ACUTE RENAL FAILURE
Diseases and conditions associated with acute renal failure during pregnancy are shown in Table 67-1. Early identification and proper management of renal failure in women with pure preeclampsia does not result in residual renal damage. Dialysis for acute renal failure in obstetrical patients is contributed to or caused by abortion (25 percent), hemorrhage (35 percent), or preeclampsia (50 percent). Hemorrhage is a cofactor in preeclampsia-related acute renal failure.
TABLE 67-1. Factors Associated with Acute Renal Failure during Pregnancy
Renal cortical necrosis follows the course of acute tubular necrosis, with oliguria or anuria, uremia, and generally death within 2 to 3 weeks unless dialysis is initiated. Differentiation from acute tubular necrosis during the early phase is not possible. The prognosis depends on the extent of the necrosis, because recovery is a function of the amount of renal tissue spared. We consider that pregnant women with serum creatinine values of 1.5 mg/dL or higher have significant acute or chronic functional renal impairment.
Acute tubular necrosis may often be prevented by the following means:
1. Prompt and vigorous replacement of blood in instances of massive hemorrhage, as in placental abruption, placenta previa, uterine rupture, and postpartum uterine atony (see Chapter 29)
2. Termination of pregnancies complicated by severe preeclampsia and eclampsia, with careful blood replacement if loss is excessive (see Chapter 29, Williams Obstetrics, 23rd ed).
3. Close observation for early signs of septic shock in women with pyelonephritis, septic abortion, amnionitis, or sepsis from other pelvic infections (see Chapter 21)
4. Avoidance of potent diuretics to treat oliguria before initiating appropriate efforts to ensure cardiac output adequate for renal perfusion
5. Avoidance of vasoconstrictors to treat hypotension, unless pathological vasodilatation is unequivocally the cause of the hypotension
Acute Obstructive Renal Failure due to Pregnancy
Rarely, bilateral ureteral compression by a very large pregnant uterus is greatly exaggerated, causing ureteral obstruction and, in turn, severe oliguria and azotemia. Partial ureteral obstruction may be accompanied by fluid retention and significant hypertension. When the obstructive uropathy is relieved (e.g., delivery), diuresis ensues and hypertension dissipates. Women with previous urinary tract surgery are more likely to have such obstructions.
Idiopathic Postpartum Renal Failure
This is a controversial syndrome of acute renal failure that develops within the first 6 weeks postpartum. See the discussion of hemolytic uremic syndrome in Chapter 70.
Identification of acute renal failure and its cause(s) is important. In most women, renal failure develops postpartum; thus, management is not complicated by fetal considerations. Oliguria is an important sign of acutely impaired renal function. Unfortunately, potent diuretics such as furosemide can increase urine flow without correcting some causes of oliguria; rather, these causes may be intensified. In obstetrical cases, both prerenal and intrarenal factors are commonly operative. When azotemia is evident and severe oliguria persists, hemodialysis should be initiated before marked deterioration of general well-being occurs. Early dialysis appears to reduce appreciably mortality and may enhance the extent of recovery of renal function. After healing has taken place, renal function usually returns to normal or near normal.
CHRONIC RENAL FAILURE
When counseling the woman with chronic renal disease regarding fertility and the risk of a complicated pregnancy, it is important to determine the degree of functional impairment and the presence or absence of hypertension.
The kidney, especially the glomerulus and its capillaries, is subject to a large number and variety of acute and chronic diseases. There are four major clinical glomerulopathic syndromes: acute, rapidly progressive glomerulonephritis; nephrotic syndrome; asymptomatic abnormalities of the urinary sediment; and chronic glomerulonephritis. The majority of these diseases are encountered in young women of childbearing age, and thus they may complicate pregnancy. Many of these disorders first become apparent because of chronic renal insufficiency.
The nephrotic syndrome, or nephrosis, is a spectrum of renal disorders of many causes. Some of these are shown in Table 67-2. Nephrotic syndrome is characterized by proteinuria in excess of 3 g/day, hypoalbuminemia, hyperlipidemia, and edema. Patients may have accompanying evidence of renal dysfunction (i.e., elevated serum creatinine level).
TABLE 67-2. Causes of the Nephrotic Syndrome in Adults
In women with mild renal insufficiency (serum creatinine less than 1.5 mg/dL), normal pregnancy is usually accompanied by a rise in renal plasma flow and glomerular filtration rate. Women with moderaterenal insufficiency (serum creatinine of 1.5 to 3.0 mg/dL) demonstrate augmented glomerular filtration rate in about half of cases, whereas those with severe disease (serum creatinine more than 3.0 mg/dL) do not.
