The renal system is the site of increased functional activity during pregnancy to maintain fluid, solute, and acid–base balance in response to the marked activity of the cardio-respiratory systems.
The primary anatomic change of the renal system is enlarge-ment and dilation of the kidneys and urinary collecting sys-tem. The kidneys lengthen by approximately 1 cm duringpregnancy as a result of greater interstitial volume as well as distended renal vasculature. The renal calyces, pelves, and ureters dilate during pregnancy because of mechani-cal and hormonal factors. Mechanical compression of the ureters occurs as the uterus enlarges and rests on the pelvic brim. The right ureter is usually more dilated than the left, possibly due to dextrorotation of the uterus and com-pression from the enlarged right ovarian venous plexus. Progesterone causes relaxation of the smooth muscle of the ureters, which also results in dilation. In addition, because progesterone also decreases bladder tone, resid-ual volume is increased. As the uterus enlarges as preg-nancy progresses, bladder capacity decreases.
The majority of pregnancy-associated functional changes in the renal system are a result of an increase in renal plasma flow. Early in the first trimester, renal plasma flow begins to increase, and, at term, it may be 75% greater than nonpreg-nant levels. Similarly, the glomerular filtration rate (GFR) increases to 50% over the nonpregnant state. This increase in GFR results in an increased load of various solutes presented to the renal system. Urinary glucose excretion increases in virtually all pregnant patients; a trace of glucose on routine prenatal colorimetric “dipstick” evaluation is normal and is usually not associated with glycemic pathol-ogy. Amino acids and water-soluble vitamins, such as vita-min B12 and folate, are also excreted to a greater extent compared with the nonpregnant state. However, there is no significant increase in urinary protein loss, which means that any proteinuria that occurs during pregnancy should engender consideration of illness. In addition, sodium metabolism remains unchanged. The potential loss of this electrolyte caused by an increased GFR is compensated for by an increase in renal tubule reabsorption of sodium.
All components of the renin-angiotensin-aldosterone system increase during pregnancy. Plasma renin activity is up to 10 times that of the nonpregnant state and renin substrate (angiotensinogen) and angiotensin increase approximately fivefold. Normal pregnant women are rel-atively resistant to the hypertensive effects of the increased levels of renin-angiotensin-aldosterone, whereas women with hypertensive disease and hypertensive disease of pregnancy are not.
The anatomic changes in the renal system result in a few common symptomatic complaints during pregnancy.
Compression of the bladder by the enlarged uterus results in urinary frequency that is not associated with urinary tract or bladder infection. In addition, 20% of women experience stress urinary incontinence, and loss of urine should be considered in the differential diagnosis when rupture of membranes is suspected. Finally, urinary stasis throughout the renal collecting system predisposes to an increased incidence of pyelonephritis in patients with asymptomatic bacteriuria.
As pregnancy advances, pressure from the presenting part on the maternal bladder can cause edema and protrusion of the bladder base into the anterior vagina. No signifi-cant changes in the renal examination are apparent dur-ing pregnancy.
The pregnancy-associated functional changes in the renal system result in a number of alterations in common tests of renal function. Serum levels of creatinine and blood-urea-nitrogen (BUN) decrease in normal pregnancy. Serumcreatinine values fall from a nonpregnant level of 0.8 mg/dL to pregnancy levels of 0.5 to 0.6 mg/dL by term. Creatinine clearance increases 30% above the nonpregnant norms of 100 to 115 mL/min. BUN also falls about 25% to levels of 8 to 10 mg/dL at the end of the first trimester, and is maintained at these levels for the remainder of the preg-nancy. Because glucosuria is common during pregnancy, quantitative urine glucose measurements are often ele-vated, but may not signify an abnormal blood sugar. By comparison, renal protein excretion is unchanged during pregnancy, and the nonpregnant range of 100 to 300 mg per 24 hours remains valid.
If imaging of the renal system is performed during pregnancy, normal dilation of the renal collecting system resembling hydronephrosis is noted on ultrasound or intravenous pyelogram.