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Proteinuria in pregnancy: Evaluation and management
Authors: Ravi I Thadhani, MD, MPH, Sharon E Maynard, MD
Section Editor: Richard J Glassock, MD, MACP
Deputy Editor: Vanessa A Barss, MD, FACOG
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2018. | This topic last updated: Jun 15, 2017.
INTRODUCTION — In non-pregnant individuals, abnormal total protein excretion is typically defined as greater
than 150 mg daily. In normal pregnancy, urinary protein excretion increases substantially; hence, total protein
excretion is considered abnormal in pregnant women when it exceeds 300 mg/24 hours [1].
Proteinuria is one of the cardinal features of preeclampsia (table 1), a common and potentially severe
complication of pregnancy. However, two important points should be noted. First, the severity of proteinuria is
only weakly associated with adverse maternal and neonatal outcomes, and severe proteinuria is no longer
considered a mandatory diagnostic feature of preeclampsia with severe features [2-6]. However, some studies
report heavy proteinuria (>3 to 5 g/day) is associated with earlier gestational age at preeclampsia onset, earlier
gestational age at delivery, and a higher incidence of fetal growth restriction as compared with milder degrees of
proteinuria [7,8].
Second, proteinuria may be absent: Up to 10 percent of women with clinical and/or histological manifestations of
preeclampsia and 20 percent of women with eclampsia have no proteinuria at the time of initial presentation
[9,10]. These observations are reflected in the 2013 American College of Obstetrics and Gynecology Task Force
on Hypertension in Pregnancy recommendations, which no longer require proteinuria for the diagnosis of
preeclampsia if other severe preeclampsia features are present (table 1). (See "Preeclampsia: Clinical features
and diagnosis".)
Although less prevalent, primary renal disease and renal disease secondary to systemic disorders, such as
diabetes or primary hypertension, are usually characterized by proteinuria and may first present in pregnancy. To
further complicate this picture, 20 to 25 percent of women with chronic hypertension and diabetes develop
superimposed preeclampsia [11,12].
It is important for clinicians caring for pregnant women to understand how to identify proteinuria, and how to
determine whether preeclampsia or renal disease (or both) is the cause. This topic will discuss the approach to
the evaluation of pregnant women with proteinuria and management of nephrotic syndrome in pregnancy. The
evaluation of proteinuria in nonpregnant individuals and measurement of protein excretion are discussed in detail
separately. (See "Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in
adults".)
RENAL CHANGES IN NORMAL PREGNANCY — Glomerular filtration rate (GFR) and renal blood flow rise
markedly during pregnancy, resulting in a physiologic fall in the serum creatinine concentration. Urinary protein
excretion increases substantially due to a combination of increased GFR and increased permeability of the
glomerular basement membrane [13]. Additionally, tubular reabsorption of filtered protein is reduced in
®

pregnancy, along with other nonelectrolytes, such as amino acids, glucose, and beta-microglobulin. (See
"Assessment of urinary protein excretion and evaluation of isolated non-nephrotic proteinuria in adults".)
Women with uncomplicated twin pregnancies have greater increases in urinary protein excretion than do women
with singleton pregnancies [14,15].
Additional information on pregnancy-related changes in renal function and the urinary tract can be found
separately. (See "Maternal adaptations to pregnancy: Renal and urinary tract physiology".)
QUALITATIVE ASSESSMENT — It is customary to test for proteinuria with a dipstick at each prenatal visit;
however, this practice has not been rigorously evaluated and proven to improve outcomes [16]. (See
"Preeclampsia: Clinical features and diagnosis", section on 'Screening'.)
Standard urine dipstick testing is commonly performed on a fresh, clean voided, midstream urine specimen
obtained before pelvic examination to minimize the chance of contamination from vaginal secretions. The urinary
dipstick for protein is a semi-quantitative colorimetric test that primarily detects albumin. Results range from
negative to 4+, corresponding to the following estimates of protein excretion:
A positive reaction (+1) for protein develops at the threshold concentration of 30 mg/dL, which roughly
corresponds to a 24-hour urinary protein excretion of 300 mg/day, depending on urine volume.
