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Kidney Disease and Hypertension in Pregnancy

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Kidney disease and hypertensive disorders in pregnancy are discussed. Pregnancy in women with kidney disease is associated with significant complications when renal function is impaired and hypertension predates pregnancy. When renal function is well preserved and hypertension absent, the outlook for both mother and fetus is excellent. The basis for the close interrelationship between reproductive function and renal function is intriguing and suggests that intact renal function is necessary for the physiologic adjustments to pregnancy, such as vasodilation, lower blood pressure, increased plasma volume, and increased cardiac output.
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Content Preview
Kidney Disease and
Hypertension in Pregnancy
Phyllis August
Kidney disease and hypertensive disorders in pregnancy are dis-
cussed. Pregnancy in women with kidney disease is associated
with significant complications when renal function is impaired
and hypertension predates pregnancy. When renal function is well
preserved and hypertension absent, the outlook for both mother and
fetus is excellent. The basis for the close interrelationship between
reproductive function and renal function is intriguing and suggests
that intact renal function is necessary for the physiologic adjustments
to pregnancy, such as vasodilation, lower blood pressure, increased
plasma volume, and increased cardiac output.
The renal physiologic adjustments to pregnancy are reviewed,
including hemodynamic and metabolic alterations. The common
primary and secondary renal diseases that may occur in pregnant
women also are discussed. Some considerations for the management of
end-stage renal disease in pregnancy are given.
Hypertensive disorders in pregnancy are far more common than is
renal disease. Almost 10% of all pregnancies are complicated by
either preeclampsia, chronic hypertension, or transient hypertension.
Preeclampsia is of particular interest because it is associated with
life-threatening manifestations, including seizures (eclampsia), renal
failure, coagulopathy, and rarely, stroke. Significant progress has been
made in our understanding of some of the pathophysiologic manifes-
tations of preeclampsia; however, the cause of this disease remains
unknown. The diagnostic categories of hypertension in pregnancy,
pathophysiology of preeclampsia, and important principles of preven-
tion and treatment also are reviewed.
C H A P T E R
10

10.2
Systemic Diseases and the Kidney
Anatomic Changes in the Kidney During Pregnancy
FIGURE 10-1
Anatomic changes in the kidney during pregnancy. During pregnancy,
kidney size increases by about 1 cm. More striking are the changes in
Increased kidney size
the urinary tract. The calyces, renal pelvis, and ureters dilate. The
dilation is more marked on the right side than the left and is apparent
as early as the first trimester. Hormonal mechanisms and mechanical
obstruction are responsible. Intravenous pyelography may demon-
strate the iliac sign in which ureteral dilation terminates at the level of
the pelvic brim where the ureter crosses the iliac artery. Ureteral dila-
Increased renal blood flow
tion and urinary stasis contribute to the increased incidence of asymp-
tomatic bacteriuria and pyelonephritis in pregnancy.
Increased glomerular filtration rate
Dilation of urinary tract
Changes in Renal Function During Pregnancy
FIGURE 10-2
↓ Uric acid reabsorption
Changes in renal function during pregnancy. Marked renal hemo-
dynamic changes are apparent by the end of the first trimester.
Both the glomerular filtration rate (GFR) and effective renal plas-

ma flow (ERPF) increase by 50%. ERPF probably increases to a
Renin
greater extent, and thus, the filtration fraction is decreased during
early and mid pregnancy. Micropuncture studies performed in ani-
mals suggest the basis for the increase in GFR is primarily the
increase in glomerular plasma flow [1]. The average creatinine level
and urea nitrogen concentration are slightly lower than in pregnant
Renal vasodilation
↑ Aldosterone
women than in those who are not pregnant (0.5 mg/d and 9
↑ Glomerular filtration rate
↑ Sodium reabsorption
mg/dL, respectively). The increased filtered load also results in
↑ Renal blood flow
↑ Water reabsorption
increased urinary protein excretion, glucosuria, and aminoaciduria.
↓ Serum creatinine
↑ Urinary calcium
The uric acid clearance rates increase to a greater extent than does
↑ Urinary protein
↑ Glucosuria
↑ Aminoaciduria
the GFR. Hypercalciuria is a result of increased GFR and of
increases in circulating 1,25-dihydroxy-vitamin D3 in pregnancy
(absorptive hypercalciuria). The renin-angiotensin system is stimu-
lated during gestation, and cumulative retention of approximately
950 mEq of sodium occurs. This sodium retention results from a
complex interplay between natriuretic and antinatriuretic stimuli
present during gestation [2].

