels of serum 1,25 dihydroxycholecalciferol (1,25 vitamin D). This hormone, which is
secreted by the placenta, augments calcium absorption in the GI tract and suppresses
parathormone production, increasing renal excretion of calcium. Additionally, dietary
supplementation of calcium during gestation further augments calcium excretion. Some
reports suggest that calcium excretion increases 200-300% compared with that in healthy
patients who are not pregnant. However, increased concentration of the aforementioned
urolithiasis inhibitors present in urine during gestation and increased urine fluid output
counters the increased risk imposed by any hypercalciuria.