Although inexpensive and commonly used, the urinary dipstick has a high false-positive and false-negative rate
when used to screen for abnormal proteinuria in pregnancy, especially at the 1+ level [17,18]. This is due
primarily to variability in urine concentration (osmolality), which can substantially affect random urine protein
concentration (ie, the dipstick result) even though there is no change in total daily urinary protein excretion.
False positive tests may occur in the presence of gross (macroscopic) blood in the urine, semen, very alkaline
urine (pH >7), quaternary ammonium compounds, detergents and disinfectants, drugs, radio-contrast agents,
and high specific gravity (>1.030). Positive tests for protein due to blood in the urine seldom exceed 1+ by
dipstick. False negatives may occur with low specific gravity (<1.010), high salt concentration, highly acidic urine,
or with nonalbumin proteinuria. False-negative urine dipstick proteinuria testing is most common in the third
trimester of pregnancy, when preeclampsia is most frequently seen [19].
QUANTIFYING PROTEIN EXCRETION — Urinary protein can be measured as either albumin or total protein.
Non-pregnant women normally excrete less than 30 mg of albumin [20] and less than 150 mg of total protein
daily. In normal pregnancy, total protein excretion increases to 150 to 250 mg daily [1], and is even higher in twin
pregnancies [14,15].
Accurate quantification of proteinuria in pregnancy is important in several clinical settings. If preeclampsia is
suspected, proteinuria quantification is helpful, though not required, for diagnosis (see "Preeclampsia: Clinical
features and diagnosis"). In women with pre-existing proteinuria, a large gestational increase in proteinuria can
herald superimposed preeclampsia. In women with chronic kidney disease, proteinuria >1 g/day is associated
Negative●
Trace - between 15 and 30 mg/dL●
1+ - between 30 and 100 mg/dL●
4+ - >1000 mg/dL●

with increased risk of adverse pregnancy and neonatal outcomes (odds ratio 3.69; 95% CI 1.63-8.36), including
preterm delivery, small for gestational age infants, and need for neonatal intensive care [21]. In women with
chronic hypertension, even mild proteinuria (50 to 300 mg/day) is associated with adverse pregnancy outcomes
[22].
There are three methods to quantify proteinuria: 24-hour urine collection, spot urine protein:creatinine ratio, and
spot urine albumin:creatinine ratio.
24-hour urine collection — The traditional method requires a 24-hour urine collection to directly determine the
daily total protein or albumin excretion. An extra benefit of this approach, if creatinine is also measured, is that it
provides the information necessary to estimate the glomerular filtration rate (GFR) from the creatinine clearance.
The 24-hour collection is begun at the usual time the patient awakens. At that time, the first void is discarded and
the exact time noted. Subsequently, all urine voids are collected with the last void timed to finish the collection at
exactly the same time the next morning. The time of the final urine specimen should vary by no more than 5 or
10 minutes from the time of starting the collection the previous morning. An inexpensive basin urinal that fits into
the toilet bowl facilitates collection. The bottle(s) may be kept at normal room temperature for a day or two, but
should be kept cool or refrigerated for longer periods of time. No preservatives are needed. (See "Patient
education: Collection of a 24-hour urine specimen (Beyond the Basics)".)
Although generally considered the "gold standard" for diagnosis of proteinuria in both preeclampsia and renal
disease, the 24-hour urine protein excretion in pregnant women is frequently inaccurate due to undercollection or
overcollection [23]. Thus, when interpreting the results of a 24-hour urine collection, it is critical to assess the
adequacy of collection by quantifying the 24-hour urine creatinine excretion, which is based on muscle mass.
The 24-hour urine creatinine excretion should be between 15 and 20 mg/kg body weight, calculated using pre-
pregnancy weight. Values substantially above or below this estimate suggest over- and undercollection,
respectively, and should call into question the accuracy of the 24-hour urine protein result.
In addition to the high rate of inaccurate/incomplete collection, the 24-hour urine sample is cumbersome for
ambulatory patients, and the result is not available for at least 24 hours while the collection is being completed
and analyzed [23]. Hence, there has been longstanding interest in alternative methods to quantify urine protein
excretion in pregnancy.
