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Hypertension in Pregnancy: Clinical-Pathological Correlations and Remote Prognosis
... Preeclampsia is a systemic disorder characterized by endothelial dysfunction that impacts multiple organ systems, including the kidney, where the most common presentation is newonset proteinuria. The impact of preeclampsia on kidney histology has been well documented, with postpartum biopsies demonstrating classic pathologic features, including glomerular endotheliosis and vascular injury [1,2]. While proteinuria typically resolves within months of delivery, there is an expanding body of evidence suggesting that there is a future risk of kidney disease after preeclampsia. ...
... In a study by Murakami et al., the authors performed postpartum renal biopsies in women with severe hypertension or proteinuria in pregnancy and found that 19 women (22.1%) had underlying kidney disease, most often IgA nephropathy [78]. In the study by Fisher et al., with 176 kidney biopsies of women with preeclampsia in the postpartum period, 31 out of 176 (17.6%) of women had glomerular disease identified on kidney biopsy [1]. Given that most of the studies linking preeclampsia to ESKD are registrybased, few women have prepregnancy testing of kidney function, even fewer have postpartum biopsies and proteinuria is not always followed to resolution, there is no good way to quantify the degree of confounding in the general population. ...
... However, there are several plausible mechanisms linking preeclampsia to future CKD, irrespective of underlying kidney disease (Fig. 2). Kidney biopsy samples have clear evidence of endothelial damage, in the form glomerular endotheliosis and vascular injury [1]. As noted previously, early onset set preeclampsia is associated with damage to the glycocalyx, which may predispose to future kidney disease [56•]. ...
Purpose of review:
Preeclampsia and chronic kidney disease have a complex, bidirectional relationship. Women with kidney disease, with even mild reductions in glomerular filtrate rate, have an increased risk of developing preeclampsia. Preeclampsia, in turn, has been implicated in the subsequent development of albuminuria, chronic kidney disease, and end-stage kidney disease. We will discuss observational evidence and mechanisms linking the two disease processes.
Recent findings:
Preeclampsia is characterized by an imbalance in angiogenic factors that causes systemic endothelial dysfunction. Chronic kidney disease may predispose to the development of preeclampsia due to comorbid conditions, such as hypertension, but is also associated with impaired glycocalyx integrity and alterations in the complement and renin-angiotensin-aldosterone systems. Preeclampsia may lead to kidney disease by causing acute kidney injury, endothelial damage, and podocyte loss. Preeclampsia may be an important sex-specific risk factor for chronic kidney disease. Understanding how chronic kidney disease increases the risk of preeclampsia from a mechanistic standpoint may open the door to future biomarkers and therapeutics for all women.
... Irreversible vascular damage due to more severe endothelial damage and inflammatory stress in EOP than in LOP cannot be disregarded [23]. Renal histology of postpartum biopsies on PE patients showed glomerular endotheliosis and vascular injury as classic pathologies features [24] support this finding. PE is suggested to develop kidney disease by causing acute renal impairment, endothelial damage, and podocyte loss [24]. ...
... Renal histology of postpartum biopsies on PE patients showed glomerular endotheliosis and vascular injury as classic pathologies features [24] support this finding. PE is suggested to develop kidney disease by causing acute renal impairment, endothelial damage, and podocyte loss [24]. ...
Background and objective: Preeclampsia (PE) has been disproportionately prevalent in developing countries and constitutes a leading cause of maternal mortality, and also has long-term impacts, including renal consequences. This study aimed to explore the risk of persistent hypertension and kidney failure in early-onset PE (EOP) and late-onset PE (LOP) in the five years after delivery.
Methods: This retrospective cohort study included women with a prior history of severe PE or normotensive pregnancy admitted to tertiary hospitals in Indonesia. The blood pressure, body mass index (BMI), urea, creatinine serum, and protein urine were analyzed, and the risk of chronic kidney disease (CKD) after five years was performed using the Kidney Disease Improvement Global Outcomes (KDIGO) classification.
Results: Twenty-seven EOP, 35 LOP, and 30 normotensive cases were included. Mean blood pressure after five years was recorded as 115.6 ± 14.25 mmHg in the normotensive group, 131.82 ± 19.34 mmHg in the LOP group, and 154.96 ± 23.48 mmHg in the EOP group. According to the KDIGO classification, the normotensive group had an average 10% risk of CKD, but severe PE had a risk of CKD greater than 90%. In the severe PE group, the risk of CKD was 20.94 times higher compared to normotensive women (OR 20.94; 95% CI 2.67-163.72, p = 0.004). The risk of CKD in the EOP group was 6.75 times higher than in the LOP group (OR 6.75; 95% CI 2.19-20.76, p = 0.001), whereas persistent hypertension in the EOP group was 5.78 times higher than in the LOP group (OR 5.78; 95% CI 1.91-17.395, p = 0.002).
Conclusions: PE women have a higher risk of CKD than normotensive women. Women with a history of EOP are more likely to develop persistent hypertension and CKD than women with a prior LOP history.
... There is also a growing body of evidence linking preeclampsia with the future development of kidney disease (29,227,303,306,423). It is well established that preeclampsia can cause pathologic changes in the kidney, including thrombotic microangiopathy and endotheliosis (134). As mentioned above, there is also evidence that preeclampsia is associated with podocyturia and reduced podocyte numbers in kidney tissue in autopsy specimens of women who died from complications of preeclampsia (150,151). ...
... In a study of postpartum kidney biopsies in women with severe hypertension or proteinuria in pregnancy, 19 women (22.1%) had underlying kidney disease, most often IgA nephropathy (297). A larger study of 176 postpartum kidney biopsies of women with preeclampsia found that 13 of 176 (17.6%) women had glomerular disease identified on kidney biopsy (134). One difficulty of observational studies investigating this relationship is that many women did not have labs, such as serum Cr or urine protein measurement, checked prior to pregnancy. ...
Preeclampsia and other hypertensive disorders of pregnancy are major contributors to maternal morbidity and mortality worldwide. This group of disorders includes chronic hypertension, gestational hypertension, preeclampsia, preeclampsia superimposed on chronic hypertension, and eclampsia. The body undergoes important physiological changes during pregnancy to allow for normal placental and fetal development. Several mechanisms have been proposed that may lead to preeclampsia, including abnormal placentation and placental hypoxia, impaired angiogenesis, excessive pro-inflammatory response, immune system imbalance, abnormalities of cellular senescence, alterations in regulation and activity of angiotensin II, and oxidative stress, ultimately resulting in upregulation of multiple mediators of endothelial cell dysfunction leading to maternal disease. The clinical implications of preeclampsia are significant as there are important short-term and long-term health consequences for those affected. Preeclampsia leads to increased risk of preterm delivery and increased morbidity and mortality of both the developing fetus and mother. Preeclampsia also commonly leads to acute kidney injury, and women who experience preeclampsia or another hypertensive disorder of pregnancy are at increased lifetime risk of chronic kidney disease and cardiovascular disease. An understanding of normal pregnancy physiology and the pathophysiology of preeclampsia is essential to develop novel treatment approaches and manage patients with preeclampsia and hypertensive disorders of pregnancy. © 2023 American Physiological Society. Compr Physiol 13:4231-4267, 2023.
... None of these diagnoses were confirmed by biomarkers such as fms-like tyrosine kinase 1 (sFlt-1) or kidney biopsy [24,25]. Fisher et al.'s study in which only 55% of women suspected of having preeclampsia were found to have preclampsia on kidney biopsy underscores the difficulty of accurate diagnosis [26]. Another limitation of these studies is the difficulty in finding appropriate comparative populations. ...
... However, this clinical sign may not be specific as worsening hypertension and a marked increase in proteinuria can be related to hyperfiltration superimposed on decreased kidney function and mild proteinuria at baseline or even acute rejection. Women with preexisting proteinuria and hypertension are at risk for augmentation of both towards the end of pregnancy [26]. In nontransplant patients, elevations in uric acid may be a clue for preeclampsia [32]. ...
Purpose of review:
To review the studies and practice guidelines on the preeclampsia risks in kidney donors and recipients.
Recent findings:
There is a small increased risk of gestational hypertension and preeclampsia in pregnancies that follow kidney donation. Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guideline (2017) and the 2015 American Society of Transplantation (AST) consensus conference statement recommends counseling kidney donors about this increased risk. There is no observed increase in fetal complications or eclampsia post-kidney donation. Preeclampsia is more commonly observed in kidney transplant recipients than the general population and these patients should be co-managed with an obstetrician with experience in managing high risk pregnancies. Although preeclampsia has not been found to have a deleterious effect on renal graft function, it can cause premature delivery. Risk calculators have been proposed and an elevated pre-pregnancy creatinine seems to be an important risk. KDIGO Clinical Practice Guidelines (2009) recommends attempting pregnancy when kidney function is stable with proteinuria of less than 1 g per day. The use of novel biomarkers for preeclampsia has not been published in this population. Preeclampsia is an important concern for female kidney donors and recipients of child-bearing age. These individuals should be appropriately counseled.
... (4 -8) Hypertensive disorder in pregnancy results in 10 -15% of all direct maternal mortality and is believed to cause long-term sequelae, such as chronic hypertension and cardiovascular disease. (2,9,10) Hypertensive disorder in pregnancy also associates with preterm labor (10%), intrauterine growth restriction (12%), and perinatal death (2.7%). (11 -13) Preterm delivery and intrauterine growth restriction increase the risk of several neonatal complications, including respiratory distress syndrome, seizure, intracranial hemorrhage, hypoglycemia, and prolonged hospitalization. ...
