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General Considerations
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Acute renal failure in pregnancy is uncommon but can be severe, requiring dialysis. Any of the causes of acute renal failure occurring in the nonpregnant population may also occur during pregnancy, but there are some specific causes of acute renal failure during pregnancy that must be considered. Determining the type of acute renal failure in a pregnant woman will depend on the history, especially the timing of the acute renal failure in terms of the pregnancy (eg, in the first, second, or third trimester or postpartum), the presence or absence of preeclampsia, findings on urine analysis (especially proteinuria, white blood cells, red blood cells), and associated laboratory abnormalities, especially anemia, platelet count, liver transaminases and bilirubin, and tests of coagulation (prothrombin time and partial thromboplastin time).
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Because plasma volume is increased in normal pregnancy, normal BUN and creatinine levels are lower in pregnancy than in the nonpregnant state (Table 55–1). Thus, during pregnancy, a creatinine >0.8 mg/dL and a BUN >14 mg/dL are abnormal and consistent with kidney disease (either acute or chronic).
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Prerenal or Hemodynamic Causes of Acute Renal Failure in Pregnancy
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Essentials of Diagnosis
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- Rising BUN and creatinine.
- History, physical examination, and laboratory data consistent with volume depletion, sepsis, or hemorrhage.
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General Considerations
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Hyperemesis gravidarum and hemorrhage may cause acute renal failure in pregnancy as a result of volume depletion. Sepsis-induced acute renal failure in pregnancy is most often associated with abortion, especially in the developing world and in areas where therapeutic abortion is illegal. Most cases of prerenal acute renal failure in pregnancy occur early in the pregnancy. As in the nonpregnant state, prerenal causes of acute renal failure in pregnancy may progress to acute tubular necrosis (ATN). Prerenal acute renal failure must be distinguished from postrenal (obstruction) and intrinsic acute renal failure.
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The history and physical examination will suggest volume depletion and/or hemodynamic compromise. Abruptio placentae may precede hemorrhage and is also associated with cortical necrosis.
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Evidence of intact kidney tubular function (low urine sodium, low urine fractional excretion of sodium and fractional excretion of urea) may often accompany prerenal acute renal failure. An elevated BUN:creatinine ratio may also be seen.
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Treatment & Prognosis
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Treatment of prerenal acute renal failure in pregnancy is to correct the underlying cause, ie, replete lost volume or blood and treat sepsis. With timely and appropriate treatment, progressive acute renal failure (ATN) may be avoided with an excellent chance of complete recovery of kidney function.
Finkielman JD et al: The clinical course of patients with septic abortion admitted to an intensive care unit. Inten Care Med 2004;30:1097.
[PubMed: 15007546]
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Postrenal Acute Renal Failure in Pregnancy
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Essentials of Diagnosis
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- Rising BUN and creatinine in a pregnant woman.
- Obstruction of the urinary tract.
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General Considerations
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Moderate dilation of the urinary collecting system is usual during pregnancy. This “functional” hydronephrosis is commonly more prominent on the right side, usually with preservation of normal kidney function. In rare cases, acute renal failure can occur if the degree of obstruction is great. In such cases, kidney function often normalizes if the woman is placed in the lateral recumbent position (relieving uterine pressure on the ureters), thereby confirming the diagnosis. In some cases, urologic intervention or delivery is needed to relieve the obstruction and resolve the acute renal failure.
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Intrinsic Acute Renal Failure in Pregnancy
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Essentials of Diagnosis
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- Rising BUN and creatinine.
- Exclusion of prerenal and postrenal causes of acute renal failure.
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General Considerations
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Although most cases of pyelonephritis during pregnancy do not result in acute renal failure, acute pyelonephritis can cause acute renal failure during pregnancy. As in the nonpregnant population, ATN, acute interstitial nephritis, and acute glomerulonephritis may also cause acute renal failure in a pregnant woman. In such cases, the history, physical examination, and urine analysis will usually lead to these diagnoses. However, there are some specific causes of acute renal failure that are seen only during pregnancy or are associated primarily with pregnancy. These include the acute renal failure seen with preeclampsia/eclampsia, acute fatty liver of pregnancy (AFLP), thrombotic microangiopathies [hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), and HELLP syndrome (hemolysis with a microangiopathic blood smear, elevated liver enzymes, and a low platelet count)], and cortical necrosis.
