1. What are the normal changes in the anatomy of the urinary system associated with pregnancy?

During normal pregnancy, the kidneys enlarge approximately 1 cm in length, with the right kidney enlarging slightly more than the left kidney. By the second month of pregnancy, the renal pelvis and ureters also begin to increase is size. Again, the right side tends to enlarge greater than the left. The ureters increase in diameter (above the pelvic brim) by as much as 2 cm, while the right and left renal pelvis dilates on average 15 mm and 5 mm, respectively.

The reason for the overall dilation appears to be related to both mechanical obstruction by the growing uterus and smooth muscle relaxation from increasing progesterone levels. Such expansion affects interpretation of urologic studies and increases the incidence of asymptomatic bacteriuria and pyelonephritis.

2. In normal pregnancy, what changes occur in renal hemodynamics?

In pregnancy, dramatic changes occur with respect to both renal plasma flow and glomerular filtration. By the second trimester, renal plasma flow increases approximately 75% above baseline, and then decreases by the end of the third trimester. The glomerular filtration rate is increased almost 50% by the end of the first trimester, and this rate is maintained throughout gestation. Glomerular filtration is clinically assessed by creatinine clearance, and because creatinine is also secreted by the renal tubules, the actual glomerular filtration rate is less than the measured creatinine clearance. The overall effect of the increase in both renal plasma flow and glomerular filtration rate causes a decrease in the filtration fraction until the third trimester, when renal plasma flow falls slightly.

3. What are the effects on serum chemistry measurements resulting from the altered renal hemodynamics?

Both serum creatinine and blood urea nitrogen levels decrease approximately 25% from nonpregnant levels as a result of the increased glomerular filtration rate. By midpregnancy, serum uric levels are decreased approximately 50% but increase to normal levels by the third trimester as renal tubular resorption increases.

4. In pregnancy, is glucosuria an abnormal finding?

No. More glucose is excreted through the glomeruli because of the increased glomerular filtration. The reabsorptive capacity of the renal tubules can be exceeded, and therefore it is normal for most pregnant women to excrete up to 10 gm of glucose a day. If glucosuria is detected, the patient should be screened for diabetes if she has risk factors, or if she had no risk factors but has not been previously screened.

While urinary protein loss should not increase, excretion of amino acids, vitamin B12, and folate is increased.

5. How is sodium balance maintained in normal pregnancy?

In normal pregnancy, plasma osmolality is decreased approximately 10 mOsm/kg H2O due to a decrease in the concentration of sodium. Despite the decreased serum concentration, there is an overall increase of almost 1000 mEq of sodium in the maternal intravascular and interstitial fluids, fetus, and placenta. Sodium loss is increased by the elevated glomerular filtration rate and by progesterone (promotes natriuresis). This is offset by a dramatic increase in renal tubular reabsorption of sodium, which is due to a dramatic increase in levels of the hormones aldosterone, deoxycortisone, and estrogen. Furthermore, angiotensinogen (renin substrate), angiotensin, and renin (the proteolytic enzyme that converts angiotensinogen to angiotensin I) levels jump, as well. The increase in these latter hormones aids in the increased production of aldosterone, which prevents sodium diuresis.

Angiotensin II, a product of angiotensin I, is a potent vasoconstrictor. In normal pregnancy, sensitivity to the vasopressor effect of angiotensin II is reduced. It is believed that increased production of uterine and placental prostaglandins, namely prostacyclin, plays an important role in blunting the normal vasoconstrictor effects of angiotensin II. It is also believed that pregnancies that do not exhibit the normal decreased sensitivity to angiotensin II are at greater risk for developing preeclampsia.

6. Are pregnant women at greater risk for developing pyelonephritis?

Yes. Pyelonephritis occurs in approximately 1-2% of all pregnancies, and it is the most common reason for nonobstetric admission during pregnancy. It is also a risk factor for increased maternal morbidity and adverse perinatal outcome. Pregnant women are at greater risk for developing asymptomatic bacteriuria, most commonly Escherichia coli. If untreated, up to 40% of women with asymptomatic bacteriuria will develop symptomatic urinary tract infections (UTIs), cystitis, and pyelonephritis.

The etiology for the increase in UTIs includes anatomic changes, increased progesterone levels, and increased glucose and amino acid levels in urine. Screening of all pregnant patients for asymptomatic bacteriuria can reduce the risk of symptomatic infections by approximately 70%, and should be done routinely at the first prenatal visit.

7. Does pregnancy increase the incidence of urolithiasis?

No. Urolithiasis affects less than 1 in 2000 pregnancies, and pregnancy does not appear to increase the incidence. The diagnosis can be made by urine microscopy, by straining urine for the presence of stones, and by ultrasound. If a patient is diagnosed with urolithiasis, consider measuring serum phosphorus and calcium levels to evaluate for hyperparathyroidism.

8. How can chronic renal disease be diagnosed in pregnancy?

In many cases, obstetricians may make the initial diagnosis of chronic renal disease in patients without other medical conditions. In general, renal disease may be silent in early stages. At a patient’s first prenatal visit, a urine analysis is performed, and the presence of glucose, protein, or casts should prompt an evaluation. A 24-hour urine collection for creatinine clearance and total protein should be done on patients with greater than trace protein on urine dip-stick analysis (and no UTI). In normal pregnancy, total protein excretion should be less than 0.3 gm per day. Creatinine clearance can decrease by almost 70% before there is an increase in serum blood urea nitrogen or creatinine.