Urine protein to creatinine ratio — The spot urine protein-to-creatinine ratio (PC ratio) has become the
preferred method for the quantification of proteinuria in the non-pregnant population due to high accuracy,
reproducibility, and convenience when compared to timed urine collection [24]. (See "Assessment of urinary
protein excretion and evaluation of isolated non-nephrotic proteinuria in adults".)
The majority of studies evaluating the urine PC ratio in pregnant women were performed in women with
suspected preeclampsia. In these studies, the PC ratio was highly correlated with the 24-hour urine protein
measurement [25,26], as it is in non-pregnant adults. Use of the PC ratio has also been validated for baseline
proteinuria quantification in early pregnancy [27]. Routine bladder catheterization for measurement of urine PC
ratio is not necessary; mid-stream clean-catch samples are accurate in pregnant women [28]. The time of day of
urine specimen collection does not impact accuracy [29].
Over a dozen studies have validated the urine PC ratio for the detection of abnormal proteinuria in women with
hypertensive pregnancy; most used the 24-hour urine collection as the "gold standard" [26,30-42]. Most studies
have focused on accurate determination of greater than 300 mg/day of proteinuria, as this is the cut-off for
preeclampsia diagnosis. Three systematic reviews have evaluated this literature, and came to similar
conclusions [43]:

Taken together, these data suggest that a urine PC ratio above 0.7 mg protein/mg creatinine strongly predicts
significant proteinuria. A urine PC ratio less than 0.15 mg protein/mg creatinine can be considered normal
(predictive of less than 300 mg protein in a 24-hour collection). Confirmatory testing with 24-hour urine collection
probably is not necessary in these individuals. Women with urine PC ratio results between 0.15 and 0.7 mg
protein/mg creatinine should have a 24-hour urine collection to accurately quantify proteinuria. Most international
organizations endorse the use of the spot urine protein:creatinine ratio ≥0.26 to 0.3 mg protein/mg creatinine for
the diagnosis of preeclampsia [47,48].
Some laboratories and international guidelines use urine protein:creatinine ratio in units of mg protein per mmol
creatinine (mg/mmol). To convert mg/mmol to mg/mg, divide by 113.6.
A calculator is available for calculating the urine protein to creatinine using spot urine protein and spot urine
creatinine values (calculator 1).
Urine albumin to creatinine ratio — The urine albumin:creatinine ratio (ACR), like the PC ratio, is measured
using a random "spot" urine specimen. (See "Assessment of urinary protein excretion and evaluation of isolated
non-nephrotic proteinuria in adults".)
The ACR can be performed using an automated analyzer, allowing immediate point-of-care testing that could be
utilized in an antenatal clinic. Like the PC ratio, the ACR (using a threshold between 20 and 60 mg albumin/g
creatinine) is strongly predictive of significant proteinuria (>300 mg protein/day by 24-hour urine collection) in a
high-risk obstetric antenatal clinic [40,49] and in women with hypertensive pregnancies [50,51]. In one study,
women with a spot urine ACR >312 mg albumin/g creatinine measured at 17 to 20 weeks of gestation were at
almost eightfold higher risk of subsequently developing preeclampsia (relative risk [RR] 7.8) compared with
women with ACR <312 mg albumin/g creatinine [52]. The ACR performs similarly to the PCR with regard to
prediction of adverse pregnancy outcomes [53]. Although more data are needed, the spot ACR has the potential
to supplant urinary dipstick as a rapid and accurate screening method for proteinuria in routine obstetric care.
Some laboratories report urine albumin:creatinine ratio in units of mg albumin per mmol creatinine (mg/mmol). To
convert mg/mmol to mg/g, divide by 0.1136.
8- or 12-hour collection — Measurement of protein in an 8-hour [54] or 12-hour [55] urine collection is a
reasonable alternative to the 24-hour urine collection for quantification of proteinuria. In a systematic review
In a 2012 meta-analysis including 2978 women from 20 studies, spot urine ratio had a pooled sensitivity of
83.6 percent (95% CI 77.5-89.7) and specificity of 76.3 percent (95% CI 72.6-80.0) using a cut-off of 0.26
mg protein/mg creatinine to predict proteinuria >300 mg/day by 24-hour urine collection [44]. The authors
concluded that a low spot protein:creatinine ratio is a reasonable "rule-out" test for excluding proteinuria
>300 mg/day in hypertensive pregnancy.
