For a discussion of renal and urinary tract function in normal pregnancy, see Chapter 7: Maternal Physiology during Pregnancy.

Urinary Tract Infection

Asymptomatic bacteriuria, acute cystitis, and acute pyelonephritis are common renal disorders in pregnancy.

Asymptomatic Bacteriuria

Asymptomatic bacteriuria is defined as the presence of actively multiplying bacteria in the urinary tract excluding the distal urethra in a patient without any obvious symptoms. The incidence during pregnancy is 2–7%. Asymptomatic bacteriuria is twice as common in pregnant women with sickle cell trait and 3 times as common in pregnant women with diabetes as in normal pregnant women. If asymptomatic bacteriuria is untreated in pregnancy, about 25–30% of women will develop acute pyelonephritis. With treatment, the rate is only 10%. The diagnosis of asymptomatic bacteriuria is based upon isolation of microorganisms with a colony count of more than 10⁵ organisms per milliliter of urine in 2 consecutive clean-catch specimens. The patient should be instructed to clean the vulvar area from front to back to avoid contamination of the urine sample. Escherichia coli is the most common offending organism for asymptomatic bacteriuria (about 80% of cases). The Klebsiella-Enterobacter-Serratia family and Proteus are responsible for the remainder of cases. Acute cystitis is rare in pregnancy (about 1%).

Acute Cystitis

The bacterial flora in acute cystitis are similar to those in asymptomatic bacteriuria. Clinically, the patient will present with symptoms of urinary frequency, urgency, dysuria, and suprapubic discomfort. An acute febrile illness with nausea, vomiting, and chills is usually absent. The characteristic cloudy, malodorous urine should be cultured for confirmation of the diagnosis.

Acute Pyelonephritis

Acute pyelonephritis occurs in 1–2% of all pregnant women (usually, although not invariably, in those with previous asymptomatic bacteriuria) and is associated with risk to the mother and fetus. Maternal effects include fever, bacterial endotoxemia, endotoxic shock, renal dysfunction leading to acute renal failure, leukocytosis, thrombocytopenia, and elevated fibrin split products. There is an increased incidence of anemia; this may be due to marrow suppression, increased erythrocyte destruction, or diminished red cell production. Pulmonary dysfunction has been described in association with acute pyelonephritis; symptoms and signs may range from minimal (mild cough and slight pulmonary infiltrate) to severe (acute respiratory distress syndrome requiring intensive therapy). Neonatal effects include prematurity and small-for-gestational-age babies.

Clinical manifestations of acute pyelonephritis include fever, shaking chills and flank pain, nausea and vomiting, headache, increased urinary frequency, and dysuria. Urine examination will reveal significant bacteriuria, with pyuria and white blood cell casts in the urinary sediment. A count of 1–2 bacteria per high-power field in unspun urine or more than 20 bacteria in the sediment of a centrifuged specimen of urine collected by bladder catheterization will help in the bedside diagnosis. The diagnosis should be confirmed by culture of urine. Associated hematuria may indicate urinary calculi.

Treatment

A midstream urine specimen should be collected for culture at the initial prenatal visit and repeated later in pregnancy. At each prenatal visit, dipstick testing should be done, and if proteinuria is present, urinalysis, culture, or both should be done. A pregnant woman with sickle cell trait should have urine culture and sensitivity testing every 4 weeks. Pregnant women should be encouraged to maintain adequate fluid intake and to void frequently.

The initial antibiotic selection should be empiric. Based on the fact that the most common offending pathogen is E. coli, sulfonamides, nitrofurantoin, ampicillin, or cephalosporins could be selected. These antibiotics should be safe for the mother and fetus, with minimal side effects. A 10- to 14-day course of one of these agents will effectively eradicate asymptomatic bacteriuria in about 65% of pregnant patients. Culture of urine should be done 1–2 weeks after therapy is begun and then monthly for the remainder of pregnancy.