... Se formarán depósitos hialinos en los túbulos renales causando necrosis del Asa de Henle según los niveles de hiperuricemia y en los que presentan depósitos de grasa se presenta proteinuria de alto peso molecular. Alrededor del 25% de las multíparas con EHE es posible constatar endoteliosis glomerular, un 13% presentarán enfermedad renal crónica asociada a la Preeclampsia y 10% histológicamente serán normales (Fisher et al., 1981). ...
La obra aborda aspectos importantes como: factores de riesgos, clasificación, algunas condiciones intrínsecas y extrínsecas vinculadas a esta patología, su etiopatogenia y fisiopatología, complicaciones maternas y perinatales; así como sus protocolos de atención, destacándose: el control de la hipertensión arterial, prevención de la convulsión eclámptica, vigilancia biológica y optimización de la extracción; con el propósito de estabilizar a la gestante en espera de la interrupción del embarazo como tratamiento definitivo que será dependiente de la edad gestacional y las condiciones clínicas materno fetales.
... One critical point is how to distinguish GD worsening from preeclampsia. This differential diagnosis is particularly challenging because of the heterogeneity of preeclampsia and its frequent association with all kidney diseases, including GD. [44][45][46][47] Recent evidence linking preeclampsia to an angiogenic-antiangiogenic imbalance 48 has led to the clinical use of various biomarkers to predict the occurrence of preeclampsia. 49 The measurement of the soluble fms-like tyrosine kinase 1/placental growth factor ratio is increasingly being recommended, but its cost-effectiveness remains to be fully assessed. ...
Our understanding of the various aspects of pregnancy in women with kidney diseases has significantly improved in the last decades. Nevertheless, little is known about specific kidney diseases. Glomerular diseases are not only a frequent cause of chronic kidney disease in young women, but combine many challenges in pregnancy: immunologic diseases, hypertension, proteinuria and kidney tissue damage. An international working group undertook the review of available current literature and elicited expert opinions on glomerular diseases in pregnancy with the aim to provide pragmatic information for nephrologists according to the present state-of-the-art knowledge. This work also highlights areas of clinical uncertainty and emphasizes the need for further collaborative studies to improve maternal and foetal health.
... This proteinuria could have been misinterpreted as pre-eclampsia as none of the above studies could confirm these findings with biomarkers such as fms-like tyrosine kinase 1 (sFlt-1) or kidney biopsy, thus suggesting just proteinuria and not exactly preeclampsia. [14,15] Fisher et al.'s study [16] showed that only 55% of women suspected of having preeclampsia had evidence of preeclampsia on kidney biopsy underscoring the difficulty of accurate diagnosis. In our study population, post-donation pregnancies females were older (25.94 ± 1.2) years to the pre-donation group (22.6 ± 1.6 years). ...
Introduction:
Recent data suggest a risk of gestational hypertension, proteinuria and pre-eclampsia among pregnancies after kidney donation.
Methods:
This retrospective study among females who donated kidneys (1997-2017) at a tertiary renal transplant center in Northern India assessed the maternal and fetal outcomes of their pregnancy. Data of participants were collected using pre-tested semi structured questionnaire.
Results:
In total, 925 female kidney donors (1332 pregnancies) in the pre-donation group and 45 females (48 pregnancies) in the post donation period were included. The mean age of first pregnancy, weight (kg) gain, proportion of history of pre-natal check-up, institutional delivery, and history of unrelated donation was statically significant among the post-donation group. The proportion of pre-eclampsia, gestational hypertension, gestational diabetes, and post-partum hemorrhage was insignificantly higher among the post-donation group with higher preterm birth with low-birth-weight babies. Proteinuria (P < 0.05) was significantly higher among post donation pregnancies. In multivariate analysis, cesarean delivery and low birth weight (<2500 g) were common among the post-donation pregnancy group.
Conclusions:
The study demonstrated no significant risk to maternal outcomes butan increased risk to fetal outcomes in terms of prematurity and low birth weight among the post-donation pregnancy group.
... Women with kidney transplants are at risk for developing preeclampsia, with the risk cited as anywhere from 25% to 40%. 6,19 The classic paper of postpreeclampsia kidney biopsies by Fisher et al. 20 did describe diffuse thickening of the arterial walls and intimal fibrous thickening in a subset of women (38 of 176), most of whom were multiparas in the affected pregnancy, suggesting they had some underlying "predisposition" to preeclampsia, such as hypertension. A recent study of 52 women with pregnancies after kidney transplant did not find that preeclampsia increased the risk of graft failure or a significant drop in eGFR in the long term, though it was associated with a larger drop in eGFR in the course of pregnancy. ...
Introduction
Women with advanced kidney disease are advised to wait until after transplant to pursue pregnancy, but the impact of pregnancy on estimated glomerular filtration rate (eGFR) decline and kidney histology is unclear.
Methods
We identified a cohort of women aged 18 to 44 years at transplant from 1996 to 2014 at our 3-site program (N = 816) and determined whether they had a pregnancy >20 weeks gestation post-transplant by chart review. Outcomes included rate of change in eGFR after pregnancy, changes in kidney histology before and after pregnancy, graft failure, and 50% reduction in eGFR.
Results
There were 37 women with one or more pregnancies lasting longer than 20 weeks gestation post-transplant. Comparing women with and without pregnancy post-transplant, there was a significant increase in the rate of eGFR decline after pregnancy (−2.4 ml/min per 1.73 m² per year vs. −1.9 ml/min per 1.73 m² per year in women with no pregnancy, P < 0.001). Pregnancy did not affect the risk of graft failure, death-censored graft failure, or 50% reduction in eGFR.
Conclusion
Pregnancy affects the rate of eGFR decline in the allograft. Postpregnancy biopsy findings revealed an increase in vascular injury, which could be a potential mechanism. We did not find a significant increase in risk of graft failure or reduction in eGFR by 50% owing to pregnancy.
... Interestingly, some early studies reported no adverse consequences of hypertensive disorder in pregnancy (HDP), PE, or eclampsia on long-term maternal health [41][42][43]. Others, however, found a correlation, especially in the event of a young primigravida [44]. ...
Over the last thirty years, evidence has been accumulating that Hypertensive Disorders of Pregnancy (HDP) and, specifically, Preeclampsia (PE) produce not only long-term effects on the pregnant woman, but have also lasting consequences for the fetus. At the core of these consequences is the phenomenon known as defective deep placentation, being present in virtually every major obstetrical syndrome. The profound placental vascular lesions characteristic of this pathology can induce long-term adverse consequences for the pregnant woman’s entire arterial system. In addition, placental growth restriction and function can, in turn, cause a decreased blood supply to the fetus, with long-lasting effects. Women with a history of HDP have an increased risk of Cardiovascular Diseases (CVD) compared with women with normal pregnancies. Specifically, these subjects are at a future higher risk of: Hypertension; Coronary artery disease; Heart failure; Peripheral vascular disease; Cerebrovascular accidents (Stroke); CVD-related mortality. Vascular pathology in pregnancy and CVD may share a common etiology and may have common risk factors, which are unmasked by the “stress” of pregnancy. It is also possible that the future occurrence of a CVD may be the consequence of endothelial dysfunction generated by pregnancy-induced hypertension that persists after delivery. Although biochemical and biophysical markers of PE abound, information on markers for a comparative evaluation in the various groups is still lacking. Long-term consequences for the fetus are an integral part of the theory of a fetal origin of a number of adult diseases, known as the Barker hypothesis. Indeed, intrauterine malnutrition and fetal growth restriction represent significant risk factors for the development of chronic hypertension, diabetes, stroke and death from coronary artery disease in adults. Other factors will also influence the development later in life of hypertension, coronary and myocardial disease; they include parental genetic disposition, epigenetic modifications, endothelial dysfunction, concurrent intrauterine exposures, and the lifestyle of the affected individual.
... al. studied association of lipid profile and uric acid levels in normotensive, preeclamptic pregnancy [15]. Few of the relevant studies and cases were reviewed [16][17][18]. Issues related to antenatal care and services in this region were reported [19][20][21][22][23][24][25]. ...
Background: The most leading cause of perinatal and maternal deaths and morbidity in developed and developing countries like India is pregnancy related hypertensive disorders especially pre-eclampsia. PIH is defined as; in previously normotensive and normoproteinuric women, hypertension of >_ 140/90 mmHg with or without proteinuria measured on two occasions 6 hours apart after gestational age (20 weeks).Women with pregnancy related hypertensive disorders experience varied and altered lipid changes. Increased TG, low-density lipoprotein cholesterol (LDL-C), cholesterol and decreased high-density lipoprotein cholesterol (HDL-C) concentrations leading to dyslipidemia was found in majority of the studies. Aim: The study aims to evaluate predictor like maternal sr. lipid profile in 2nd trimester in pregnancy related hypertensive disorders. Objective: To evaluate the occurrence of normal maternal and altered maternal serum lipid profile serum lipid profile in 2nd trimester of pregnancy in pregnancy related hypertensive disorders and compare them . Materials and Methods: The design of the study will be prospective as well as observational conducted from September 2020 to august 2022 with an estimated sample size of 1000. Patients included were nnormotensive and non-proteinuric in second trimester (13-20 weeks of gestation). Subjects will be evaluated on the basis of preformed and pretested proforma consisting of history, clinical symptoms and presentation and investigations. Blood samples for serum lipid profile will be collected in plain bulb with aseptic conditions and analyzed at the biochemistry laboratory by enzymatic method. Expected Results: We expect that from our results, altered maternal serum lipid profile in 2nd trimester will be positively associated with pregnancy related hypertensive disorders.
