Acute renal failure (ARF) is a syndrome characterized by the rapid (hours to weeks) decline in renal function, resulting in the retention of nitrogenous waste products such as BUN and creatinine along with the inability to maintain normal fluid and electrolyte balances. Nonpregnant patients with ARF are often asymptomatic, but, when seen in pregnancy, ARF is rarely encountered in the absence of significant clinical findings or events complicating the gestation. ARF may complicate a host of diseases that, for purposes of diagnoses and management, are conveniently divided into 3 categories (Table 13-2).
Diseases characterized by renal hypoperfusion in which the integrity of renal parenchymal tissue is preserved (prerenal azotemia, prerenal ARF). This is the most common form of ARF and has the best prognosis.
Diseases involving renal parenchymal tissue (intrarenal azotemia, or intrinsic renal ARF).
Diseases associated with an acute obstruction of the urinary tract (postrenal azotemia, postrenal ARF).
TABLE 13-2.Acute Renal Failure in Pregnancy ||Download (.pdf) TABLE 13-2. Acute Renal Failure in Pregnancy
|Differential diagnosis |
Intrarenal azotemia or acute tubular necrosis
Bilateral renal cortical necrosis
Acute interstitial nephritis
Post renal azotemia
Most acute intrinsic renal azotemia is caused by ischemia or nephrotoxins, and is classically associated with acute tubular necrosis (ATN). Thus, in clinical practice, the term ATN is commonly used to denote ischemic or nephrotoxic ARF.
In prerenal ARF, impaired renal perfusion is the problem and this may be secondary to true intravascular volume depletion, decreased effective circulating volume to the kidneys secondary to impaired cardiac output, or due to agents that alter renal perfusion. Prerenal ARF may be rarely seen in the first trimester of pregnancy as a complication of severe hyperemesis gravidarum. In the second and third trimesters, severe blood loss as a complication of uterine hemorrhage in the antepartum, intrapartum, or postpartum periods is an important and not an uncommon cause of hypovolemia and subsequent ARF. It is important to remember that maternal bleeding may be concealed behind the placenta in some patients with serious placental abruption, and this condition may also be accompanied by varying degrees of a consumptive coagulopathy that can further complicate the degree of renal dysfunction.
Pregnancy is associated with a higher incidence of both bladder infections and pyelonephritis. This increased incidence of both upper and lower urinary tract infections, estimated to complicate approximately 2% of all pregnancies, is believed to result from both hormonal and mechanical changes that result in stasis within the urinary collecting system. Unlike their nonpregnant counterparts, pregnant women with pyelonephritis can manifest a substantial decrease in creatinine clearance and rarely may experience some degree of transient ARF. Patients with pyelonephritis in pregnancy, complicated with ARF, often have evidence of chronic renal parenchymal infection and recovery after appropriate antimicrobial therapy may be incomplete.
Severe preeclampsia and eclampsia account for the majority of ARF unique to pregnancy. Renal failure is unusual even with severe disease, unless there has also been significant blood loss with hemodynamic instablility or severe disseminated intravascular coagulopathy. Usually, the clinical picture of ARF seen in such patients is that of ATN, and typically resolves spontaneously within the first 2 weeks postpartum. Whereas in the short term, some of these patients with preeclampsia/eclampsia-induced ATN may require dialytic support, in general, even these more seriously affected patients experience complete recovery and have an excellent long-term prognosis. In those patients with ATN secondary to preeclampsia in whom the disease persists and long-term dialysis is necessary, frequently, it appears that pregnancy and/or preeclampsia have unmasked a chronic renal disorder or there has been some degree of renal cortical necrosis. When ARF develops in patients with severe preeclampsia or eclampsia, consideration should be given to effecting delivery as safely and as expeditiously as possible because maternal condition will frequently dramatically improve postpartum.
Preeclamptic/eclamptic patients, patients who develop placental abruption with or without coagulopathy, pregnancies in which there is a prolonged intrauterine fetal demise complicated with DIC, or women experiencing an amniotic fluid embolism are at an increased risk of developing renal cortical necrosis. Renal cortical necrosis, a pathologic process that destroys the renal cortex partially or completely while sparing the medulla, is heralded by the abrupt onset of oliguria or anuria that may be accompanied by flank pain, gross hematuria, and hypotension. This triad of anuria, gross hematuria, and flank pain is unusual in the other causes of renal failure in pregnancy. Renal cortical necrosis is not unique to pregnancy. However, pregnancy-related cases account for up to 70% of all cases. This entity is diagnosed based on the clinical presentation and can usually be established with ultrasonography or CT scanning of the kidneys. The characteristic findings are hypoechoic or hypodense areas in the renal cortex. There is no specific therapy that has been shown to be effective for patients with renal cortical necrosis with many women requiring chronic hemodialysis. Approximately 30% to 40% of patients experience at least partial recovery and have markedly compromised creatinine clearances.
Other clinical entities, more commonly associated with pregnancy and ARF with varying degrees of proteinuria, are seen in patients with HELLP (hemolysis, elevated liver transaminases, low platelets) syndrome, acute fatty liver of pregnancy, postpartum renal failure due to adult hemolytic uremic syndrome (HUS), and thrombotic thrombocytopenic purpura (TTP). Some investigators group these disease processes and preeclampsia under the same rubric of microangiopathic hemolytic processes of pregnancy, because they share a common histologic feature of anemia with evidence of red cell destruction on peripheral smears. The clinical manifestation and the nomenclature of the disease reflect the primary target organ. However, it is believed that there may be a unifying pathophysiologic process of profound vasoconstriction of arterioles resulting from an, as yet, unidentified “toxin” or mechanism likely involving the vascular endothelium. Consequently, in acute fatty liver of pregnancy, although this rare complication of pregnancy is associated with ARF in up to 60% of cases, the target organ is primarily the liver, with accompanying alterations of normal laboratory values such as transaminases, bilirubin, glucose metabolism, and various clotting factors (eg, antithrombin III, fibrinogen). Similarly, in postpartum renal failure resulting from HUS, the kidneys appear to be the target organs with resultant alterations in normal renal functions assays and, in comparison to renal dysfunction associated with HELLP syndrome or acute fatty liver of pregnancy, protracted ARF may result. Though HUS is generally a postpartum disease and HELLP syndrome is a form of severe preeclampsia usually confined to the late second or third trimesters, TTP almost always occurs antepartum and, although it may occur in the third trimester, many cases appear before 24 weeks of gestation. TTP is characterized by the pentad of microangiopathic hemolytic anemia, thrombocytopenia, renal insufficiency, fever, and neurologic abnormalities. The severity of renal dysfunction is usually mild particularly in comparison with the more striking neurologic involvement, fever, and thrombocytopenia.