Sulfa drugs must be avoided in mothers with glucose-6-phophatase deficiency. Additionally, sulfa drugs are best avoided late in pregnancy because of the increased likelihood of neonatal hyperbilirubinemia. Trimethoprim is a folic acid antagonist, so trimethoprim-sulfamethoxazole should be avoided in pregnancy. Nitrofurantoin should be avoided at term or before (when labor is imminent) because it may induce hemolytic anemia in the newborn.

Any woman with acute pyelonephritis in pregnancy should be admitted to the hospital for therapy. Antibiotics should be given parenterally and dehydration corrected. Antipyretic agents are given where indicated, and vital signs and urinary output are closely monitored. Ampicillin or a cephalosporin is usually administered intravenously in doses of 1–2 g every 6 hours.

If there is no appropriate response in 48–72 hours, an aminoglycoside (eg, entamicin or tobramycin, 3–5 mg/kg/24 h in 3 divided doses) is administered. With persistent flank pain and fever despite proper therapy, perinephric abscess must be ruled out with ultrasound examination. This is generally a complication of obstruction associated with infection. With confirmation of the diagnosis, the abscess must be drained to avoid maternal death. An intravenous pyelogram may also be useful in evaluating patients who do not improve despite adequate therapy. A preliminary film and a 15-minute film are usually adequate for the diagnosis of urinary tract obstruction. In selected cases of persistent infection, cystoscopy and retrograde pyelographic studies may be useful.

Cunningham noted that 28% of women with pyelonephritis developed recurrent bacteriuria and 10% had recurrent acute pyelonephritis during the same pregnancy. Such women should be given long-term prophylactic treatment. Nitrofurantoin, 100 mg every night, has been suggested, although the efficacy of such therapy is questionable.

Periodic culture of the urine will assist in detecting recurrence. Relapse is defined as recurrent infection due to the same species and type-specific strain of organism present before treatment; this represents a treatment failure. Most relapses occur less than 2 weeks after completion of therapy. Reinfection is recurrent infection due to a different strain of bacteria following successful treatment of the initial infection, occurring more than 3 weeks after completion of therapy.

Urinary Calculi

The incidence of urinary calculi is not altered by pregnancy (overall incidence is 0.24% [1 in 425 persons]). This condition predisposes pregnant women to urinary tract infection, recurrent hospitalization, premature labor, and operative intervention. The causes of urinary calculi in pregnant women are the same as in nonpregnant women, ie, chronic urinary tract infection, hyperparathyroidism, congenital or familial cystinuria (or oxaluria), gout, and obstructive uropathy. Most stones are composed of calcium, and they are more common as pregnancy progresses, being rare during the first trimester. Although physiologic hydroureter is more pronounced on the right side, stones occur with equal frequency in both tracts.

Clinical Findings

Patients may present with a variety of symptoms, including classic renal or ureteric colic or vague abdominal or back pain. The differential diagnosis must include other acute abdominal conditions, ie, acute appendicitis, biliary colic, adnexal torsion, preterm labor, and placental abruption. The patient may present with fever, bacteriuria, flank pain, and nausea and vomiting suggestive of acute pyelonephritis. The persistence of fever after 48 hours of parenteral antibiotics is strongly suggestive of urinary tract obstruction with calculus. Although hematuria (varying from gross to microhematuria) may be present, it is not always pathognomonic of calcular disease. A high index of suspicion will help in the diagnosis, particularly in cases with negative culture of urine in suspected pyelonephritis, persistent hematuria, and recurrent urinary tract infection.

Clinical diagnosis may be difficult. In most cases, diagnostic imaging is necessary. For preliminary screening, an ultrasonic examination could be useful. In selected cases, excretory urography (a single film taken 20 minutes after infusion) should be done. This exposes the fetus to only 0.2 rad.

Treatment

Treatment consists of admission to the hospital, hydration, culture of urine, appropriate intravenous antibiotic therapy, correction of electrolyte imbalance, and analgesics. Fortunately, most stones are passed spontaneously. Surgical intervention (ureteral stenting, cystoscopic extraction, open surgery) will be needed in a few cases with persistent severe pain, infection not responding to antibiotics, and obstructive uropathy.