... El manejo debe ser ambulatorio. (22) Hígado graso agudo del embarazo En lo • s casos de complicación aguda de la preeclampsia (eclampsia. síndrome Hellp, rotura hepática), debe procederse a terminar la gestación de inmediato y por cesárea. ...
La ocurrencia de convulsiones en asociación con preeclampsia constituye una causa importante de morbimortalidad materna. A pesar de reconocerse desde la antigüedad, el tratamiento en la práctica es todavía inadecuado. La respuesta al ineficiente manejo de la eclampsia consiste en mejorar la capacitación de todos los ginecoobstetras, anestesiólogos, médicos generales y obstetrices en el diagnóstico y tratamiento de la preeclampsia severa y eclampsia. En el Instituto Nacional Materno Perinatal se ha adoptado los criterios diagnósticos del Colegio Americano de Obstetras y Ginecólogos, los que se plasman en las guías clínicas y procedimientos para la atención obstétrica del Instituto. Los objetivos terapéuticos a conseguir son controlar la hipertensión arterial, prevenir la ocurrencia de convulsiones o su repetición, optimizar el volumen intravascular, mantener una oxigenación arterial adecuada, diagnosticar y tratar precozmente las complicaciones y culminar la gestación por la vía más rápida. Palabras clave: Hipertensión, embarazo, preeclampsia, morbilidad materna, mortalidad materna, diagnóstico, tratamiento.
... 25 It has been reported that moderate glomerular endotheliosis develops in pregnancies complicated with preeclampsia. 26 In women with preeclampsia, subendothelial fibrinoid deposits and mesangial cell interposition have been observed, and it has been stated that these findings were specific to preeclampsia. The presence of proteinuria in preeclampsia is explained by this physiological mechanism. ...
Aim:
To evaluate whether there is a statistically significant difference between the cord blood gas parameters of pregnancies complicated with preeclampsia and uncomplicated pregnancies and to show whether the amount of proteinuria affects fetal cord blood gas parameters in pregnancies complicated with preeclampsia.
Methods:
The study was designed retrospectively. Between 2016 and 2019, the neonatal results and cord blood gas results of 109 pregnant women who were diagnosed with preeclampsia and 75 nonpreeclamptic randomly selected pregnant women were compared. The preeclampsia group was divided into groups according to amount of proteinuria. SPSS 21.0 statistics program was used, and comparative analysis was carried out.
Results:
The data of the 109 preeclampsia cases and 75 control groups included in the study were compared, and there was no statistical difference between the fetal cord blood gas parameters between the groups (p > 0.05). The median first and fifth minute Apgar scores were found significantly lower in the preeclampsia group compared to the control group (6, 8 and 8, 9, respectively; p < 0.001). Also, the amount of proteinuria does not alter cord blood gas parameters (p > 0.05).
Conclusion:
Preeclampsia poses a risk for the neonatal period as it reduces the neonatal Apgar scores due to the chronic hypoxic process it creates. However, it was observed that the amount of proteinuria, which is one of the diagnostic criteria, did not affect neonatal results on Apgar scores or fetal cord blood gas parameters.
... Pre-eclampsia may worsen all other hypertensive disorders. Although the evidence from renal biopsy studies suggest that the diagnosis of superimposed pre-eclampsia may be often erroneous [4]. The probability of pre-eclampsia is double to four times greater if a patient has a first-degree relative with a history of the disorder and is sevenfold greater if a previous pregnancy was pre-eclampsia-complicated [5,6]. ...
... Women with the pattern of hypertension outlined above but with no proteinuria were classified as mild preeclampsia. Because preeclampsia is considered a disease of first pregnancies [22,23], only those women with the above-mentioned features in their first pregnancies were included. Women with preexisting hypertension or other medical conditions known to predispose them to preeclampsia (e.g. ...
Objective:
Preeclampsia is a common and serious heritable disorder of human pregnancy. Although there have been notable successes in identification of maternal susceptibility genes a large proportion of the heritability of preeclampsia remains unaccounted for. It is has been postulated that rare variation may account for some of this missing heritability. In this study, we performed whole-exome sequencing (WES) in multiplex families to identify rare exonic risk variants.
Methods:
We conducted WES in 244 individuals from 34 Australian/New Zealand multiplex preeclampsia families. Variants were tested for association with preeclampsia using a threshold model and logistic regression.
Results:
We found significant association for two moderately rare missense variants, rs145743393 (Padj = 0.0032, minor allele frequency = 0.016) in the chromosome 1 open reading frame 35 (C1orf35) gene, and rs34270076 (Padj = 0.0128, minor allele frequency = 0.024) in the pyroglutamylated RFamide peptide receptor (QRFPR) gene. To replicate these associations we performed imputation in our Australian genome wide association scan for preeclampsia and found no significant exonic variants in either C1orf35 or QRFPR. However, 11 variants demonstrating nominal significance (P < 0.05) in the genomic region between QRFPR and annexin A5 (ANXA5) were identified. We further leveraged publicly available genome-wide available summary data from the UK Biobank to investigate association of these two variants with the underlying clinical phenotypes of preeclampsia and detected nominal association of the QRFPR variant (rs34270076, P = 0.03) with protein levels in females.
Conclusion:
The study represents the first to use WES in multiplex families for preeclampsia and identifies two novel genes (QRFPR and C1orf35) not previously associated with preeclampsia and find nominal association of rs34270076 with protein levels, a key clinical feature of preeclampsia. We find further support for ANXA5 previously associated with pregnancy complications, including preeclampsia.
... Thrombocytopenia is observed by 6-10% during pregnancy, and the case of preeclampsia and HELLP syndrome account for 2% of thrombocytopenia [1]. Many risk factors are involved in preeclampsia and HELLP syndrome that may develop in pregnancy, and multiple pregnancy is among these factors [4]. ...
... 17 Others argue that only a renal biopsy showing glomerular endotheliosis can prove PE and that 76% of multiparas are misdiagnosed (25% of primiparas); therefore, only the latter should be included in related research. 28 Recently, Myatt and Roberts 29 advocated consideration of PE as a syndrome rather than a specific disease. By restricting our comparison group to those patients diagnosed with severe features, we hoped to identify parameters present in those most in need of a higher level of care. ...
( Anesth Analg . 2018;126:913–919)
Nearly one-third of patients with preeclampsia (PE) do not present clearly, and there currently is no predictive test with adequate discrimination power. Analysis of peripheral pulse waveforms has long been recognized to indicate arterial resistance characteristics. The authors of the present study hypothesized it may be possible to distinguish women with PE with severe features from nonpreeclamptic patients, using parameters of photoplethysmographic (PPG) pulse and electrocardiogram (ECG) alone. To that end, the authors of the present study determined a set of timing, shape, and statistical features available through these noninvasive measures.
... Fisher et al. stellten bereits 1981 fest, dass eine Präeklampsie mit einem erhöhten Langzeitri- siko für kardiovaskuläre Erkrankungen einhergeht ( Fisher et al., 1981). Zudem konnte gezeigt werden, dass Präeklampsiepatientinnen häufiger an einer kardiovaskulären Erkrankung ver- ...
Um das Gehirn vor den Gefahren der Hypo- oder Hyperperfusion zu schützen, ist eine Konstanthaltung der zerebralen Durchblutung trotz Schwankungen im systemischen Blutdruck essentiell. Dies wird durch den Mechanismus der zerebralen Autoregulation (CA) ermöglicht. Es ist bekannt, dass es bei Präeklampsie zu einer Störung der CA kommen kann. Zudem wur-de nach stattgehabter Präeklampsie ein erhöhtes zerebrovaskuläres Langzeitrisiko beobachtet.
Ziel der vorliegenden Arbeit war es zu untersuchen, ob eine gestörte CA nach Präeklampsie langfristig persistiert.
... Studies in the past have shown an increased risk of kidney biopsy [2] indicating kidney disease or end-stage renal failure [3,4]. There is also evidence of increased risk of chronic hypertension following an episode of preeclampsia [5][6][7]. ...
Abstract Background Data on the prevalence of persistent symptoms in the first year after preeclampsia are limited. Furthermore, possible risk factors for these sequelae are poorly defined. We investigated kidney function, blood pressure, proteinuria and urine sediment in women with preeclampsia 6 months after delivery with secondary analysis for possible associated clinical characteristics. Methods From January 2007 to July 2014 all women with preeclampsia and 6-months follow up at the University Hospital Basel were analyzed. Preeclampsia was defined as new onset of hypertension (≥140/90 mmHg) and either proteinuria or signs of end-organ dysfunction. Hypertension was defined as a blood pressure ≥ 140/90 mmHg or the use of antihypertensive medication. Proteinuria was defined as a protein-to-creatinine ratio in a spot urine > 11 mg/mmol. Urine sediment was evaluated by a nephrologist. Secondary analyses were performed to investigate for possible parameters associated with persistent symptoms after preeclampsia. Results Two hundred two women were included into the analysis. At a mean time of follow up of 172 days (+/− 39.6) after delivery, mean blood pressure was 124/76 mmHg (+/− 14/11, range 116–182/63–110) and the mean serum-creatinine was 61.8 μmol/l (33–105 μmol/l) (normal 60 mml/min/1.73m2). 20.3% (41/202) had a blood pressure of 140/90 mmHg or higher (mean 143/89 mmHg) or were receiving antihypertensive medication (5.5%, 11/202). Proteinuria was present in 33.1% (66/199) (mean 27.5 mg/mmol). Proteinuria and hypertension was present in 8% (16/199). No active urine sediment (e.g. signs of glomerulonephritis) was observed. Age and gestational diabetes were associated with persistent proteinuria and severe preeclampsia with eGFR decline of ≥ 10 ml/min/1.73m2. Conclusion Hypertension and proteinuria are common after 6 months underlining the importance of close follow up to identify those women who need further care.