During pregnancy, blood volume expansion is dependent on the severity of renal disease, and, therefore, proportional to the serum creatinine. In women with mild-to-moderate dysfunction, there is normal pregnancy-induced hypervolemia that averages 50 percent. However, in women with severe renal insufficiency, volume expansion is attenuated, and averages only about 25 percent. Finally, although there is some degree of pregnancy-induced erythropoiesis in these women, it is not proportional to the plasma volume increase; thus, preexisting anemia is intensified.
The most common causes of end-stage renal disease are diabetes, hypertension, glomerulonephritis, and polycystic kidney disease. In many cases of chronic renal disease, biopsy will be necessary to determine the underlying cause. We believe that biopsy is usually best reserved until after pregnancy, unless the results will significantly alter the management of renal disease.
Women with chronic renal disease should have frequent prenatal visits to determine blood pressure. Serial creatinine measurements, the intervals determined by severity, are done to estimate renal function, and protein excretion is monitored if indicated. Women should be screened and treated for bacteriuria to decrease the risk of acute pyelonephritis. Although protein-restricted diets are prescribed for nonpregnant patients with chronic renal disease, these are not recommended during pregnancy. Anemia associated with chronic renal insufficiency responds to recombinant erythropoietin given subcutaneously; however, hypertension is a well-documented side effect. The appearance of hypertension is managed as described in Chapter 23, and suspected fetal growth restriction as in Chapter 38.
The prognosis for a successful pregnancy outcome in general is related not to the underlying kidney disorder but, rather, to the degree of functional impairment. Except for an increased risk of superimposed preeclampsia, women with relatively normal renal function and no hypertension before pregnancy usually have a normal pregnancy. As renal impairment worsens, so does the likelihood of pregnancy complications. At least half of women with renal insufficiency will develop hypertension. Worsening of hypertension or superimposed preeclampsia develops in 80 percent of those with moderate insufficiency and almost 90 percent who have severe disease.
Dialysis during Pregnancy
For those women requiring dialysis, increased dialysis time may improve pregnancy outcome. The type of dialysis—hemodialysis versus peritoneal—does not appear to significantly influence pregnancy outcome.
A longstanding unresolved issue is whether pregnancy accelerates chronic renal insufficiency. It seems reasonable to conclude that, at least in most women, in the absence of superimposed preeclampsia plus hemorrhage or severe placental abruption, pregnancy does not appreciably accelerate deterioration in baseline renal function. Importantly, because of the inevitable likelihood of long-term progression of the chronic disease, the ultimate maternal prognosis is guarded.
PREGNANCY AFTER RENAL TRANSPLANTATION
It is recommended that women who have undergone kidney transplantation satisfy a number of requisites before attempting pregnancy:
1. They should be in good general health for at least 2 years after transplantation.
2. There should be stable renal function without severe renal insufficiency (serum creatinine, 2 mg/dL, and preferably less than 1.5 mg/dL), none to minimal proteinuria, no evidence of graft rejection, and absence of pyelocalyceal distention by urography.
3. Absent or easily controlled hypertension.
4. Drug therapy is reduced to maintenance levels (i.e., prednisone dosage to 15 mg/day or less, azathioprine at 2 mg/kg/day or less, and cyclosporine at 5 mg/kg/day or less).
Covert bacteriuria must be treated, and if recurrent, suppressive treatment for the remainder of pregnancy is given. Serial hepatic enzyme concentrations and blood counts are monitored for toxic effects of azathioprine and cyclosporine. Renal function is monitored, at first with serum creatinine determinations, but if abnormal, determination of 24-hour creatinine clearance is performed. A decline of less than 30 percent in clearance during the third trimester is normal. Throughout pregnancy, the woman is carefully monitored for development of preeclampsia. Management of hypertension in these women is the same as for nontransplanted patients. Graft infection or rejection should prompt admission for aggressive management. Because of the significantly increased incidence of fetal growth restriction and preterm delivery, fetal surveillance is indicated (see Chapter 38). Cesarean delivery is reserved for obstetrical indications, unless the transplanted kidney is expected to obstruct labor.
For further reading in Williams Obstetrics, 23rd ed.,
see Chapter 48, “Renal and Urinary Tract Disorders.”