●
In a 2008 meta-analysis including 1717 women from seven studies, a lower cut-off of 0.13 to 0.15 mg
protein/mg creatinine provided higher (90 to 99 percent) sensitivity, albeit with more false-positive results
(specificity 33 to 65 percent) [45]. A higher cutoff of 0.6 to 0.7 mg protein/mg creatinine had a high specificity
(96 percent) for significant proteinuria (>300 mg in a 24-hour specimen), but at the cost of lower sensitivity
(85 to 87 percent). Midrange protein/creatinine ratios (greater than 0.15 mg/mg but less than 0.7 mg/mg) did
not reliably predict abnormal proteinuria.
●
Another 2012 meta-analysis, including 2790 women from 15 studies, had similar findings. A single
diagnostic threshold of approximately 0.30 mg protein/mg creatinine had sensitivity and specificity of 81 and
76 percent, respectively, for the detection of >300 mg/day proteinuria by 24-hour urine collection [46]. A
lower cut-off (0.13 mg/mg) had better (89 percent) sensitivity for the exclusion of proteinuria.
●

including seven studies, >150 mg of protein in a 12-hour collection was highly predictive of >300 mg protein in a
24-hour collection (pooled sensitivity 92 percent [95% CI 86-96], specificity 99 percent [75-100]) [55].
DIFFERENTIAL DIAGNOSIS OF PROTEINURIA
Renal disease versus preeclampsia — In the evaluation of a pregnant patient with proteinuria, the first
consideration is to determine whether the proteinuria is due to preeclampsia or some other renal disease,
whether pre-existing or de novo (table 2). In patients with established renal disease before conception or in
whom proteinuria is documented before the 20th week of gestation, the diagnosis of pre-existing renal disease
can be readily made because preeclampsia rarely occurs before that time. (See "Pregnancy in women with
underlying renal disease".)
Conversely, new-onset proteinuria after 20 weeks of gestation suggests preeclampsia. Approximately one-third
of women who present with new proteinuria after 20 weeks gestation eventually progress to preeclampsia
[56,57], and 25 percent of women with preeclampsia have proteinuria as their initial presenting sign [58]. In such
cases, adverse pregnancy and neonatal outcomes are more common as compared with women in whom
hypertension was the first presenting sign of preeclampsia [58,59].
Of course, de novo renal disease (for example, lupus nephritis) can also occur later in pregnancy. Especially
when information on the presence of proteinuria (and hypertension) in early pregnancy is lacking, distinguishing
between underlying renal disease and preeclampsia can be difficult. For this reason, it is useful to quantify
protein excretion in early pregnancy in women at risk for underlying renal disease (ie, women with chronic
hypertension, diabetes mellitus, and systemic lupus erythematosus). Diagnostic evaluation in women when the
etiology of proteinuria is unclear should include renal ultrasound, as urinary tract dilatation has been associated
with proteinuria in pregnancy [60].
A novel serum test for early diagnosis of preeclampsia has been developed, which relies on detection of
abnormal levels of placentally-derived angiogenic factors, sFlt1 (soluble fms-like tyrosine kinase-1) and PlGF
(placental growth factor) [61,62]. This diagnostic test is available in Europe (Roche Diagnostics, Rotkreuz,
Switzerland and Thermo Fisher/Brahms, Hennigsdorf, Germany) and is being evaluated by the FDA for use in
the United States. Although more studies are needed to validate its use, this blood test may prove useful and
cost-effective in distinguishing preeclampsia from other causes of proteinuria in pregnancy [63,64], and appears
to be predictive of adverse maternal and neonatal outcomes in women with clinical suspicion of preeclampsia
[65,66]. The sFlt1:PlGF ratio may be particularly helpful in distinguishing chronic kidney disease and
preeclampsia [67]. (See "Preeclampsia: Pathogenesis", section on 'sFlt-1, VEGF, PlGF'.)