... The longest follow-up after pregnancy was 39 years after delivery and the risk of chronic kidney disease was 1.9 times higher [20]. In 37% of multiparas [21] classical glomerular lesions or other lesions were found on renal biopsy after delivery. Focal glomerulosclerosis, nephroarteriosclerosis and IgA nephropathy dominated in renal biopsies done 10 years after previous preeclampsia [22]. ...
Preeclampsia is a condition characterized by hypertension, proteinuria after 20th week of gestation, dysfunction of other maternal organs or uteroplacentary dysfunction and is associated with short-term renal damage. Recent studies report on potential association of preeclampsia with chronic kidney disease in later life. The aim of this study was to determine this potential association by literature review and our results.
A Pubmed (Medline) literature search on the association of preeclampsia and subsequent chronic kidney disease was carried out. Our study was conducted at the Department of Nephrology of the University Clinical Centre Skopje in 2010 and included women who consulted the Clinic due to hypertension or impaired renal function and who had either preeclampsia or hypertensive disorders in pregnancy. Thirty patients with decreased glomerular filtration that occurred 1-28 years after pregnancy with hypertensive disorder were included in the study.
Literature search yielded 227 abstracts, of which 19 papers were selected, and they referred only to chronic kidney disease in the period after delivery in patients with preeclampsia. Various risks for emergence of chronic kidney disease in later life were reported in recent literature, varying from 1.2 to 14 for preeclampsia and in patients with superimposed preeclampsia, the risk was 45 times higher. In our study, risk of reduction in glomerular filtration rate was highest in the first 5 years (OR 3.6, 95% CI 1.06-22.5). Delivery before 27 weeks of gestation insignificantly increased the risk of reduced glomerular filtration in the later period (OR 1.33 95% CI 0.2-8.5). Preeclampsia is not a direct risk factor for chronic kidney disease, however, proteinuria over 0.3 g/24h in the group of patients with hypertension or preeclampsia in pregnancy, increased the risk of reduced glomerular filtration rate by 28 times (OR 28.5, 95% CI 2.7-30.9).
Patients with preeclampsia need careful monitoring in postpartal and long-term period, not only for cardiovascular but for chronic kidney disease.
... Поражение почек при ПЭ -одно из наиболее ярких проявлений дисфункции эндотелия. Еще в 1959 г. были описаны значительные морфологические изменения гломерулярного аппарата почек, выражающиеся в набухании и вакуолизации эндотелиальных клеток нефронов, отложении фибрина в эндотелии, что породило термин «гломерулярный эндотелиоз» [40]. Электронно-микроскопические исследования показали исчезновение фенестрации гломерулярного эпителия [15]. ...
... [1][2][3] La definición clásica de preeclampsia, sustentada en hipertensión arterial y proteinuria, es pobre para predecir resultados maternos y perinatales adversos con un valor predictivo positivo de 30%. 4 Además, es inespecífica porque en un estudio clínico de mujeres diagnosticadas con preeclampsia, las biopsias renales revelaron que el diagnóstico fue incorrecto en 20% de las primigestas y en más de 30% de las multíparas; la glomerulonefritis fue el hallazgo más común. 5 Los factores angiogénicos son marcadores potencialmente útiles para la predicción, diagnóstico y estratificación del riesgo de preeclampsia. 6 En la actualidad se dispone de pruebas, como el inmunoensayo Elecsys sFlt-1 y PIGF para diagnosticar preeclampsia temprana con sensibilidad de 95% y especificidad de 99.5% en embarazos menores de 34 semanas; en gestaciones mayores de 34 semanas se reporta una sensibilidad de 74%. ...
OBJETIVO:
determinar la relación entre las concentraciones séricas de factores angiogénicos con la severidad de la preeclampsia e hipertensión gestacional y con el resultado materno y perinatal adverso.
MATERIALES Y MÉTODOS:
estudio transversal y comparativo efectuado en pacientes atendidas entre los meses de septiembre de 2013 y agosto de 2015 en la Unidad Médica de Alta Especialidad. La población de estudio se dividió en cinco grupos: 1) hipertensión gestacional leve, 2) preeclampsia leve, 3) hipertensión gestacional severa, 4) preeclampsia severa y 5) preeclampsia severa complicada. Además, el total de pacientes se analizó según el resultado materno o perinatal adverso. Las concentraciones séricas de sFlt-1, PlGF y su relación sFlt1/PlGF se midieron con electroquimioluminiscencia.
RESULTADOS:
se estudiaron 196 mujeres con embarazo único ≥ 20 semanas de gestación, con hipertensión gestacional y preeclampsia. Las concentraciones de sFlt-1, PlGF y la relación sFlt1/PlGF fueron significativamente diferentes entre los cinco grupos de estudio (p < 0.001). La diferencia en la concentración de los factores angiogénicos fue más marcada conforme mayor fue la severidad de la enfermedad hipertensiva en el embarazo (p < 0.001). La relación sFlt-1/PIGF fue significativamente mayor en las pacientes con resultado materno o perinatal adverso en comparación con quienes no lo tuvieron (222.5 vs 112.8 y 158.3 vs 53.1, respectivamente) p < 0.001.
CONCLUSIÓN:
conforme mayor fue la severidad de la enfermedad hipertensiva en el embarazo se observó mayor alteración en la concentración de factores angiogénicos (p < 0.001). Así mismo, la relación sFlt-1/PIG fue mayor en pacientes con resultado materno y perinatal adverso (p < 0.001).
Background
Early-onset preeclampsia (EOP) and late-onset preeclampsia (LOP) are associated with different maternal and fetal outcomes, biochemical markers, and clinical characteristics. Nevertheless, only a few data were presented about its long-term effects on kidney function later in life.
Objective
This study aimed to explore the risk of persistent hypertension and kidney failure in EOP and LOP in five years after delivery. Study Design: This retrospective cohort study included women with prior history of severe preeclampsia or normotensive pregnancy admitted to one of tertiary hospitals in Indonesia. The blood pressure, body mass index, urea and creatinine serum, and protein urine were analyzed, and risk of chronic kidney disease (CKD) was performed using KDIGO classification.
Results
A total of 27 EOP, 35 LOP and 30 normotensive cases were included. Mean blood pressure after five years recorded respectively 115.6 ± 14.25 mmHg in normotensive group, 131.82 ± 19.34 mmHg in LOP group, and 154.96 ± 23.48 mmHg in EOP group. Percentage of women with positive protein urine varied from 13.3–31.4% and 66.7% in normotensive, LOP, and EOP, respectively. According to KDIGO classification, normotensive group had 90% of low-risk CKD, whereas the severe preeclampsia group had 41.9% of high-risk CKD. In the severe preeclampsia group, the risk of CKD was 20.94 times higher compared to normotensive women (OR 20.94; 95% CI [2.67-163.72], p = 0.004). Then risk of CKD in EOP group was 6.75 times higher than LOP group (OR 6.75; 95% CI [2.19–20.76], p = 0.001), whereas persistent hypertension in EOP group was 5.78 times higher than LOP group (OR 5.78; 95% CI [1.91-17.395], p = 0.002).
Conclusions
Preeclampsia women have a higher risk of CKD than normotensive women. Women with a history of EOP are more likely to develop persistent hypertension and CKD than women with prior LOP history.
The developing human placenta undergoes extensive angiogenesis (neovascularization from preexisting blood vessels) and vasculogenesis (blood vessel generation from angioblast precursor cells), along with a process of vascular mimicry (pseudo-vasculogenesis) as cytotrophoblasts convert from an epithelial to an endothelial phenotype. Failure of these changes has been linked to the pathogenesis of preeclampsia. Placentas in preeclamptic subjects produce an excess of antiangiogenic factors that enter the maternal circulation and impair vascular endothelial cell signaling of proangiogenic factors. In this chapter we discuss evidence that measurement of circulating angiogenic factors in the plasma accurately reflects the morbidity of severe disease and the risk of adverse outcomes related to preeclampsia. The mechanisms as to how antiangiogenic proteins cause preeclamptic and eclamptic signs and symptoms are reviewed, as are their implications for prevention or cure.
Renal function profoundly changes during normal pregnancy, and many of these physiological alterations are disrupted in preeclampsia. In Chapter 14, The Kidney in Normal Pregnancy and Preeclampsia, the authors first discuss the changes in renal blood flow and glomerular filtration and in the renal handling of proteins and uric acid that occur during normal pregnancy, and then describe the perturbation of these gestational alterations of kidney function in preeclampsia. Osmoregulatory changes of pregnancy , as well as a comprehensive description of renal morphology in normal pregnancy and preeclampsia, and the indications for renal biopsy in pregnancy are presented. The clinical implications of changes in kidney function and morphology during normal pregnancy and preeclampsia are also described, including underlying cellular and molecular mechanisms. Finally, a thorough examination of the epidemiology, pathophysiology, and diagnosis of superimposed preeclampsia in women with chronic kidney disease is presented. This extensively revised and updated Chapter for the 5th edition of Chesley’s Hypertensive Disorders in Pregnancy should be informative for both the basic scientist and clinician interested in learning more about the kidney during normal pregnancy and preeclampsia.