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Preeclampsia/Eclampsia-Associated Acute Renal Failure
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Essentials of Diagnosis
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- Typically develops late in the third trimester.
- Preeclampsia does not occur before 20 weeks of gestation.
- Preeclampsia = hypertension, edema, and proteinuria.
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General Considerations
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Kidney function is usually normal or near normal in women with preeclampsia unless hemodynamic instability develops with excessive bleeding or disseminated intravascular coagulation (DIC) occurs. Mild degrees of kidney dysfunction may be seen with preeclampsia, likely because of reduced glomerular permeability. Delivery of the fetus usually results in resolution of the preeclampsia in 24–48 hours. Severe preeclampsia may also present with thrombotic microangiopathic acute renal failure (see below and the section on eclampsia/preeclampsia).
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Thrombotic Microangiopathies
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Essentials of Diagnosis
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- Thrombocytopenia.
- Microangiopathic anemia.
- Normal prothrombin time.
- Abnormal kidney function.
- Usually occurs late in pregnancy or early postpartum.
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General Considerations
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It can be difficult to make a specific diagnosis when acute renal failure associated with thrombocytopenia and microangiopathic hemolytic anemia occurs late in pregnancy. In addition to TTP and HUS, severe preeclampsia and HELLP (hemolysis with a microangiopathic blood smear, elevated liver enzymes, and a low platelet count) can cause acute renal failure as a result of thrombotic microangiopathy. Although TTP and HUS are considered distinct entities, because their clinical presentations are often indistinguishable, they are best considered as part of a spectrum of disease. Differentiating severe preeclampsia or HELLP from TTP-HUS is important for both therapeutic and prognostic reasons. The most useful distinguishing features are the timing of the onset of acute renal failure and the blood pressure and urine protein during the pregnancy.
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Severe preeclampsia is more common than TTP-HUS and usually presents with proteinuria, hypertension, and edema late in pregnancy. TTP-HUS often occurs postpartum without an antecendent history of pregnancy-associated hypertension or proteinuria. When TTP-HUS occurs antepartum, it often presents early in the second or even during the first trimester. Importantly, unlike TTP-HUS, acute renal failure with preeclampsia and HELLP usually resolves with delivery.
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Thrombocytopenia and microangiopathic anemia are the cardinal findings. Elevated liver enzymes may occur with TTP-HUS, but if they are extremely high, it should suggest HELLP (Figure 55–2). Patients with TTP generally have very low levels of plasma ADAMTS13 while HELLP is associated with only mildly to moderately low ADAMTS13 levels.
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Differential Diagnosis
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In addition to severe preeclampsia and HELLP, acute renal failure occurring late in pregnancy may also be associated with AFLP, disseminated intravascular coagulation with sepsis, hemorrhage, or obstetric catastrophe (eg, abruptio placentae). The differential diagnosis may also include severe ATN and cortical necrosis. In most cases, the clinical history and laboratory findings will narrow the diagnostic possibilities.
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The optimal treatment of TTP-HUS in pregnancy is the same as in the nonpregnant population. Plasma infusion with or without plasma exchange is the mainstay of treatment and has significantly improved mortality. Renal replacement therapy may be required depending on the clinical circumstances. The treatment of HELLP is more controversial, although delivery is clearly indicated. Some of the abnormal laboratory results may transiently worsen after delivery, but usually normalize within postpartum week one.
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Before the use of plasma exchange, the mortality of pregnancy-associated TTP-HUS approached 90%. Today, with appropriate treatment, mortality has improved, although a significant proportion of women may be left with CKD or, less often, ESRD requiring dialysis.
George JN: The association of pregnancy with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Curr Opin Hematol 2003;10:339.
[PubMed: 12913787]
Lattuada A et al: Mild to moderate reduction of a von Willebrand factor cleaving protease (ADAMTS13) in pregnant women with HELLP microangiopathic syndrome. Haematologica 2003;88:1029.