The distinction between renal disease and preeclampsia is important because it affects clinical management. In
patients with renal disease, the usual aim is term delivery, while patients with preeclampsia often develop
progressive disease culminating in the need for iatrogenic preterm delivery. (See "Pregnancy in women with
underlying renal disease" and "Preeclampsia: Management and prognosis".)
In instances where the distinction between renal disease and preeclampsia cannot be resolved, it is prudent to
assume preeclampsia as the working diagnosis, as it has the potential for rapid development of serious maternal
and fetal complications.
In some cases, the distinction between renal disease and preeclampsia can only be made in retrospect, as
clinical signs of preeclampsia generally resolve within 12 weeks after delivery [68], while proteinuria due to
underlying renal disease does not. However, resolution of proteinuria after preeclampsia, especially when
severe, can sometimes take much longer. In one cohort study of 205 women with preeclampsia, 14 percent had
persistent proteinuria at 12 weeks after delivery, which resolved by two years postpartum in all but 2 percent of
subjects [69]. Nevertheless, proteinuria (or hypertension) which persists longer than three months after delivery

should prompt close follow-up and consideration of further evaluation and appropriate referral, so that underlying
renal disease or chronic hypertension is detected and treated expeditiously.
Superimposed preeclampsia — When preeclampsia develops in women with preexisting renal disease and/or
hypertension, it often occurs earlier in gestation and may be particularly severe. In such cases, significant clues
to the diagnosis of superimposed preeclampsia can be provided by the systemic manifestations of the disorder, if
present, such as thrombocytopenia, an increase in levels of liver enzymes, hemolysis, and/or evidence of fetal
compromise (including intrauterine growth restriction) (table 3) [70].
Alternatively, worsening hypertension and proteinuria in a woman with renal disease may represent an
exacerbation of the underlying disease. Studies in women with documented primary renal disease predating
pregnancy have demonstrated that the majority of women with glomerular disease exhibit increasing proteinuria
during the course of their gestation and nephrotic syndrome in the third trimester [71,72].
The differential diagnosis for hypertension and proteinuria in pregnancy is discussed in detail separately. (See
"Preeclampsia: Clinical features and diagnosis", section on 'Differential diagnosis'.)
Nephrotic syndrome — Nephrotic-range proteinuria (>3.0 g/24 hours) is a sign of glomerular injury. Pathology
limited to the renal tubules and interstitium typically results in protein excretion rates less than 2.0 g/24 hours
unless glomerular disease is also present. Patients with protein excretion less than 3.0 g/24 hours are usually
asymptomatic. In contrast, rates greater than 3.0 g/24 hours may cause the nephrotic syndrome, which consists
of nephrotic-range proteinuria together with edema, hypoalbuminemia, and hyperlipidemia. (See "Overview of
heavy proteinuria and the nephrotic syndrome".)
Kidney biopsy in pregnancy — Preeclampsia is the most common cause of de novo nephrotic-range
proteinuria in pregnancy, and rarely requires kidney biopsy [73]. However, the nephrotic syndrome in pregnancy
may also be caused by preexisting renal disease (which is often accompanied by a large increase in proteinuria
during pregnancy), and de novo renal disease that presents during pregnancy (eg, associated with invasive
trophoblastic tumors [74]). Once it has been determined that the patient has heavy proteinuria, the etiology may
be suggested from the history and physical examination. This is particularly true for patients who have a
systemic disease such as diabetes mellitus, systemic lupus erythematosus, HIV infection, or use of a medication
known to cause nephrotic syndrome (NSAIDs, pamidronate, lithium, interferon-alpha). In some cases, however,
renal biopsy is required to establish the diagnosis. The decision to perform renal biopsy during pregnancy, or to
defer until after delivery, is based on several factors, including the stage of pregnancy, the severity of the renal
disease, and the suspected underlying diagnosis.