The changes in the cardiovascular system during normal pregnancy include increases in cardiac output and arterial compliance, while blood pressure and systemic vascular resistance fall, and the vasculature becomes resistant to pressor hormones, all without significant changes in myocardial contractility. The onset of preeclampsia is characterized by marked reversal of vasculature resistance to pressor hormones, decreases in cardiac output, and a high systemic vascular resistant state. Some note a hyperdynamic, low-resistance disease state preceding this that may indicate a subset of women with, or destined to have, chronic hypertension. However, the hyperdynamic state is hard to reconcile with the early change in vascular reactivity, a decrease in intravascular volume preceding, and the exaggerated rise in circulating antiangiogenic proteins that impede vasodilatation. Steady and pulsatile arterial loads decrease in normal pregnancy but fail to do so in preeclampsia. Abnormal vascular responses during preeclampsia may be secondary to changes in vascular tone—autonomic nervous system, hormonal regulation—and/or vascular wall elements. While left ventricular contractility, as measured by load-independent indices, seems to be unaltered during preeclampsia, left ventricular diastolic function seems to be depressed in early-onset preeclampsia. Evidence is accumulating in support of the notion that pregnancy can be considered as a cardiometabolic “stress test,” capable of unmasking underlying subclinical cardiovascular and metabolic abnormalities that increase the risk of both pregnancy disorders such as preeclampsia and later-life cardiovascular disease.
Preeclampsia is a heritable quantitative trait disorder characterized by hypertension and often proteinuria. The confounders associated with quantitative traits (e.g., polygenic, multifactorial, non-Mendelian inheritance) have been a hallmark when exploring its pathogenesis which has remained elusive despite years of research. Immune function at the uteroplacental interface leading to poor placental implantation evidenced by abnormal invasion of spiral arteries by the extra-villous cytotrophoblast may be the earliest clues to its origins. Abnormal implantation provides a rationale for the resolution of this condition, namely delivery of the fetus and placenta. Placental-derived vasoactive substances have been implicated in the hypertensive phenotype and perturbation of organs remote from the uterus (e.g., kidneys, liver, brain). Placental-derived biomarkers have made their way into clinical practice with the promise of being predictive of disease later in pregnancy. Reliable prediction allows the opportunity to use low dose aspirin therapy as a proven prophylaxis.
Rationale & Objective
Though studies have demonstrated a relationship between hypertensive disorders of pregnancy (HDP) and chronic kidney disease, there are limited data on the risk of acute kidney injury (AKI) following HDP. We examined the risk of AKI following the occurrence of HDP.
Study Design
Retrospective population-based cohort study.
Setting & Participants
Pregnant women of Ontario, Canada, aged 14-50 years who delivered at ≥ 20-weeks gestation between April 1, 2002 and March 31, 2015.
Exposure
Preeclampsia, gestational hypertension, or neither.
Outcomes
The primary outcome was AKI with receipt of dialysis (AKI-D) ≥ 90 days after delivery. The main secondary outcome was AKI based on a hospitalization with a diagnostic code for AKI ≥ 90 days after delivery.
Analytical Approach
Time-dependent Cox proportional and cause-specific hazards models were used to evaluate the relationship between HDP and outcomes of interest. Models were adjusted for baseline and time-varying covariates.
Results
Our cohort comprised 1,142,656 women and 1,826,235 deliveries, of which 1.7% were associated with gestational hypertension and 4.4% with preeclampsia. After a mean follow-up of 6.7 years, there were 322 episodes of AKI-D (0.41 per 10,000 person-years), and 1598 episodes of AKI based on diagnostic codes (2.04 per 10,000 person-years). After adjustment, neither preeclampsia nor gestational hypertension was associated with AKI-D. Preeclampsia was associated with AKI (HR 1.22, 95% CI 1.03-1.45) but gestational hypertension was not.
Limitations
Retrospective design and possible unmeasured confounding. Cases of HDPs and AKI may have been undetected.
Conclusions
Preeclampsia was a risk factor for AKI occurring ≥ 90 days after delivery. Our findings suggest the potential importance of obtaining a pregnancy history as part of a comprehensive risk profile for acute kidney disease and suggest that women with a history of HDP may benefit from monitoring of kidney function.
Blood pressure; extracellular fluid volume; renal plasma flow; glomerular filtration rate; plasma concentrations of renin, angiotensin, aldosterone, desoxycorticosterone, and prostaglandins; responses to infused angiotensin; and many other factors are altered during normal and hypertensive gestation. The diagnosis of the exact disease process responsible for hypertension in pregnancy in an individual patient is extremely difficult if based solely on clinical criteria. The American College of Obstetricians and Gynecologists has suggested the following clinical classifications: (1) preeclampsia-eclampsia, (2) chronic hypertension of whatever cause, (3) chronic hypertension with superimposed preeclampsia, and (4) late or transient hypertension. The three broad categories of renal disease responsible for these clinical syndromes are: (1) preeclampsia-eclampsia, (2) hypertensive changes, and (3) various primary renal diseases.
Controversy abounds regarding the aggressiveness of therapy in this syndrome. We prefer a middle-of-the-road approach, bringing blood pressure down to the range of 95 to 100 mm Hg. Hydralazine and Aldomet are the usual drugs of choice. Any intervening nervous system hyperexcitability suggests impending eclampsia and should be immediately treated with magnesium sulfate.
The long-term prognosis for the mother with pure preeclampsia appears to be excellent. Most infants born of hypertensive gestations are small for date, with a prognosis that is also affected by the underlying disease of the mother.
Objective
To examine whether maternal race could affect the relationship between fetal sex and preeclampsia.
Material and methods
This study was a cohort analysis using prospectively collected data from pregnant women who participated in the Vitamin Antenatal Asthma Reduction Trial (VDAART). Preeclampsia was the secondary outcome of VDAART. We examined the association of fetal sex with preeclampsia and its potential interaction with maternal race in 813 pregnant women (8% with preeclampsia) in logistic regression models with adjustment for preterm birth (<37 weeks of gestation), maternal age, education, and body mass index at enrollment and clinical center. We further conducted a race stratified analysis and also examined whether any observed association was dependent on the gestational age at delivery and prematurity.
Results
In an analysis of all races combined, preeclampsia was not more common among pregnant women with a male fetus compared to those with a female fetus (odds ratio [OR] = 1.3, 95% CI = 0.81, 2.24). There was an interaction between African American race and fetal sex in association with preeclampsia after adjustment for preterm delivery and other potential confounders (p = .014). In race stratified analyses, we observed higher odds of preeclampsia among African American pregnant women who carried male fetuses after adjustment for preterm delivery and other potential confounders (adjusted OR = 2.4, 95% CI = 1.12, 5.60).
Conclusion
We observed fetal sexual dimorphic differences in the occurrence of preeclampsia in African American women, but not in Whites. Information on fetal sex may ultimately improve the prediction of pre-eclampsia in African American mothers, who might be at higher risk for this adverse condition in pregnancy.
Preeclampsia is characterized by angiogenic imbalance (AI), sFlt-1 (soluble fms-like tyrosine kinase-1)/PlGF (placental growth factor) is useful for its diagnosis and prediction of adverse outcomes, but the relationship among the degrees of AI as assessed by this ratio with the correct diagnosis, clinical characteristics, and outcomes in women with clinical diagnosis of preeclampsia are unclear. We studied 810 women with clinical diagnosis of preeclampsia. Patients were divided into 3 groups based on their degree of AI, evaluated by the sFlt-1/PlGF ratio: no AI (≤38), mild AI (>38-<85), and severe AI (≥85). Patients with no AI were more likely to have comorbidities and false significant proteinuria compared with patients with mild and severe AI (P<0.001). The rates of preterm delivery, delivery within 14 days, and small-for-gestational-age infant were higher among patients with severe AI than in patients with no and mild AI (P<0.001) and in patients with mild AI that in those with no AI (P≤0.01). The occurrence of any adverse maternal outcome (HELLP syndrome, elevated liver enzymes, thrombocytopenia, placental abruption, acute kidney injury) was only present in patients with severe AI. Interestingly, the frequency of misdiagnosis of preeclampsia was progressively lower as the degrees of AI increased (no AI: 100%, mild AI: 88.2%, and severe AI: 15.6%). We concluded that in women with clinical diagnosis of preeclampsia, severe AI is characterized by high frequency of true preeclampsia and preeclampsia-related adverse outcomes, in contrast, no and mild AI, are characterized by unnecessary early deliveries, often due to misdiagnosis.
The centuries-old approach to the prevention of eclampsia and its associated maternal morbidity and mortality is based on the recognition of the presence of premonitory signs and symptoms such as hypertension and proteinuria. The spectrum of preceding signs and symptoms came to be known as preeclampsia, which is debatably considered to be an early stage on a clinical continuum possibly leading to eclampsia. The premonitory signs and symptoms were then construed as diagnostic criteria for the poorly understood syndrome of preeclampsia, and this led to a perpetual debate that remains subject to wide disagreement and periodic updates. In this commentary, we will draw attention to the fact that the criteria for preeclampsia should be viewed from the prism of a screening test rather than as diagnostic of a condition in itself. Focusing research on developing better diagnostic and screening methods for what is clinically important, namely maternal and perinatal morbidity and mortality from hypertensive disorders of pregnancy, a long overdue upgrade from what was possible centuries ago, will ultimately lead to better management approaches to what really matters.
Women with advanced chronic kidney disease (CKD) may have impaired fertility making conception difficult. In addition, in these women, pregnancy is high risk and associated with increased complications. This is further complicated by having an endocrinopathy such as thyroid disease or diabetes. As a result, a multidisciplinary team consisting of an endocrinologist, nephrologist, obstetrician, or maternal-fetal-medicine physician is warranted. Management requires consideration of hormonal levels and non-teratogenic medications.
