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Acute kidney injury (AKI) is costly and is associated with increased mortality and morbidity. An understanding of the renal physiologic changes that occur during pregnancy is essential for proper evaluation, diagnosis, and management of AKI. As in the general population, AKI can occur from prerenal, intrinsic, and post-renal causes. Major causes of pre-renal azotemia include hyperemesis gravidarum and uterine hemorrhage in the setting of placental abruption. Intrinsic etiologies include infections from acute pyelonephritis and septic abortion, bilateral cortical necrosis, and acute tubular necrosis. Particular attention should be paid to specific conditions that lead to AKI during the second and third trimesters, such as preeclampsia, HELLP syndrome, acute fatty liver of pregnancy, and TTP-HUS. For each of these disorders, delivery of the fetus is the recommended therapeutic option, with additional therapies indicated for each specific disease entity. An understanding of the various etiologies of AKI in the pregnant patient is key to the appropriate clinical management, prevention of adverse maternal outcomes, and safe delivery of the fetus. In pregnant women with pre-existing kidney disease, the degree of renal dysfunction is the major determining factor of pregnancy outcomes, which may further be complicated by a prior history of hypertension.
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PMID:Acute kidney injury in the pregnant patient. 2316 15

HELLP syndrome is a collection of symptoms described as hemolysis, elevated liver enzymes and low platelets. HELLP syndrome complicates 0.01-0.6% of pregnancies and can be considered a severe variant of preeclampsia. The occurrence of HELLP syndrome diagnosed before the 20th week of gestation has been most commonly reported in association with antiphospholipid antibody syndrome (APS) or triploid chromosomal anomalies. A 41-year-old primigravida was admitted at 17 weeks and 6 days gestation with hypertension, proteinuria, hemolytic anemia and acute renal injury. She was diagnosed with HELLP syndrome, and subsequently suffered from an intrauterine fetal demise. After delivery, the clinical manifestations of HELLP syndrome resolved within 7 days with the exception of her acute renal failure. Interdisciplinary teams of physicians were able to exclude other imitators of preeclampsia, such as hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), APS, lupus and acute fatty liver of pregnancy. This case is difficult to diagnose, given the similar presentation of several microangiopathic hemolytic anemias. The clinical manifestations and laboratory findings of HELLP and its mimicking conditions seem as if they are mirror images of each other. However, the discrete differences in our patient presentation, clinical findings, laboratory results and overall postpartum course leave HELLP syndrome as the most consistent diagnosis. It is imperative to investigate for all possible etiologies as HELLP syndrome at 17 weeks gestation is extremely rare and mimicking conditions may require alternative management strategies.
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PMID:HELLP Syndrome at 17 Weeks Gestation: A Rare and Catastrophic Phenomenon. 2580 1

Pre-eclampsia complicated by severe HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome is a multi-organ disease, and can be difficult to differentiate from thrombotic microangiopathy (appearing as thrombotic thrombocytopenic purpura or hemolytic uremic syndrome), acute fatty liver, systemic erythematous lupus, antiphospholipid syndrome and severe sepsis. Many papers have highlighted the risks of misdiagnosis resulting in severe consequences for maternal health, and this can be fatal when thrombotic thrombocytopenic purpura is misdiagnosed as severe HELLP syndrome. The aim of this paper is to propose relevant markers to differentiate pre-eclampsia complicated by severe HELLP syndrome from its imitators, even in the worrying situation of apparently indistinguishable conditions, and thereby assist clinical decision-making regarding whether or not to commence plasma exchange. Relevant identifiers to establish the most accurate diagnosis include the frequency of each disease and anamnestic data. Frank hemolysis, need for dialysis, neurological involvement and absence of disseminated intravascular coagulation are indicative of thrombotic microangiopathy. The definitive marker for thrombotic thrombocytopenic purpura is undetectable ADAMTS 13 activity.
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PMID:Differentiation between severe HELLP syndrome and thrombotic microangiopathy, thrombotic thrombocytopenic purpura and other imitators. 2587 92