9. What are the effects of pregnancy on chronic renal disease?

In general, the long-term effects of pregnancy on renal disease are unclear. Creatinine clearance will still increase in patients with baseline dysfunction. As pregnancy nears completion, creatinine clearance decreases in those with underlying renal disease, and this fall reverses after delivery. In patients with mild renal disease (serum creatinine < 1.4 mg/dL), pregnancy should not cause a worsening of renal function, but these patients are at greater risk for pyelonephritis. Patients with moderate to severe renal insufficiency (serum creatinine > 1.4 mg/dL and 2.5 mg/dL, respectively) can experience deterioration of renal function that may not improve after delivery.

Comorbid conditions such as hypertension and diabetes can also increase the risk for irreversible renal function with pregnancy. Hypertension should be controlled above levels of 160 mmHg systolic and 110 mmHg diastolic. These patients are at high risk for developing complications from their hypertension-aside from worsening renal disease and superimposed preeclampsia. Worsening proteinuria is common, and this can make the diagnosis of superimposed preeclampsia difficult.

Key points: renal disease in pregnancy

  • During pregnancy, increased renal plasma flow and increased glomerular filtration rate lead to decreased serum BUN and creatinine.
  • Pregnancy increases the risk of pyelonephritis due to anatomic changes, changes in urine content, and increased progesterone, but it does not increase urolithiasis.
  • Because early renal disease may be asymptomatic, women are often first diagnosed with chronic renal disease during obstetric care.
  • Worsening renal function during pregnancy usually only occurs in women with moderate to severe disease (creatinine >1.4, 2.5 respectively), but blood pressure elevations can occur in all renal patients.
  • Maternal chronic renal disease increases the risk of miscarriage, IUGR, preeclampsia and preterm delivery.

10. What are the effects of chronic renal disease on pregnancy outcome?

In general, patients with renal insufficiency are at greater risk for miscarriage, intrauterine growth restriction, preeclampsia, and preterm delivery (both spontaneous and iatrogenic, due to preeclampsia). Perinatal mortality has decreased as a result of advances in neonatal care, maternal administration of antenatal steroids, and increased antepartum surveillance, but it is still significantly increased in patients with moderate to severe renal dysfunction.

11. In the nondiabetic gravida, what is the most common cause of nephrotic syndrome?

Etiologies for nephrotic syndrome (> 3.5 gm protein/24 h) include diabetes, systemic lupus erythematosus, minimal change disease, membranous glomerulonephritis, and membranoproliferative glomerulonephritis. Some of these diseases respond to steroids, and therefore when significant proteinuria is documented, it is important to identify the etiology. Pregnancy outcome depends on the etiology of the proteinuria, the presence of other medical conditions such as hypertension, and the gestational age at diagnosis.

The most common etiology for nephrotic-range proteinuria remains preeclampsia, and again, pregnancy outcome depends on gestational age at presentation as well as the presence of other manifestations of severe preeclampsia (pulmonary edema, liver function abnormalities, oliguria, fetal growth restriction, and coagulopathy).

12. Can women requiring dialysis therapy conceive?

Women with chronic renal failure usually have oligomenorrhea, and therefore have significantly decreased fertility. If they do become pregnant, they usually require more frequent and longer dialysis sessions. Hemodialysis can cause significant fluid shifts, and fetal monitoring should be used when fetal viability is attained. Treat anemia with transfusion and erythropoietin. Patients on dialysis have a significantly increased risk of miscarriage, fetal demise, fetal growth restriction, and preterm delivery. There is some evidence that patients on peritoneal dialysis may have better outcomes with fewer complications than those receiving hemodialysis.

13. Should women who have had renal transplantation and become pregnant stop or change their medication regimen?

Many women who experienced oligomenorrhea with chronic renal disease regain fertility as renal function improves after renal transplantation. Immunosuppressive medications (steroids, azathioprine, and cyclosporine) should not be stopped after conception. The rate of fetal malformations does not appear to be increased. Azathioprine and cyclosporine can be associated with fetal growth restriction. While there may be some maternal and fetal side effects to these medications, these risks must be weighed against the risk of rejection.

14. What are the risks in pregnancy for women who have had renal transplantation?

The risk for allograft rejection in pregnancy is about 9%, no different than in nonpregnant women. Making the diagnosis of rejection can be difficult in the pregnant patient. Pregnancies in women with renal transplantation are at greater risk for preeclampsia (approximately 30%), fetal growth restriction (approximately 20%), spontaneous abortion, fetal death, and preterm delivery (up to 45%). Because the kidney is denervated, pain may not be experienced when pyelonephritis is present. Women should be screened frequently for urinary tract colonization and infection, and treated appropriately. In late pregnancy, renal function may decrease in up to 15% of patients.

In general, it is recommended that women defer conception for 1 year after receiving a transplant from a living donor and 2 years after a cadaveric transplant.

15. Does pregnancy adversely affect women with adult polycystic kidney disease?

Adult polycystic kidney disease is an autosomal dominant disorder with an incidence of 1 in 400 to 1000 that usually presents in the fourth or fifth decade of life. The disease is associated with hypertension, and pregnancy could worsen the hypertension. In general, pregnancy does not appear to worsen the course of this disease.

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