Acute renal failure complicating severe preeclampsia requiring admission to an obstetric intensive care unit

Drakeley, Andrew J.; Roux, Paul A. le; Anthony, John; Penny, James

doi:10.1067/mob.2002.120279

Cited by 130 publications

(83 citation statements)

References 5 publications

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“…AKI occurs in 3%-15% of cases of HELLP syndrome, and HELLP syndrome accounts for 40% of all cases of P-AKI and up to 60% of severe cases (13,(63)(64)(65). AKI associated with HELLP syndrome, even in its severe forms requiring dialysis, usually retains a favorable renal outcome.…”

Section: Tma In Pregnancy: the Great Paradigm Shiftmentioning

confidence: 99%

“…These lesions usually recover starting in early postpartum, and in most but not all cases, they completely disappear by 3-6 months postpartum with the parallel resolution of proteinuria and hypertension. PE/E accounts for 15%-20% of P-AKI cases (13), and the risk of P-AKI is higher in the setting of early-onset (,32 weeks gestation) PE/E (2). Convincing data have linked the pathophysiologic changes observed in PE to an increase in the circulating antiangiogenic factors sFlt 1 and endoglin.…”

Section: Pe and Antiangiogenic Factorsmentioning

confidence: 99%

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Obstetric Nephrology

Fakhouri

Vercel

Frémeaux‐Bacchi

2012

Clinical Journal of the American Society of Nephrology

145

121

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Summary AKI in pregnancy remains a cause of significant fetomaternal mortality and morbidity, particularly in developing countries. Hypertensive complications of pregnancy (preeclampsia/eclampsia or hemolysis, elevated liver enzymes, and low platelets count syndrome) are the leading cause of AKI in pregnancy worldwide. Thrombotic microangiopathy is another peculiar and devastating cause of AKI in pregnancy. During the last decade, our understanding, and in some cases, our management, of these causes of AKI in pregnancy has dramatically improved. For instance, convincing data have linked pre-eclampsia/eclampsia to an increase in circulating antiangiogenic factors soluble Flt 1 and endoglin, which induce endothelial cell dysfunction, hypertension, and proteinuria. Several distinct pathogenic mechanisms underlying thrombotic microangiopathy, including thrombotic microangiopathy occurring during pregnancy, have been established. Thrombotic microangiopathy, which can present as hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, can be reclassified in four potentially overlapping subtypes: disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 deficiency-related thrombotic microangiopathy, complement alternative pathway dysregulation-related thrombotic microangiopathy, secondary thrombotic microangiopathy (verotoxin and antiangiogenic drugs), and thrombotic microangiopathy of undetermined mechanism. In most cases, pregnancy is only a precipitating factor for thrombotic microangiopathy. Treatment of thrombotic microangiopathy occurring during pregnancy should be tailored to the underlying pathogenic mechanism: (1) restoration of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 serum activity in the setting of thrombotic thrombocytopenic purpura through plasma exchanges and in some cases, B cell-depleting therapy and (2) inhibition of complement alternative pathway activation in atypical hemolytic uremic syndrome using antiC5 blocking antibody (eculizumab).

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Section: Tma In Pregnancy: the Great Paradigm Shiftmentioning

confidence: 99%

Section: Pe and Antiangiogenic Factorsmentioning

confidence: 99%

Obstetric Nephrology

Fakhouri

Vercel

Frémeaux‐Bacchi

2012

Clinical Journal of the American Society of Nephrology

145

121

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“…19 In women with post-partum HELLP syndrome, risk of renal failure and pulmonary oedemaincreased significantly compared to those with an antenatal onset. 20,21 In another study, the mortality rate for women with HELLP syndrome was 1.1% where one to twentyfive percent of affected women developed serious complications such as disseminated intravascular coagulation, abruptio placentae, acute respiratory distress syndrome, hepatorenal failure, pulmonary edema, subcapsular hematoma and hepatic rupture. A significant percentage of patients received blood products.…”

Section: 11mentioning

confidence: 99%

Overview of Eclampsia at a Tertiary Care Hospital

Shakya

Vaidya

2014

Nepal j. obstet. gynaecol.

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Results: Out of 31,674 obstetric admissions, 45 (0.14%) were eclampsia cases of which 42.2% belonged to 20 -<25 years and 28.8% in 17-<20 years age group occurring mostly in primipara (71.1%). Antepartum and postpartum eclampsia were 77.7% and 22.2% respectively. Majority of them presented at 36-40 weeks'(46.6%), unbooked cases being 80% and 20% had antenatal check-up at this hospital. The diastolic blood pressure on admission recorded was 110-130 mmHg (55.5%), headache being the most common symptom(53.3%), blurred vision (22.2%), HELLP syndrome (4.4%) and urine albumin 3+ (46.6%) at the time of admission. Magnesium sulphate was used as anticonvulsant, loading and maintenance dose (40%) and only as loading dose (33.3%). Though fetal outcome was normal in 44.4% cases, rest were premature (24.4%), intrauterine growth restriction (17.7%) and intrauterine fetal demise (13.3%). Three (6.6%) cases were referred to multidisciplinary center. Maternal mortality occurred in two (4.4%) cases (cardiopulmonary arrest and prolonged hypoxia). Conclusions:When patients with eclampsia presented late, significant morbidity like HELLP syndrome, renal failure and central nervous disorder occurred and muti-organ damage leading to maternal mortality.

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“…The development of hemolysis (H), elevated liver enzyme (EL), low platelets (LP) is called HELLP syndrome [2] [3]. During normal pregnancy, the placenta vascularizes to allow for the exchange blood [4], water, gases, solute, including nutrient and wastes between the mother and fetal circulation [5].…”

mentioning

confidence: 99%

Estimation of Plasma D-Dimer Levels in Sudanese Women with Preeclampsia

Abdelgadir¹,

Gaufri²

2017

OALib

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Background: The literature suggests that the haemostatic abnormalities have taken a big part in preeclampsia. D-dimer is a biomarker of fibrin formation and degradation. Objective: The present study was aimed to estimate and evaluation of the plasma D-dimer levels in Sudanese preeclampsia women. Material and Methods: This is an analytical descriptive case control study done during March 2016. A total of 100 participants were enrolled in this study, classified into two groups: the first group consisted of 50 Sudanese women diagnosed by preeclampsia as patients group, while the second group consisted of 50 normotensive women and their age matched to patients, designated as normal control group. 3 milliter of veins blood samples were collected in containers containing 3.2% tri sodium citrate as anticoagulant, then the platelet-poor plasma was prepared immediately by centrifuging for 15 minutes at approx 3000 rpm. The plasma D-dimer levels were done using MISPA-i2 (Switzerland). The data were analyzed by using SPSS (version 20). Results: The current study showed that the D-dimer level was statistically significant higher in preeclampsia women compared with normotensive pregnant women (Mean ± SD: 1.016 ± 0.158 vs 0.168 ± 0.045 with P value 0.000, respectively). Conclusion: This study concluded that the plasma D-dimer level was significantly elevated in Sudanese women with preeclampsia. Subject AreasHematology

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Acute renal failure complicating severe preeclampsia requiring admission to an obstetric intensive care unit

Cited by 130 publications

References 5 publications

Obstetric Nephrology

Obstetric Nephrology

Overview of Eclampsia at a Tertiary Care Hospital

Estimation of Plasma D-Dimer Levels in Sudanese Women with Preeclampsia

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