[PubMed: 12969811]
Vesely SK et al: Pregnancy outcomes after recovery from thrombotic thrombocytopenic purpura-hemolytic uremic syndrome. Transfusion 2004;44:1149.
[PubMed: 15265118]
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Acute Fatty Liver of Pregnancy
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Essentials of Diagnosis
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- Jaundice and liver dysfunction.
- Occurs at the end of pregnancy or in early puerperium.
- Usually simultaneous coagulation disorders.
- Liver biopsy is diagnostic.
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General Considerations
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AFLP is characterized by microvesicular fatty infiltration of hepatocytes without necrosis or inflammation. This disorder is unique to human pregnancy and is relatively uncommon, occurring in one in 7000–16,000 deliveries. It usually occurs late in pregnancy, close to term. Some patients may present after delivery.
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As with Reye's syndrome, microvesicular fatty infiltration is seen histologically with AFLP. Affected women may have an inherited enzyme deficiency in β-oxidation of fatty acids that predisposes them to AFLP. The accumulation of long-chain 3-hydroxyacyl metabolites produced by the fetus or the placenta is toxic to the maternal liver and may be the cause of the disease.
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Women with AFLP often present with nausea and vomiting, abdominal pain, lethargy, jaundice, headache, bleeding, or altered mental status due to hepatic encephalopathy. However, in some patients incidentally elevated liver test results lead to the diagnosis.
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See Figure 55–2. Abnormal liver function tests occur with modest to severe elevations of aminotransferase. The platelet count is normal unless progression to DIC has occurred. In such cases, antithrombin III levels will be low. In severe cases of AFLP, elevations of ammonia may occur as well as profound hypoglycemia. Acute renal failure occurs in up to 60% of cases.
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Imaging studies are primarily used to exclude hepatic infarct or hematoma. Fat may be seen on ultrasound or computed tomography (CT) of the liver but is rarely diagnostic.
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Liver biopsy is diagnostic and shows pericentral pallor with lobular disarray and vacuolization of the centrizonal hepatocytes. Special stains should be done to identify the microvesicular fat. Because of the coagulopathy accompanying AFLP, liver biopsy caries a high risk of bleeding and is reserved for cases in which the diagnosis is in doubt and/or treatment is being delayed.
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Differential Diagnosis
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Acute renal failure associated with severe preeclampsia, HELLP, and thrombotic microangiopathies comprises the diagnostic possibilities (Figure 55–2). Hepatic infarction or hematoma and other causes of acute liver failure should be excluded.
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Treatment is delivery after stabilization. Supportive therapy is usually required and may include monitoring in an intensive care unit. Glucose infusion and reversal of the associated coagulopathy are usually required.
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Today most women recover without sequelae, but a mortality rate of 10% has been reported. AFLP can recur in subsequent pregnancies. One out of four infants born to women with AFLP will have an inherited disorder of long-chain 3-hydroxyacyl CoA dehydrogenase deficiency (LCHAD). When stressed, such infants are at risk of fatal nonketotic hypoglycemia. Additionally, some forms of LCHAD deficiency are associated with neonatal dilated cardiomyopathy or progressive neuromyopathy.
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Essentials of Diagnosis
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- Seen with complications of pregnancy, eg, abruptio placentae, placenta previa, amniotic fluid embolism, prolonged intrauterine death.
- Usually associated with severe renal ischemia and/or DIC.
- Abrupt onset of oliguria or anuria.
- Often a triad of anuria, gross hematuria, and flank pain.
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General Considerations
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Bilateral cortical necrosis is an unusual cause of acute renal failure, but when seen it often occurs in the obstetric setting. It usually follows a complication of pregnancy and is associated with DIC and/or severely impaired renal blood flow. Cortical necrosis is usually diagnosed clinically and confirmed radiologically by finding hypoechoic or hypodense areas of renal cortex on ultrasound or CT scan. Renal calcification on plain film may be seen 1–2 months after the event. There is no specific treatment for cortical necrosis and many women require chronic dialysis; 20–40% may have some recovery of kidney function and be left with CKD. Most women with acute renal failure from cortical necrosis will remain dialysis dependent.