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Acute kidney injury (acute renal failure) in pregnancy

Phyllis August, MD, MPH
Section Editors
Charles J Lockwood, MD, MHCM
Paul M Palevsky, MD
Deputy Editor
Alice M Sheridan, MD


Acute kidney injury (AKI) is the abrupt loss of kidney function, resulting in the retention of urea and other nitrogenous waste products and in the dysregulation of extracellular volume and electrolytes. The term, AKI, has largely replaced acute renal failure (ARF), reflecting the recognition that smaller declines in kidney function that do not result in overt organ failure are of substantial clinical relevance and are associated with increased morbidity and mortality.

AKI during pregnancy can be caused by any of the disorders leading to AKI in the general population. There are also, however, pregnancy complications characteristic of each trimester that can be associated with kidney injury [1,2]. This topic reviews causes of AKI that are most commonly encountered during pregnancy. Causes of AKI in the general population are discussed elsewhere. (See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting", section on 'Major causes and pathogenesis of kidney disease'.)

Nephrolithiasis during pregnancy is discussed elsewhere. (See "Nephrolithiasis during pregnancy".)


AKI is defined by the abrupt loss of kidney function. Several consensus definitions of AKI have been developed for use in the general population in order to provide a uniform, quantitative definition of AKI. These include the RIFLE and Acute Kidney Injury Network (AKIN) definitions and the Kidney Disease: Improving Global Outcomes (KDIGO) modifications of the AKIN definition. (See "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting", section on 'Major causes and pathogenesis of kidney disease'.)

However, it is not clear that the consensus criteria for AKI are useful in pregnancy. This is because, during pregnancy, glomerular filtration rate (GFR) increases significantly (by approximately 50 percent), resulting in a lower baseline serum creatinine compared with similarly healthy, nonpregnant individuals (see "Maternal adaptations to pregnancy: Renal and urinary tract physiology", section on 'Increase in GFR'). Most obstetricians do not routinely check the serum creatinine either prior to or early in pregnancy. Thus, seemingly "normal" serum creatinine levels (eg, 0.7 to 0.9 mg/dL) may represent significant increases from baseline, which may not be appreciated at the time of presentation.

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Literature review current through: Sep 2017. | This topic last updated: May 08, 2017.
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