Literature DB >> 20356704

[Kidney and preeclampsia].

B Moulin1, A Hertig, E Rondeau.   

Abstract

During normal pregnancy, renal blood flow and GFR increase gradually until they reach a peak of about 150% of their normal values by the end of the 1(st) trimester. This increase in GFR is secondary to the extra-cellular compartment expansion caused by a positive sodium balance of about 500-900 mmol which is in turn associated with a water retention amounting 6 to 8 liters. Blood pressure decreases during a normal pregnancy because of the decrease in peripheral vascular resistance. This drop in blood pressure is limited by the renin-angiotensin system. Blood pressure gradually recovers during the 3(rd) trimester. Systemic hypertension, proteinuria >0.3 g/day and edema are the usual signs leading to the diagnosis of PE. However, any of the above listed signs found in isolation can be a tell tale sign of PE and must therefore prompt for the identification of a possible fetal effect The differential diagnosis of PE includes essential hypertension and hypertension secondary to a pre-existing renal failure. In the latter, signs of renal impairment early in the pregnancy, or (and) renal failure prior to the pregnancy are of important diagnostic clues. Causes of acute renal failure during pregnancy are numerous. PE associated acute renal failure presents in 5-10% of severe forms of PE. This is always a bad prognostic sign with a predicted mortality of 10%. Histological features are those of acute tubular necrosis with "endotheliosis" an inflammation of the glomerular endothelium. This renal impairment is frequently complicated by pulmonary edema. Passed the acute phase, the recovery of the renal function is usually complete. An acute renal failure during pregnancy can also be secondary to a pre-existing renal impairment suddenly aggravated by PE. In this setting, the probability of these patients requiring long term dialysis is high. Post-partum Haemolytic-Uremic Syndrome (HUS), although rare, is a serious condition which, following delivery, will require an early diagnosis (haemolysis, hypertension, acute renal failure) and urgently require symptomatic, perhaps specific, treatment (Plasma exchange transfusion). Copyright 2010 Elsevier Masson SAS. All rights reserved.

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Year:  2010        PMID: 20356704     DOI: 10.1016/j.annfar.2010.02.022

Source DB:  PubMed          Journal:  Ann Fr Anesth Reanim        ISSN: 0750-7658


  5 in total

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Authors:  S Masoura; I Kalogiannidis; T Dagklis; T Theodoridis; T Agorastos
Journal:  Hippokratia       Date:  2011-10       Impact factor: 0.471

2.  Prediction of fluid responsiveness in severe preeclamptic patients with oliguria.

Authors:  Clément Brun; Laurent Zieleskiewicz; Julien Textoris; Laurent Muller; Jean-Pierre Bellefleur; François Antonini; Maxime Tourret; Denis Ortega; Armand Vellin; Jean-Yves Lefrant; Léon Boubli; Florence Bretelle; Claude Martin; Marc Leone
Journal:  Intensive Care Med       Date:  2012-12-06       Impact factor: 17.440

3.  Pregnancy-related acute kidney injury: experience of the nephrology unit at the university hospital of fez, morocco.

Authors:  Mohamed Arrayhani; Randa El Youbi; Tarik Sqalli
Journal:  ISRN Nephrol       Date:  2012-12-20

4.  Oxidative and Inflammatory Imbalance in Placenta and Kidney of sFlt1-Induced Early-Onset Preeclampsia Rat Model.

Authors:  Álvaro Santana-Garrido; Claudia Reyes-Goya; Pablo Espinosa-Martín; Luis Sobrevia; Luis M Beltrán; Carmen M Vázquez; Alfonso Mate
Journal:  Antioxidants (Basel)       Date:  2022-08-19

5.  Low-Dose Aspirin Prevents Kidney Damage in LPS-Induced Preeclampsia by Inhibiting the WNT5A and NF-κB Signaling Pathways.

Authors:  Guanlin Li; Wei Wei; Lingge Suo; Chun Zhang; Haiyan Yu; Hui Liu; Qing Guo; Xiumei Zhen; Yang Yu
Journal:  Front Endocrinol (Lausanne)       Date:  2021-03-11       Impact factor: 5.555

  5 in total

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