Acute Renal Failure

Acute renal failure in pregnancy is rare but carries a high mortality rate and therefore must be prevented where possible and treated aggressively. Most cases are due to acute hypovolemia. Clinically, acute renal failure is a condition in which the kidneys are temporarily unable to perform their excretory and regulatory functions. Urine output is usually less than 40 mL/24 h, and blood urea nitrogen and serum creatinine levels are elevated. Acute renal failure during pregnancy may result in abortion, low birthweight, premature labor, and stillbirth. Hypotension and vaginal hemorrhage may occur during dialysis, although successful outcomes without adverse effects have been reported.

Based on the cause, acute renal failure may be classified as prerenal, renal, or postrenal. In the prerenal type, acute renal failure occurs due to renal hypoperfusion secondary to maternal hypovolemia (eg, hemorrhage, dehydration, abruptio placentae, septicemia), circulating nephrotoxins (eg, aminoglycosides), mismatched blood transfusion, preeclampsia-eclampsia, disseminated intravascular coagulation, and hypoxemia (eg, chronic lung disease and heart failure). In the renal type, a variety of intrinsic renal diseases such as acute glomerulonephritis, acute pyelonephritis, and amyloidosis are responsible for acute renal failure. The postrenal type is caused by urinary obstruction from ureteric stone, retroperitoneal tumor, or other diseases. Bilateral ureteral obstruction due to polyhydramnios is fortunately rare.

The state of renal hypoperfusion is reversible within 24–36 hours with volume restoration and treatment of the precipitating factors. Acute tubular necrosis may develop following reduction of the outer cortical blood flow in the absence of such treatment. The most serious condition arising secondary to acute renal failure is acute cortical necrosis in damaged glomerular capillaries and small kidney vessels. Acute cortical necrosis is rare but carries a poor prognosis; partial recovery may be anticipated in patients with patchy lesions.

Clinical Findings

The clinical course has been divided into an oliguric phase, a diuretic phase, and a recovery phase. In the oliguric phase, urine output drops below 30 mL/h, with accumulation of blood urea nitrogen and potassium. The patient becomes acidotic with the increase in hydrogen ion and loss of bicarbonate. In the diuretic phase, large volumes of dilute urine are passed, with loss of electrolytes due to absence of function of the renal tubules. As tubular function returns to normal in the recovery phase, the normal volume and composition of urine returns. Clinical manifestations and complications include anorexia, nausea and vomiting, lethargy, cardiac arrhythmia (secondary to electrolyte disturbance), anemia, renal or extrarenal infection, thrombocytopenia, metabolic acidosis, and electrolyte imbalance (hyperkalemia, hyponatremia, hypermagnesemia, hyperphosphatemia, hypocalcemia).

Infection in an operative site or the respiratory or urinary tract remains the main cause of death. Other causes of death include azotemia, pulmonary edema, and cardiac arrhythmia (induced by hyperkalemia).

Treatment

In obstetric practice, prevention of acute renal failure should be the aim, with appropriate volume replacement to maintain urine output of 60 mL/h or more. Proper management of high-risk obstetric conditions (eg, preeclampsia-eclampsia, abruptio placentae, chorioamnionitis), careful typing and cross-matching of blood, and avoidance of nephrotoxic antibiotics are also important.

Specific treatment includes the following:

Emergency Treatment

Underlying causes of acute renal failure (eg, hemorrhagic shock) may require emergency treatment.

Surgical Measures

Surgical measures include determination of any obstructive uropathy or sepsis due to infected products of conception. Such problems should be treated appropriately.

Routine Measures

Routine measures include achieving fluid and electrolyte balance. Fluid intake may be calculated from the urinary output, loss of fluid from other sources (eg, diarrhea, vomiting), and insensible loss of about 500 mL/d (correcting for fever may be necessary). Intake and output must be recorded carefully. The patient should be weighed daily and should maintain a constant weight or lose weight slowly (250 g/d, if one assumes a room temperature of 22–23 °C [71–73 °F]). Hyperkalemia is a significant problem that can be controlled by giving glucose and insulin. The diet should be high in calories, low in protein and electrolytes, and high in carbohydrates. Parenteral feeding may be given in cases of nausea and vomiting. Prophylactic antibiotics should not be used, but infections may be treated with antibiotics without renal toxicity. Indwelling bladder catheters are to be avoided.