Nephrotic range proteinuria during pregnancy due to primary glomerular disease is associated with a high risk of
several adverse outcomes, including preeclampsia, acute kidney injury, preterm birth, low birthweight, and the
need for neonatal intensive care [75]. Nevertheless, conservative management until delivery, particularly in
patients who present in the third trimester, is a reasonable management approach. When nephrotic syndrome
presents early in pregnancy, and/or there is progressive decline in renal function, timely treatment of the
underlying kidney disease is often indicated. In such cases, the potential benefits of kidney biopsy may outweigh
the risks.
Data on the safety of renal biopsy during pregnancy are limited. The major complication of kidney biopsy is
bleeding. In a systematic review of reports of renal biopsies performed during pregnancy or postpartum, the risk
of bleeding was higher when the biopsy was performed during pregnancy as compared with postpartum (7
percent [16/197] versus 1 percent [3/268]) [76]. All observed cases of major bleeding (ie, requiring blood
transfusion) occurred in biopsies performed between 23 to 26 weeks of gestation, suggesting women in this
gestational age range may be particularly vulnerable to complications. During this gestational window, however,
the benefit of a biopsy (accurate diagnosis and subsequent tailored management) may outweigh its risks. Later

in gestation, the gravid uterus makes the standard prone position difficult. In such cases, renal biopsy is
frequently deferred until the patient has stabilized postpartum.
MANAGEMENT OF NEPHROTIC SYNDROME IN PREGNANCY — The management of the nephrotic
syndrome in pregnancy is based on expert opinion, as very little data are available to support evidence-based
practice.
Edema — A major goal in the management of nephrotic syndrome is to reduce edema to a level that allows
comfort during ambulation. The dietary intake of sodium may be limited to 1.5 g (approximately 60 mEq) of
sodium per day, provided normal blood pressure is maintained. Bed rest and leg elevation are safe and often
effective methods to facilitate resolution of edema.
Historically, the use of diuretics has been discouraged because of the theoretical risk that they will impair the
normal pregnancy-associated expansion of plasma volume, possibly decreasing placental perfusion. However,
there is no clear evidence of adverse fetal effects, and loop diuretics are appropriate in pregnant women with
severe, refractory edema [77]. In such cases, therapy should aim to reduce excessive edema at a slow rate of no
more than 1 to 2 pounds per day with a loop diuretic, while a low sodium diet is maintained. A written record of
daily weights, taken by the patient, is highly recommended. Diuretics should not be used in preeclampsia
because plasma volume is already reduced.
Anticoagulation — Nephrotic syndrome is associated with an increased risk of deep venous thrombosis (DVT).
Routine prophylactic anticoagulation in severe nephrotic syndrome (ie, serum albumin <2.0 mg/dL) is
controversial, and generally recommended only if another risk factor for thrombosis is present (see "Renal vein
thrombosis and hypercoagulable state in nephrotic syndrome"). Since pregnancy is a prothrombotic state, we
believe prophylactic anticoagulation should be considered in pregnant women with nephrotic syndrome and
severe hypoalbuminemia (serum albumin <2.0 mg/dL, or <2.8 mg/dL in membranous nephropathy), especially if
another risk factor (eg, bedrest) is present. However, this decision needs to be made on a case-by-case basis
with consideration of the patient’s specific risk factors for bleeding complications, including pregnancy-related
bleeding.
Low-molecular weight heparin or unfractionated heparin is appropriate for prophylactic anticoagulation in
pregnancy. Warfarin should be avoided during pregnancy because it crosses the placenta and can have adverse
fetal effects, but can be used postpartum, even in breastfeeding women. Anticoagulation should be continued in
the immediate postpartum period, particularly in women undergoing cesarean delivery, as this period carries a
particularly high risk for DVT [78]. (See "Use of anticoagulants during pregnancy and postpartum".)
Hyperlipidemia — Statins are avoided in pregnancy because of limited and contradictory data suggesting an
increased risk of birth defects with first trimester exposure. This discordance may reflect confounding by
indication. We suggest discontinuing statins in women who are planning pregnancy and resuming these drugs
after delivery/breast feeding. (See "Statins: Actions, side effects, and administration", section on 'Risks in
pregnancy and breastfeeding'.)