Preeclampsia is a heterogenous, systemic disorder that is caused by maternal and placental factors. Preexisting renal disease and chronic hypertension are significant risk factors for the development of preeclampsia, and the degree of renal insufficiency prior to pregnancy is an important determinant of the risk of maternal complications in pregnancy. While pregnancy itself may accelerate renal decline in some patients, it is not clear whether preeclampsia contributes additional damage. There are currently no clinically used biomarkers that can differentiate preeclampsia from intrinsic renal disease, and an interdisciplinary care approach is the best way to help manage these complex cases. There is evidence that preeclampsia is associated with the future low but increased risk of maternal renal disease. It is still unclear whether it is truly an independent risk factor, but preeclampsia may still identify women early in life who are at future risk of developing renal disease. The optimal long-term follow-up of women with preeclampsia is still not known, but providers should appreciate the significant overlap of renal disease and preeclampsia and have a high index of suspicion in women who do not follow a typical clinical course.
The use of renal biopsy during pregnancy remains controversial. While it is considered safe by some authors, a risk/benefit ratio must still be considered whenever the procedure is contemplated, weighing the risks to maternal health and ultimate pregnancy outcome. One must keep in mind potentiation of bleeding risk in a woman who is preeclamptic or who has uncontrolled hypertension. If the performance of a kidney biopsy is thought to result in a potential change in therapeutic management, it may be reasonable to perform this procedure. Preeclampsia is an important clinical concern but does not usually require biopsy for diagnosis. However, in some situations it may be important to distinguish preeclampsia from other clinicopathologic entities that can mimic or be superimposed upon it. The pathologic features of preeclampsia are well established, but they are not specific to preeclampsia and may even be seen during normal pregnancy.
The International Journal of Gynecology and Obstetrics regrets that, in the above article, an error appeared in the 5.3.4 Measurement of uterine artery pulsatility index section on page 17, 5th paragraph, second last sentence: The first-trimester abnormal UTPI is defined as less than the 90th percentile, achieving a detection rate of 48%, at 8% false-positive rate, for the identification of early-onset PE. should have been: The first-trimester abnormal UTPI is defined as greater than the 90th percentile, achieving a detection rate of 48%, at 8% false-positive rate, for the identification of early-onset PE. Affiliation of the author, Mary D'Alton has been corrected to the following: Obstetrician and Gynecologist in-Chief, Columbia University Irving Medical Center, NewYork-Presbyterian The online version is corrected with the above changes after first online publication. We apologize for the inconvenience caused.
Pre‐eclampsia (PE) is a multisystem disorder that typically affects 2%–5% of pregnant women and is one of the leading causes of maternal and perinatal morbidity and mortality, especially when the condition is of early onset. Globally, 76 000 women and 500 000 babies die each year from this disorder. Furthermore, women in low‐resource countries are at a higher risk of developing PE compared with those in high‐resource countries.
Although a complete understanding of the pathogenesis of PE remains unclear, the current theory suggests a two‐stage process. The first stage is caused by shallow invasion of the trophoblast, resulting in inadequate remodeling of the spiral arteries. This is presumed to lead to the second stage, which involves the maternal response to endothelial dysfunction and imbalance between angiogenic and antiangiogenic factors, resulting in the clinical features of the disorder.
Accurate prediction and uniform prevention continue to elude us. The quest to effectively predict PE in the first trimester of pregnancy is fueled by the desire to identify women who are at high risk of developing PE, so that necessary measures can be initiated early enough to improve placentation and thus prevent or at least reduce the frequency of its occurrence. Furthermore, identification of an “at risk” group will allow tailored prenatal surveillance to anticipate and recognize the onset of the clinical syndrome and manage it promptly.
PE has been previously defined as the onset of hypertension accompanied by significant proteinuria after 20 weeks of gestation. Recently, the definition of PE has been broadened. Now the internationally agreed definition of PE is the one proposed by the International Society for the Study of Hypertension in Pregnancy (ISSHP).
According to the ISSHP, PE is defined as systolic blood pressure at ≥140 mm Hg and/or diastolic blood pressure at ≥90 mm Hg on at least two occasions measured 4 hours apart in previously normotensive women and is accompanied by one or more of the following new‐onset conditions at or after 20 weeks of gestation:
1.Proteinuria (i.e. ≥30 mg/mol protein:creatinine ratio; ≥300 mg/24 hour; or ≥2 + dipstick);
2.Evidence of other maternal organ dysfunction, including: acute kidney injury (creatinine ≥90 μmol/L; 1 mg/dL); liver involvement (elevated transaminases, e.g. alanine aminotransferase or aspartate aminotransferase >40 IU/L) with or without right upper quadrant or epigastric abdominal pain; neurological complications (e.g. eclampsia, altered mental status, blindness, stroke, clonus, severe headaches, and persistent visual scotomata); or hematological complications (thrombocytopenia–platelet count <150 000/μL, disseminated intravascular coagulation, hemolysis); or
3.Uteroplacental dysfunction (such as fetal growth restriction, abnormal umbilical artery Doppler waveform analysis, or stillbirth).
It is well established that a number of maternal risk factors are associated with the development of PE: advanced maternal age; nulliparity; previous history of PE; short and long interpregnancy interval; use of assisted reproductive technologies; family history of PE; obesity; Afro‐Caribbean and South Asian racial origin; co‐morbid medical conditions including hyperglycemia in pregnancy; pre‐existing chronic hypertension; renal disease; and autoimmune diseases, such as systemic lupus erythematosus and antiphospholipid syndrome. These risk factors have been described by various professional organizations for the identification of women at risk of PE; however, this approach to screening is inadequate for effective prediction of PE.
PE can be subclassified into:
1.Early‐onset PE (with delivery at <34+0 weeks of gestation);
2.Preterm PE (with delivery at <37+0 weeks of gestation);
3.Late‐onset PE (with delivery at ≥34+0 weeks of gestation);
4.Term PE (with delivery at ≥37+0 weeks of gestation).
These subclassifications are not mutually exclusive. Early‐onset PE is associated with a much higher risk of short‐ and long‐term maternal and perinatal morbidity and mortality.
Obstetricians managing women with preterm PE are faced with the challenge of balancing the need to achieve fetal maturation in utero with the risks to the mother and fetus of continuing the pregnancy longer. These risks include progression to eclampsia, development of placental abruption and HELLP (hemolysis, elevated liver enzyme, low platelet) syndrome. On the other hand, preterm delivery is associated with higher infant mortality rates and increased morbidity resulting from small for gestational age (SGA), thrombocytopenia, bronchopulmonary dysplasia, cerebral palsy, and an increased risk of various chronic diseases in adult life, particularly type 2 diabetes, cardiovascular disease, and obesity. Women who have experienced PE may also face additional health problems in later life, as the condition is associated with an increased risk of death from future cardiovascular disease, hypertension, stroke, renal impairment, metabolic syndrome, and diabetes. The life expectancy of women who developed preterm PE is reduced on average by 10 years. There is also significant impact on the infants in the long term, such as increased risks of insulin resistance, diabetes mellitus, coronary artery disease, and hypertension in infants born to pre‐eclamptic women.
The International Federation of Gynecology and Obstetrics (FIGO) brought together international experts to discuss and evaluate current knowledge on PE and develop a document to frame the issues and suggest key actions to address the health burden posed by PE.
FIGO's objectives, as outlined in this document, are: (1) To raise awareness of the links between PE and poor maternal and perinatal outcomes, as well as to the future health risks to mother and offspring, and demand a clearly defined global health agenda to tackle this issue; and (2) To create a consensus document that provides guidance for the first‐trimester screening and prevention of preterm PE, and to disseminate and encourage its use.
Based on high‐quality evidence, the document outlines current global standards for the first‐trimester screening and prevention of preterm PE, which is in line with FIGO good clinical practice advice on first trimester screening and prevention of pre‐eclampsia in singleton pregnancy.1
It provides both the best and the most pragmatic recommendations according to the level of acceptability, feasibility, and ease of implementation that have the potential to produce the most significant impact in different resource settings. Suggestions are provided for a variety of different regional and resource settings based on their financial, human, and infrastructure resources, as well as for research priorities to bridge the current knowledge and evidence gap.
To deal with the issue of PE, FIGO recommends the following:
Public health focus: There should be greater international attention given to PE and to the links between maternal health and noncommunicable diseases (NCDs) on the Sustainable Developmental Goals agenda. Public health measures to increase awareness, access, affordability, and acceptance of preconception counselling, and prenatal and postnatal services for women of reproductive age should be prioritized. Greater efforts are required to raise awareness of the benefits of early prenatal visits targeted at reproductive‐aged women, particularly in low‐resource countries.
Universal screening: All pregnant women should be screened for preterm PE during early pregnancy by the first‐trimester combined test with maternal risk factors and biomarkers as a one‐step procedure. The risk calculator is available free of charge at https://fetalmedicine.org/research/assess/preeclampsia. FIGO encourages all countries and its member associations to adopt and promote strategies to ensure this. The best combined test is one that includes maternal risk factors, measurements of mean arterial pressure (MAP), serum placental growth factor (PLGF), and uterine artery pulsatility index (UTPI). Where it is not possible to measure PLGF and/or UTPI, the baseline screening test should be a combination of maternal risk factors with MAP, and not maternal risk factors alone. If maternal serum pregnancy‐associated plasma protein A (PAPP‐A) is measured for routine first‐trimester screening for fetal aneuploidies, the result can be included for PE risk assessment. Variations to the full combined test would lead to a reduction in the performance screening. A woman is considered high risk when the risk is 1 in 100 or more based on the first‐trimester combined test with maternal risk factors, MAP, PLGF, and UTPI.
Contingent screening: Where resources are limited, routine screening for preterm PE by maternal factors and MAP in all pregnancies and reserving measurements of PLGF and UTPI for a subgroup of the population (selected on the basis of the risk derived from screening by maternal factors and MAP) can be considered.