Pregnancy-related acute kidney injury (AKI) has declined in incidence in the last three decades, although it remains an important cause of maternal and fetal morbidity and mortality. Pregnancy-related causes of AKI such as preeclampsia, acute fatty liver of pregnancy, HELLP (Hemolysis, Elevated Liver function tests, Low Platelets) syndrome, and the thrombotic microangiopathies (thrombotic thrombocytopenic purpura, atypical hemolytic-uremic syndrome [HUS]) exhibit overlapping features and often present as diagnostic dilemmas. Differentiating among these conditions may be difficult or impossible based on clinical criteria only. In difficult and rare cases, a renal biopsy may need to be considered for the exact diagnosis and to facilitate appropriate treatment, but the risks and benefits need to be carefully weighed. The use of eculizumab for the treatment of atypical HUS has demonstrated efficacy in early case reports. Non-pregnancy related causes such as volume depletion and pyelonephritis require early and aggressive resuscitative as well as antibiotic measures respectively. We will discuss in this review the various etiologies of AKI in pregnancy, current diagnostic approaches, and the latest treatment strategies. Given the recent trends of increasing maternal age at the time of pregnancy, and the availability of modern reproductive methods increase the risks of AKI in pregnancy in the coming years.
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PMID:Acute Kidney Injury in Pregnancy. 2871 Oct 77

Pregnancy-related acute kidney injury (Pr-AKI) remains a large public health problem, with decreasing incidences in developing countries but seemingly increasing incidences in the United States and Canada. These epidemiologic changes are reflective of the advances in medical and obstetric care, as well as changes in underlying maternal risk factors. The risk factors associated with advanced maternal age, such as hypertension, diabetes, chronic kidney disease, and those associated with reproductive technologies such as multiple gestations, are increasing. Traditional causes of Pr-AKI, such as septic abortions and puerperal sepsis, have been replaced by hypertensive diseases, such as preeclampsia and thrombotic microangiopathies comprising thrombotic thrombocytopenic purpura (TTP) and atypical hemolytic uremic syndrome (aHUS). In this review, we discuss the global impact of Pr-AKI on maternal and fetal outcomes, the predominant etiologies, and key clinical features to distinguish diagnoses, such as preeclampsia/hemolysis elevated liver function test and low platelet (HELLP) syndrome, acute fatty liver disease of pregnancy (AFLP), and other thrombotic microangiopathies. New insights into the pathogenesis of preeclampsia, TTP/aHUS, and AFLP that have unearthed possible therapeutic targets are summarized. We also delve into special consideration needed to give to pyelonephritis and postobstructive causes of Pr-AKI. With each diagnosis, we offer the latest treatment recommendations, such as the positive reports from the use of eculizumab to treat aHUS. In the end, we hope to arm the clinician with the best tools to understand and address this morbid problem that does not seem to be disappearing.
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PMID:Acute Kidney Injury in Pregnancy: The Changing Landscape for the 21st Century. 2972 29

HELLP syndrome is a disorder associated with serious maternal morbidity and mortality. Distinguishing HELLP from other pregnancy-related disorders is often challenging and may result in delay of treatment. Differential diagnoses include acute fatty liver of pregnancy, thrombotic thrombocytopenic purpura, antiphospholipid syndrome, and hemolytic uremic syndrome, and are reviewed in this chapter. While there is not any current treatment for HELLP, the mainstay of treatment involves maternal stabilization and timely delivery. Various treatment strategies have been attempted to help decrease the morbidity and mortality of HELLP, including the maternal use of corticosteroids. The authors review the studies and controversies surrounding the maternal use of corticosteroids, plasma exchange, and low molecular weight heparin for the treatment of HELLP, as well as the role of the complement system in HELLP. Further large, well-designed, randomized controlled trials are needed to address the role corticosteroids may play in the treatment of women with HELLP and to help improve maternal and fetal outcomes.
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PMID:HELLP Syndrome: Pathophysiology and Current Therapies. 2999 1

Thrombocytopenia during pregnancy presents unique challenges for the hematologist. Obstetricians generally manage many of the pregnancy-specific etiologies, ranging from the benign (gestational thrombocytopenia) to the life-threatening (preeclampsia; hemolysis, elevated liver enzymes and low platelets syndrome; and acute fatty liver of pregnancy). However, hematologists may be consulted for atypical and severe presentations and to help manage non-pregnancy specific etiologies, including immune thrombocytopenia, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome and antiphospholipid syndrome, among others, in which maternal and fetal risks must be considered. This review provides a general approach to the diagnosis and management of thrombocytopenia in pregnancy for the consulting hematologist.
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PMID:Thrombocytopenia in pregnancy: Diagnosis and approach to management. 3175 23


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