Bile acid sequestrants and fibrates have no established teratogenic effects and can be safely used in pregnancy
to treat severe hyperlipidemia due to nephrotic syndrome.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries
and regions around the world are provided separately. (See "Society guideline links: Glomerular disease in
adults" and "Society guideline links: Hypertensive disorders of pregnancy".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and
"Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5 to 6 grade
reading level, and they answer the four or five key questions a patient might have about a given condition. These
th th

articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond
the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written
at the 10 to 12 grade reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)
SUMMARY AND RECOMMENDATIONS
th th
Beyond the Basics topic (see "Patient education: Protein in the urine (proteinuria) (Beyond the Basics)")●
Evaluation of a fresh midstream urine specimen obtained as a clean voided specimen before pelvic
examination minimizes the chance of contamination from vaginal secretions. (See 'Qualitative assessment'
above.)
●
Urine dipstick to screen for proteinuria is associated with frequent false-positive and false-negative results,
especially when the urine is particularly concentrated or dilute, respectively. It is most predictive of abnormal
24-hour proteinuria if +2 or greater. Positive urine dipsticks should be followed-up with a quantitative test.
(See 'Qualitative assessment' above.)
●
The urinary protein-to-creatinine (PC) ratio (mg protein/mg creatinine) is an accurate, convenient, and
relatively rapid method to quantify proteinuria in pregnancy. A urine PC ratio less than 0.15 mg/mg may be
considered normal (predictive of less than 300 mg protein in a 24-hour collection) and values above 0.7
mg/mg are very likely to indicate significant proteinuria (more than 300 mg protein in a 24-hour collection).
Ratios between 0.15 and 0.7 mg/mg should be further evaluated by 24-hour urine collection. If a 24 hour
urine collection is not obtained, a protein:creatinine ratio of 0.26 mg/mg (30 mg/mmol) in a random urine
sample is suggested as the threshold for significant proteinuria. (See 'Quantifying protein excretion' above.)
●
The gestational age at which proteinuria is first documented is important in establishing the likelihood of
preeclampsia versus other renal disease. Proteinuria documented prior to pregnancy or in early pregnancy
(before 20 weeks of gestation) suggests preexisting renal disease. In late pregnancy, the presence of
hypertension or other signs/symptoms of severe preeclampsia (eg, thrombocytopenia, elevated liver
transaminases), if present, also helps to distinguish preeclampsia from underlying renal disease. (See
'Differential diagnosis of proteinuria' above.)
●
Preeclampsia is the most common cause of proteinuria in pregnancy and is the most likely diagnosis in all
women with proteinuria first identified after 20 weeks of gestation. If hypertension is absent, then the
presence of primary or secondary renal disease should be considered. If renal biopsy is indicated for
diagnosis, it is often better to wait until the patient is postpartum unless unexplained progressive loss of
renal function is occurring. (See 'Differential diagnosis of proteinuria' above.)
●
For women with nephrotic range proteinuria, discomfort from severe leg edema can be managed with
sodium restriction (1.5 g, approximately 60 mEq), bedrest, and leg elevation. If edema persists despite these
measures, loop diuretics may be used with caution. Prophylactic anticoagulation is reasonable in pregnant
women with nephrotic syndrome and severe hypoalbuminemia (serum albumin <2.0 mg/dL, or <2.8 mg/dL in
membranous nephropathy), especially if another risk factor (eg, bedrest) is present. Bile acid sequestrants
and fibrates can be safely used in pregnancy to treat severe hyperlipidemia due to nephrotic syndrome;
statins should be avoided. (See 'Management of nephrotic syndrome in pregnancy' above.)