Prophylactic measures: Following first‐trimester screening for preterm PE, women identified at high risk should receive aspirin prophylaxis commencing at 11–14+6 weeks of gestation at a dose of ~150 mg to be taken every night until 36 weeks of gestation, when delivery occurs, or when PE is diagnosed. Low‐dose aspirin should not be prescribed to all pregnant women. In women with low calcium intake (<800 mg/d), either calcium replacement (≤1 g elemental calcium/d) or calcium supplementation (1.5–2 g elemental calcium/d) may reduce the burden of both early‐ and late‐onset PE.
Background:
Among the severe complications of preeclampsia (PE), acute kidney injury (AKI) is problematic if features of thrombotic microangiopathy (TMA) are present. Although a haemolysis enzyme liver low-platelets syndrome is considerably more frequent, it is vital to rule out a flare of atypical haemolytic and uraemic syndrome (aHUS). Our objective was to improve differential diagnosis procedures in post-partum AKI.
Methods:
A total of 105 cases of post-partum AKI, admitted to nine different regional French intensive care units from 2011 to 2015, were analysed. Analysis included initial and final diagnosis, renal features, haemostasis and TMA parameters, with particular focus on the dynamics of each component within the first days following delivery. A classification and regression tree (CART) was used to construct a diagnostic algorithm.
Results:
AKI was attributed to severe PE (n = 40), post-partum haemorrhage (n = 33, including 13 renal cortical necrosis) and 'primary' TMA (n = 14, including 10 aHUS and 4 thrombotic thrombocytopenic purpura). Congruence between initial and final diagnosis was low (63%). The dynamics of haemoglobin, haptoglobin and liver enzymes were poorly discriminant. In contrast, the dynamic pattern of platelets was statistically different between primary TMA-related AKI and other groups. CART analysis independently highlighted the usefulness of platelet trajectory in the diagnostic algorithm. Limitations of this study include that only the most severe cases were included in this retrospective study, and the circumstantial complexity is high.
Conclusion:
Trajectory of platelet count between admission and Day 3 helps to guide therapeutic decisions in cases of TMA-associated post-partum AKI. Our study also strongly suggests that during the post-partum period, there may be a risk of transient, slowly recovering TMA in cases of severe endothelial injury in women without a genetic mutation known to induce aHUS.
Preeclampsia and eclampsia have the potential to produce significant maternal and fetal complications. This chapter addresses therapy for pregnant women with chronic hypertension and focuses on pharmacologic management that may diminish risk of superimposed preeclampsia. Preeclampsia is sometimes manifested by severe systemic hypertension. Careful control of hypertension must be achieved to prevent complications, such as maternal cerebral vascular accidents and placental abruption. Pregnancy‐related blindness has been associated with eclampsia, cavernous sinus thrombosis, and hypertensive encephalopathy. Thrombosis and vasospasm develop and lead to multi‐organ involvement, including renal, hepatic, neurologic, hematologic, and uteroplacental dysfunction. Unlike most forms of preeclampsia, HELLP syndrome is not primarily a disease of primigravidas. The clinical signs and symptoms of patients with HELLP syndrome are classically related to the impact of vasospasm on the maternal liver. Thus, most patients present with signs or symptoms of liver compromise.
Kidneys may fail post-partum in a number of circumstances due, for example, to post-partum haemorrhage, preeclampsia, amniotic fluid embolism or septic abortion. All these conditions in pregnancy and post partum represent a threat not only to the endothelium but also to the renal tubular epithelium, and as such may lead to rapid and also irreversible impairment of the renal function. This paper is a non-systematic review of the literature and of our experience, in which we discuss the main open issues on kidney disease in pregnancy and following delivery, in particular as regards tubular damage, with the aim to help reasoning on acute kidney injury (AKI) following delivery. The review will emphasize the often under-estimated importance of the tubular epithelium in the peri-partum period and will: (1) describe the main characteristics of the renal tissues around delivery; (2) define pregnancy-related AKI according to recent Kidney Disease/Improving Global Outcome (KDIGO) guidelines; (3) discuss the most common circumstances of post-partum AKI; and (4) describe the input expected from urinalysis, renal imaging and kidney biopsy.
Cardiovascular disease, including ischaemic heart disease and cerebrovascular disease, has become the number one cause of death in women worldwide. Having had a pregnancy complicated by pre-eclampsia may be more than just a risk factor for the development of cardiovascular disease later in life. Pre-eclampsia causes significant morbidity and mortality in the acute setting with multisystem involvement. We are now learning that while these acute effects resolve in the short to medium term, their legacy is long-lasting. In this chapter we explore the mechanisms involved in the development of long-term hypertension, chronic kidney disease, ischaemic heart and cerebrovascular disease, diabetes and venous thromboembolism. Ways in which the post-partum period can be used to improve the long-term health of these women are reviewed, including the difficulties in identifying subtle abnormalities in parameters such as post-partum blood pressure because normal values have been based on studies often done on middle-aged men. Unfortunately diet and exercise on their own appear to be ineffective in reducing the risk but are important first steps for new mothers to alter their longer-term risks and improve their journey through subsequent pregnancies.
The experience of pregnancy and childbirth transforms the lives of mothers and their families. As it may be anticipated, a large number of medical and surgical complications in the pregnant mother may affect development of the fetus and health of the newborn infant. Since the early nineteenth century (Bard 1807), volumes may be devoted to a consideration of these (Creasy et al. 2014; Reece and Hobbins 2007); however, in the light of space limitations, only several will be considered here.
Background:
The goal of this study was to determine a set of timing, shape, and statistical features available through noninvasive monitoring of maternal electrocardiogram and photoplethysmography that identifies preeclamptic patients.
Methods:
Pregnant women admitted to Labor and Delivery were monitored with pulse oximetry and electrocardiogram for 30 minutes. Photoplethysmogram features and heart rate variability were extracted from each data set and applied to a sequential feature selection algorithm to discriminate women with preeclampsia with severe features, from normotensive and hypertensive controls. The classification boundary was chosen to minimize the expected misclassification cost. The prior probabilities of the misclassification costs were assumed to be equal.
Results:
Thirty-seven patients with clinically diagnosed preeclampsia with severe features were compared with 43 normotensive controls; all were in early labor or beginning induction. Six variables were used in the final model. The area under the receiver operating characteristic curve was 0.907 (standard error [SE] = 0.004) (sensitivity 78.2% [SE = 0.3%], specificity 89.9% [SE = 0.1%]) with a positive predictive value of 0.883 (SE = 0.001). Twenty-eight subjects with chronic or gestational hypertension were compared with the same preeclampsia group, generating a model with 5 features with an area under the curve of 0.795 (SE = 0.007; sensitivity 79.0% [SE = 0.2%], specificity 68.7% [SE = 0.4%]), and a positive predictive value of 0.799 (SE = 0.002).
Conclusions:
Vascular parameters, as assessed noninvasively by photoplethysmography and heart rate variability, may have a role in screening women suspected of having preeclampsia, particularly in areas with limited resources.
Pre-eclamptic focal glomerular sclerosis, hitherto an undescribed complication of IgA nephropathy, was diagnosed in two patients. A 37-year-old female (case 1) was first found to have microscopic hematuria at age 10, and had mild proteinuria during four prior pregnancies. At 26 weeks in her fifth pregnancy urinary proteinuria was noted again in association with elevation of blood pressure to 158/90 mmHg, followed by development of a nephrotic syndrome at 34 weeks and by cesarean section at 35 weeks. Renal biopsy, carried out beyond 2 months after delivery, because of persistences of proteinuria of more than 2.0 g per day and high blood pressure, revealed swelling of glomerular endothelial cells and hyalinosis together with foam cells and focal glomerular sclerosis, which was already known as a type of pre-eclamptic glomerular lesions, as well as typical lesions of IgA nephropathy composed of mild mesangial proliferation and mesangial IgA and C3c deposits. A 28-year-old female (case 2), presented with intermittent proteinuria following upper respiratory tract infection, was histologically proven to have IgA nephropathy. At 34 weeks in her second pregnancy, she showed (_??_) proteinuria and hypertension of 140/100 mmHg. As (_??_) proteinuria persisted for more than one month after delivery, renal biopsy was carried out, revealing almost the same pathological findings as observed in case1. After delivery, proteinuria decreased to 0.8 g per day in case 1 and became negligible in case 2 ultimately and final determination of GFR was estimated as 92 and 104 ml/ min, respectively. These results suggest that worsening of renal symptoms observed in the two patients may be attributed to a complication of pre-eclamptic focal glomerular sclerosis rather than exacerbation of underlying IgA nephropathy. This is the first report, which described the pre-eclamptic focal glomerular sclerosis as a complication of IgA nephropathy.