Dialysis

Dialysis is indicated if serum potassium levels rise to 7 mEq/L or more, serum sodium levels are 130 mEq/L or less, the serum bicarbonate is 130 mEq/L or less, blood urea nitrogen levels are more than 120 mg/dL or there are daily increments of 30 mg/dL in patients with sepsis, and dialyzable poisons or toxins are present.

Glomerulonephritis

Acute glomerulonephritis during pregnancy is rare. There is increased perinatal loss with this condition. The clinical course is variable during pregnancy. In some patients, the condition may resolve early in pregnancy, with return to normal renal function. These cases may be mistaken for preeclampsia. Microscopic hematuria with red blood cell casts, low serum complement, and a rising antistreptolysin O titer indicate acute glomerulonephritis. Treatment consists of control of blood pressure, prevention of congestive heart failure, administration of fluids and electrolytes, and close follow-up.

The outcome of pregnancy with chronic glomerulonephritis will depend on the degree of functional impairment of the kidneys, blood pressure levels prior to conception, and the exact histology of the glomerulonephritis. Patients are more likely to develop superimposed preeclampsia or hypertensive crisis earlier in pregnancy. Successful pregnancy should be anticipated, although renal function is expected to decrease. The incidence of fetal intrauterine growth retardation, premature labor, abruptio placentae, and intrauterine fetal demise is significantly high. Routine prenatal care must include periodic renal function tests, control of blood pressure, ultrasonic evaluation of fetal growth, and biophysical monitoring of fetal well-being. Early delivery is indicated after evaluation of pulmonary maturity with lecithin:sphingomyelin ratios and phosphatidylglycerol levels in amniotic fluid. Nephrotoxic drugs must be avoided, and acute renal failure should be anticipated, particularly during the postpartum period.

Solitary Kidney

A solitary kidney may be the result of developmental aberration or disease requiring removal of one kidney. A single kidney may be abnormally developed or it may be placed low, perhaps even within the true pelvis. A second small, virtually functionless kidney may not be discovered by the usual diagnostic tests. Anatomic and functional hypertrophy of the kidney usually occurs and is augmented by pregnancy. There is no medical contraindication to pregnancy with a solitary kidney. However, if infection occurs in a solitary kidney and does not respond to antibiotics quickly, consideration must be given to termination of the pregnancy to preserve renal function.

Renal Transplantation

Successful renal transplantation has not prevented pregnancy in the limited number of cases to date. Patients with adequate renal function prior to pregnancy will experience little if any deterioration in graft function during pregnancy. The likelihood of graft rejection during pregnancy remains the same as in nonpregnant graft recipients. The spontaneous abortion rate is not increased, but many patients choose to terminate the pregnancy. Pregnancy-induced hypertension occurs in about 30% of patients with renal transplant, and there is a 60% incidence of proteinuria in the third trimester.

The risk of infection is considerably higher during pregnancy in renal transplant patients. Primary or reactivated herpesvirus infection is a significant risk. The incidence of hepatitis B surface antigenemia has been noted to be about 50% among patients receiving dialysis.

Prematurity with its related complications, intrauterine growth restriction, and fetal abnormalities caused by immunosuppressive agents taken by the mother may occur. The route of delivery depends primarily on obstetric indications. A transplanted kidney in the false pelvis does not usually cause obstruction leading to dystocia. In patients with aseptic necrosis of the hip joints or other bony dystrophy secondary to long-term use of immunosuppressive agents, cesarean section may be required.

Ectopic Kidney

An ectopic kidney in the true pelvis with an aberrant blood supply may cause obstruction interfering with delivery. Cesarean section should be done in this situation with great caution to avoid injury to the kidney or its blood supply.