●

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Topic 4808 Version 26.0

GRAPHICS
Criteria for the diagnosis of preeclampsia
Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on two occasions at least four
hours apart after 20 weeks of gestation in a previously normotensive patient
If systolic blood pressure is ≥160 mmHg or diastolic blood pressure is ≥110 mmHg, confirmation within minutes is
sufficient
and
Proteinuria ≥0.3 g in a 24-hour urine specimen or protein/creatinine ratio ≥0.3 (mg/mg) (30 mg/mmol)
Or dipstick ≥1+ if a quantitative measurement is unavailable
OR
Systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg on two occasions at least four
hours apart after 20 weeks of gestation in a previously normotensive patient with the new onset of any of
the following (with or without proteinuria):
Platelet count <100,000/microL
Serum creatinine >1.1 mg/dL (97.2 micromol/L) or doubling of the creatinine concentration in the absence of other
renal disease
Liver transaminases at least twice the upper limit of the normal concentrations for the local laboratory
Pulmonary edema
Cerebral or visual symptoms (eg, new-onset and persistent headaches not responding to usual doses of analgesics*;
blurred vision, flashing lights or sparks, scotomata)
Superimposed preeclampsia is defined by the new onset of proteinuria, significant end-organ dysfunction, or both
after 20 weeks of gestation in a woman with chronic/preexisting hypertension. For women with chronic/preexisting
hypertension who have proteinuria prior to or in early pregnancy, superimposed preeclampsia is defined by worsening
or resistant hypertension (especially acutely) in the last half of pregnancy or development of signs/symptoms of the
severe end of the disease spectrum.
* Response to analgesia does not exclude the possibility of preeclampsia.
Adapted from: American College of Obstetricians and Gynecologists, Task Force on Hypertension in Pregnancy. Hypertension
in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy.
Obstet Gynecol 2013; 122:1122.
Graphic 79977 Version 28.0

Causes of proteinuria in pregnancy
Primary renal diseases
IgA nephropathy
Minimal change disease
Membranous nephropathy
Focal segmental glomerulosclerosis
Primary glomerulonephritis
Allergic interstitial nephritis
Polycystic kidney disease
Systemic causes
Preeclampsia
Diabetic nephropathy
Lupus nephritis (diffuse proliferative, focal proliferative, membranous)
Hypertensive nephrosclerosis
Thrombotic thrombocytopenic purpura (TTP)
Infection-associated glomerular disease (eg, HIV, hepatitis B/C)
Systemic vasculitis
Multiple myeloma
Chronic vesicoureteral reflux
Antiphospholipid syndrome
Symptomatic urinary tract obstruction

Findings which increase the certainty of the diagnosis of preeclampsia
Systolic blood pressure ≥160 mm Hg
Diastolic blood pressure ≥110 mm Hg
Proteinuria occurring for the first time during pregnancy, especially if ≥2 g in 24 hours. A qualitative result of 2+ or 3+
is also suggestive.
Serum creatinine >1.2 mg/dL (106 mmol/L)
Platelet count <100,000 cells per cubic millimeter
Evidence of microangiopathic hemolytic anemia (eg, elevated indirect bilirubin or lactic acid dehydrogenase)
Elevated liver chemistries (eg, alanine aminotransferase or aspartate aminotransferase)
Persistent headache or other cerebral or visual disturbances
Persistent epigastric pain
Working group report on high blood pressure in pregnancy. National Instititutes of Health, Washington, DC 2000.

Contributor Disclosures
Ravi I Thadhani, MD, MPH Nothing to disclose Sharon E Maynard, MD Patent Holder: Beth Israel Deaconess
Medical Center [Angiogenic biomarkers for preeclampsia (Elecsys Preeclampsia sFlt-1 & PlGF)]. Richard J
Glassock, MD, MACP Speaker's Bureau: Genentech [Vasculitis (Rituximab)]. Consultant/Advisory Boards:
Bristol-Myers Squibb [Lupus Nephritis, Focal Segmental Glomerulosclerosis (Abatacept)]; ChemoCentryx
[Vasculitis, C3 Glomerulopathy, Focal Segmental Glomerulosclerosis (CCX-168, CCX-140)]; Retrophin [Focal
Segmental Glomerulosclerosis (Sparsentan)]; Omeros [IgA Nephropathy]; Ionis [C3 Glomerulopathy]; Apellis
[Complement Inhibition on Glomerular Disease]. Employment: American Society of Nephrology [Nephrology Self-
Assessment Program]; Karger Publishers [American Journal of Nephrology]. Equity Ownership/Stock Options:
Reata [Alport Syndrome, Pulmonary Hypertension, Diabetic Nephropathy (Bardoxolone)]. Vanessa A Barss,
MD, FACOG Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
Conflict of interest policy

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