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15 - Pre-eclampsia-related renal impairment

from SECTION 5 - ACUTE RENAL IMPAIRMENT

Published online by Cambridge University Press:  05 September 2014

Louise Kenny
Affiliation:
National University of Ireland
John Davison
Affiliation:
University of Newcastle
Catherine Nelson-Piercy
Affiliation:
St Thomas’s Hospital, London
Sean Kehoe
Affiliation:
John Radcliffe Hospital, Oxford
Philip Baker
Affiliation:
University of Alberta
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Summary

Introduction

Pre-eclampsia is the most common cause of impaired renal function arising de novo in late pregnancy. Pre-eclampsia typically presents in the third trimester with hypertension accompanied by proteinuria and is the most common cause of nephrotic syndrome in pregnancy. Pre-eclampsia remains a leading cause of maternal mortality. In recent years, an improved understanding of the renal pathophysiology of pre-eclampsia has improved clinical management of severe cases, particularly with respect to fluid balance, and this has had an appreciable impact on morbidity caused by fluid overload. In this chapter the renal pathophysiology of pre-eclampsia and the differential diagnosis of renal impairment, particularly in late pregnancy, are discussed. The investigation and management of renal impairment of pre-eclampsia, particularly with respect to intrapartum and immediate postpartum care, are described.

Renal pathophysiology in pre-eclampsia

In normal pregnancy, the glomerular filtration rate (GFR) increases by 40—60% during the first trimester, resulting in a fall in serum markers of renal clearance, urea, creatinine and uric acid. In pre-eclampsia, both GFR and renal plasma flow are decreased by 30—40% compared with normal pregnancy of the same duration and this results in a corresponding relative increase in serum urea and creatinine. However, it is important to note that, in pre-eclampsia, urea and creatinine often remain in the normal range for nonpregnant women despite a significant decrease in GFR from the high level of normal pregnancy.

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Publisher: Cambridge University Press
Print publication year: 2008

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