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English Abstract
Journal Article
[Nephrotic syndrome due to preeclampsia: Presentation, management and clinical evolution observed in 5 years experience].
INTRODUCTION: Nephrotic syndrome (NS) is rare during pregnancy. The main cause is severe pre-eclampsia (PR). Our aim was to describe the clinical presentation, analytical features, medical management, and progress of women with NS due to PE.
MATERIALS AND METHODS: A descriptive, retrospective study, conducted from 01/01/2017 to 01/01/2022 (5years). Women with a gestational age (GA) ≥20weeks were included in the study, hospitalised due to hypertensive disorders in pregnancy (HDP), with no evidence of kidney damage prior to gestation.
RESULTS: Of the 652 HDP, 452 PE and 21 NS were identified. Maternal age was 25±5.7 years, GA at diagnosis was 33.1±5.1 weeks. All the women had facial and peripheral oedema: 5 pleural effusion, 3 pericardial effusion, and 2 anasarca. Their p24 was 6.17±2.34grams (3.10-10.8), serum albumin 2.5±0.27g/dL (2.10-2.90), and serum cholesterol 281.4±21.7mg/dL (251-316). Thirteen developed maternal complications: acute kidney damage, pulmonary oedema, dilated cardiomyopathy, eclampsia, and HELLP syndrome. They all remained hypertensive postpartum, and required a combination of two to three antihypertensive drugs. They all received statins postpartum, and angiotensin converting enzyme (ACE) inhibitors to manage proteinuria. None developed hyperkalaemia or creatinine elevation. Hospital stay was 10.4±3.7days. All nephrotic range proteinuria parameters reversed prior to discharge. No deaths were recorded.
CONCLUSION: Presentation ranged from peripheral oedema to serous involvement. Severity of proteinuria varied. Use of ACE inhibitors did not precipitate hyperkalaemia or kidney failure. Maternal complications were frequent, but no deaths were recorded.
MATERIALS AND METHODS: A descriptive, retrospective study, conducted from 01/01/2017 to 01/01/2022 (5years). Women with a gestational age (GA) ≥20weeks were included in the study, hospitalised due to hypertensive disorders in pregnancy (HDP), with no evidence of kidney damage prior to gestation.
RESULTS: Of the 652 HDP, 452 PE and 21 NS were identified. Maternal age was 25±5.7 years, GA at diagnosis was 33.1±5.1 weeks. All the women had facial and peripheral oedema: 5 pleural effusion, 3 pericardial effusion, and 2 anasarca. Their p24 was 6.17±2.34grams (3.10-10.8), serum albumin 2.5±0.27g/dL (2.10-2.90), and serum cholesterol 281.4±21.7mg/dL (251-316). Thirteen developed maternal complications: acute kidney damage, pulmonary oedema, dilated cardiomyopathy, eclampsia, and HELLP syndrome. They all remained hypertensive postpartum, and required a combination of two to three antihypertensive drugs. They all received statins postpartum, and angiotensin converting enzyme (ACE) inhibitors to manage proteinuria. None developed hyperkalaemia or creatinine elevation. Hospital stay was 10.4±3.7days. All nephrotic range proteinuria parameters reversed prior to discharge. No deaths were recorded.
CONCLUSION: Presentation ranged from peripheral oedema to serous involvement. Severity of proteinuria varied. Use of ACE inhibitors did not precipitate hyperkalaemia or kidney failure. Maternal complications were frequent, but no deaths were recorded.
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