Background: The Glomerular Filtration Rate (GFR) is the best indicator of renal function. Serum cystatin C has been introduced as an endogenous marker of GFR. However, there are conflicting reports regarding its use in pregnancy and pre-eclampsia. We aimed to assess the GFR changes in pre-eclampsia, evaluate the use of serum cystatin C as an indicator of GFR and to identify other biomarkers for detection of pre-eclampsia. Methods: This was a case-control study, conducted between December 2008 and December 2010, in Omdurman Maternity Hospital. The study group was 72 pre-eclamptic cases compared to 96 normal pregnant and 63 non-pregnant Sudanese women. Clinical and laboratory parameters including blood samples and 24-hour urine output were recorded. Total blood count, serum liver enzymes, renal function tests and serum cystatin C. Creatinine clearance and GFR were calculated. Results: Serum cystatin C level in the pre-eclamptic cases was significantly higher than the normal pregnant (P=0.000) and the non–pregnant participants (P=0.0001). Mean GFR of the pre-eclamptic cases was significantly lower than that of normal pregnant (P=0.0001) and the non-pregnant (P=0.0001). GFR of pre-eclamptic cases did not correlate with serum cystatin C nor with serum uric acid, but was negatively correlated with serum creatinine (r=-0.31, P=0.02). Serum cystatin C correlated with serum albumin (r=-0.41, P=0.0001), serum aspartate aminotransferase (r=0.26, P=0.03) and serum uric acid (r=0.60,P=0.0001) in the pre-eclamptic group. The diagnostic accuracy tests showed that serum cystatin C was a good detector of pre-eclampsia but not a reliable marker of GFR changes in pre-eclampsia. Conclusions: In pre-eclampsia, serum cystatin C level was significantly higher than in normal pregnancy. Serum cystatin C was superior to serum uric acid and serum creatinine in detection of pre-eclampsia but not a reliable indicator of GFR. Serum albumin and serum aspartate transferase can be used as additional biomarkers in pre-eclampsia.
An immunofluorescent study of renal biopsies from patients with toxemia of pregnancy has been performed. It was found that the glomeruli consistently showed bright staining for fibrin within endothelial cells, as well as occasional deposits along the basement membrane. Gamma globulin was only occasionally demonstrable, generally in the form of irregular deposits along the basement membrane. ß1C was absent and albumin was not seen in glomeruli, except sometimes in the form of droplets within epithelial cells.
In biopsies from pregnant patients without toxemia only equivocal staining for fibrin was seen.
On the basis of these observations and other evidence discussed, it is proposed that the accumulation of fibrin in glomeruli reflects a prolonged state of intravascular clotting in toxemia and that the arrest in glomeruli of some form of circulating fibrin constitutes the basic pathogenic mechanism of the glomerular damage in this disease.
Renal biopsies from two patients with classical toxaemia of pregnancy demonstrated heavy deposition of IgG and IgA in a predominantly finely granular pattern. It is suggested that this may be a manifestation of immune complex formation and may provide further evidence for an immunological basis for the renal lesion of this poorly understood disease process.
Renal biopsy specimens from 11 women with severe pre-eclamptic toxaemia were examined by light and electron microscopy linked with immunofluorescence and immuno-electron microscopy. The part played by the mesangium in causing capillary loop thickening is stressed, and the progress of this 'strangulation' is illustrated. In contrast to the findings of most previous authors, IgM was demonstrated by direct immunofluorescence in all biopsy specimens, and its presence and site within the glomerulus were shown by immuno-electron microscopy in three cases.
Heavy proteinuria and/or the nephrotic syndrome rarely occur late in pregnancy. We report the clinical and renal biopsy findings on 11 patients with the nephrotic syndrome occurring during pregnancy in whom light and electron microscopic findings were characteristic of pre-eclampsia. Immunofluorescent microscopy revealed deposits of IgG, IgM, IgA, beta 1C globulin, and fibrinogen, predominantly in the subendothelial position. Only two patients were primigravid; three were in their second or third pregnancy; in six, pre-eclampsia first occurred in the fourth to eighth pregnancy. Clinical abnormalities appeared first between the 23rd and 39th week of gestation. All patients had marked elevation of blood pressure and of serum uric acid levels. Of the 12 infants, eight were alive and well, including one set of twins; four were stillborn. Following delivery, clinical resolution was similar to that in less severe pre-eclampsia. The findings suggest the possible importance of the role of intravascular coagulation in the genesis of pre-eclampsia.
Thirteen nephrosclerotic women were followed for 2 to 7 years from the time a diagnosis was made following a pregnancy complicated by hypertension. Ten patients developed sustained hypertension. Twelve women who were examined responded with a hypertensive pattern to acute salt load. Of the 10 patients who were examined, seven had a reduced renal plasma flow (RPF) demonstrated by the phenolsulfonphthalein (PSP) excretion test. The present observations support the view that the vascular lesion in the kidneys precedes and persists independently of pregnancy. The pregnant state brings the hypertensive disease to clinical expression.
During a retrospective study of 100 patients who underwent renal biopsy because of pregnancy complicated by hypertension, we found 19 patients whom proteinuria exceeded 5.0 Gm. per 24 hours and an additional eight patients in whom excretion ranged between 3.5 and 5 Gm. per day. Of these 27 patients, 23 had the kidney lesion of pre-eclampsia, and three of them had superimposed hypertensive changes in the vasculature. The remaining four had other renal diseases. We located and re-examined 10 of the 23 pre-eclamptic women, 12 to 104 (mean, 36) months after delivery. Serum creatinine levels were normal in all but one, who was discovered to have polycystic kidney disease. During the same time period, we located the records of six women who had heavy proteinuria during gestation but were normotensive. Thus, at our institution, pre-eclampsia is the most common cause of the nephrotic syndrome in pregnancy. The frequency of nephrotic proteinuria in pre-eclampsia appears higher than previously suspected, but, despite this fact, recovery was complete in most instances.
Three hundred and forty-six nulliparous women with pregnancy-induced hypertension prior to term were monitored in a high-risk pregnancy unit while awaiting fetal maturity. Management included ambulation as desired, regular hospital diet without salf restriction, blood pressure measured 4 times daily, weight and urine protein determined 3 times each week, creatinine clearance determined weekly, and serial sonography to monitor fetal growth. Sedation and antihypertensive agents were not prescribed. Delivery was delayed until term unless hypertension persisted or recurred following an initial salutary response. Factors other than hypertension that contributed to the decision to effect delivery were 1) rapid weight gain, 2) decreasing creatinine clearance, 3) appearance of significant proteinuria, 4) suspected fetal growth retardation, and 5) the development of severe headache or scotomata. With this method of management the perinatal mortality rate was 9/1000. Only 5 infants developed the respiratory distress syndrome and all survived. There were 26 women who left the unit against medical advice. Severe hypertension subsequently developed in 7 of these women and 4 of their fetuses were stillborn. The perinatal mortality rate among this group of patients was 154/1000. It is concluded that the nulliparous patient with pregnancy-induced hypertension prior to term can be safely managed by hospitalization and close observation as a viable alternative to prompt delivery.
Six primigravid women developed the nephrotic syndrome in pregnancy during a 4 year period of observation, including 12,707 deliveries. Clinical evaluation and examination of renal tissue by light and electron microscopy were carried out in each case. Four of the initial pregnancies ended with the delivery of viable infants. Four subsequent pregnancies also terminated successfully. A variety of morphologic lesions was found, including diffuse membranous glomerulonephritis, poststreptococcal glomerulonephritis, and pre-eclampsia. Four patients were followed from 1 to 4 years after delivery. Three women showed minimal clinical and histologic evidence of renal disease at the end of the follow-up period, although one with morphologic abnormalities of pre-eclampsia relapsed transiently 9 months post partum. The fourth patient with an initial kidney biopsy specimen compatible with pre-eclampsia progressed into end-stage renal failure. The findings suggest that the histologic characteristics of pre-eclampsia may not be specific but may be associated with other renal diseases occurring during pregnancy.
All but 2 of the 270 women surviving eclampsia at the Margaret Hague Maternity Hospital in the period 1931 through 1951 were traced to 1966; 9 patients refused examination. In white women having eclampsia in the first pregnancy carried to viability the remote mortality is the same as in unselected women; in all Negro and in white women having eclampsia as multiparas, the remote mortality is 2.6 to 3.8 times the expected number. The prevalence of hypertension and frequency distribution of diastolic blood pressures is virtually identical in primiparous eclamptic women and the women in several epidemiologic studies of blood pressure; there is a considerable increase in the prevalence of hypertension in women having had eclampsia as multiparas, and that has accounted for their increased death rates. The prevalence of diabetes, developing many years after eclampsia, is 5 times the expected rate in primiparous and 10 times the expected rate in multiparous eclamptic women. We conclude that eclampsia does not cause chronic hypertension and that posteclamptic women found with hypertension either had it before pregnancy or would have developed it even though they had never been pregnant.
Percutaneous renal biopsies obtained during the immediate postpartum period from 57 subjects who had been hypertensive during pregnancy were studied by pathologists who had no knowledge of the clinical data. Although the degree of glomerular endotheliosis, mesangiosis, and basement membrane deposits showed some correlation with the clinical severity of the hypertension and toxemia, there was a wide range of observed tissue changes. It is concluded that such renal alterations are suggestive but not pathognomonic of preeclampsiaeclampsia. © 1969 The American College of Obstetricians and Gynecologists.
A case of lupus erythematosus during pregnancy, erroneously diagnosed, is presented with the suggestion that the signs and symptoms of abnormal renal function during pregnancy may indicate the presence of lupus rather than nephrosis, nephritis, or toxemia of pregnancy.
With the possible exception of a unique glomerular lesion, the morphological changes in patients dying with convulsions, coma, and other complications of acute hypertension are not specific for a pathological entity initiated by aberrations peculiar to the pregnant state. Renal biopsies afford a means for classifying pregnant patients with acute hypertension. The glomerular lesion, believed to be pathognomonic of preeclampsia, was not found in 25% of 63 primiparas who fulfilled the clinical criteria for preeclampsia; chronic renal disease was present without the toxemic lesion in 30% of 214 pregnant patients with acute hypertension. These findings suggest that chronic renal disease plays a more important role in the acute hypertension of pregnancy than current statistics indicate, and that data pertaining to the hypertensive disorders of pregnancy must be interpreted with caution when their differentiation is based upon clinical criteria alone.