Kidney Disease and Hypertension in Pregnancy
10.3
Serum Electrolytes in Pregnancy
FIGURE 10-3
A Altered osmoregulation:
B Serum chloride levels are
Serum electrolytes in pregnancy. A, During normal gestation, serum
↓ Serum sodium and ↓ Posm
unchanged compared with
osmolality decreases by 10 mosm/L and serum sodium (Na+) decreases
with ↓ Osmotic Threshold
women who are not pregnant
by 5 mEq/L. A resetting of the osmoreceptor system occurs, with
for the argenine vasopressin
decreased osmotic thresholds for both thirst and vasopressin release
release and thirst
[3]. B, Serum chloride (Cl-) levels essentially are unchanged during
pregnancy. C, Despite significant increases in aldosterone levels
during pregnancy, in most women serum potassium (K+) levels are
Na+
Cl-
either normal or, on average, 0.3 mEq/L lower than are values in
136 mEq/L
104 mEq/L
women who are not pregnant [4]. The ability to conserve potassi-
3.7 mEq/L
20 mEq/L
um may be a result of the elevated progesterone in pregnancy [5].
K+
HCO3
D, Arterial pH is slightly increased in pregnancy owing to mild
respiratory alkalosis. The hyperventilation is believed to be an
effect of progesterone. Plasma bicarbonate (HCO-3) concentrations
C Mild hypokalemia may be
D Mild respiratory alkalosis is
decrease by about 4 mEq/L [6].
observed due to ↑ glomerular
associated with small decreases
filtration rate, ↑ urine flow,
in plasma bicarbonate
and ↑ aldosterone

Blood Pressure and the Renin-Aldosterone
System in Pregnancy
PRA
120
Postpartum angiotensinogen values
14
110
12
*
100
10
e
,
mmHg
90
Sitting
8
,

ng/mL/h
Standing
essur
A
80
PR
6
**
70
*
Blood pr
4
***
60
2
*
*
(N)
(7)
(16)
(18) (18)
(18) (19) (18) (18)(15)
(19)
50
0
4
8
12
16
20
24
28
32
36
40
PP
4
8
12
16
20
24
28
32
36 38
PP
A
Gestation, wk
B
Gestation, wk
FIGURE 10-4
Blood pressure and the renin-aldosterone system in pregnancy.
pregnancy and often approaches prepregnancy levels at term.
Normal pregnancy is associated with profound alterations in
B, Despite the decrease in blood pressure, plasma renin activity
cardiovascular and renal physiology. These alterations are
(PRA) increases during the first few weeks of pregnancy; on
accompanied by striking adjustments of the renin-angiotensin-
average, close to a fourfold increase in PRA occurs by the end of
aldosterone system. A, Blood pressure and peripheral vascular
the first trimester, with additional increases until at least 20
resistance decrease during normal gestation. The decrease in
weeks. The source of the increased renin is thought to be the
blood pressure is apparent by the end of the first trimester of
maternal renal release of renin.
(Continued on next page)

10.4
Systemic Diseases and the Kidney
Urine aldosterone
Urine sodium
Plasma aldosterone
200
Urine potassium
120
150
100
100
P
l
,
mEq
a
+
µ
g/d
s
ma aldost
,
100
80
80
and K
one
+
er
er
one
60
60
24-hr Na
,
ng/100mL
50
r
ine aldost
U
40
40
0
20
20
8
12
16
20
24
28
32
36
38
PP
C
0
0
D
Gestation, wk
FIGURE 10-4 (Continued)
C, Changes in renin are associated with commensurate changes in
increases in late gestation to a greater degree than does plasma
the secretory rate of aldosterone. Although a correlation exists
aldosterone, which may reflect an increased production of the
between the increase in renin and that of aldosterone, the latter
3-oxo conjugate measured in urine. D, Despite the marked increas-
increases to a greater degree in late pregnancy. This observation
es in aldosterone during pregnancy, 24-hour urinary sodium and
suggests that other factors may regulate secretion to a greater degree
potassium excretion remain in the normal range. PP— postpartum.
than does angiotensin II in late gestation. Urinary aldosterone
(From Wilson and coworkers [7]; with permission.)
Functional Significance of the Stimulated
Renin-Angiotensin System in Pregnancy
FIGURE 10-5
Pregnant (n = 9)
Nonpregnant (n = 8)
Functional significance of the stimulated renin-angiotensin system
(RAS) in pregnancy. We determine whether changes in the RAS in
85
25
pregnancy are primary, and the cause of the increase in plasma vol-
80
20
ume, or whether these changes are secondary to the vasodilation
and changes in blood pressure. To do so, we administered a single
75
15
*
P < .05
dose of captopril to normotensive pregnant women in their first
and second trimesters and age-matched normotensive women who
P
,

mm Hg 70
,

mg/mL/h 10
A
were not pregnant. We then measured mean arterial pressure (MAP)
MA
PR
and plasma renin activity (PRA) before and 60 minutes after the dose.
65
P < 0.005
5
*
A, Despite similar baseline blood pressures, blood pressure decreased
60
0
more in pregnant women compared with those who were not preg-
T = 0
T = 60
T = 0
T = 60
nant in response to captopril. This observation suggests that the
A
B
RAS plays a greater role in supporting blood pressure in pregnan-
cy. B, Baseline PRA was higher in pregnant women compared with
those who were not pregnant, and pregnant women had a greater
increase in renin after captopril compared with those who were not
pregnant. T—time. (From August and coworkers [8]; with permission.)

Kidney Disease and Hypertension in Pregnancy
10.5
Pregnancy and the Course of Renal Disease
FIGURE 10-6
INTERRELATIONSHIPS BETWEEN
Pregnancy may influence the course of renal disease. Some women
PREGNANCY AND RENAL DISEASE
with intrinsic renal disease, particularly those with baseline azotemia
and hypertension, suffer more rapid deterioration in renal function
after gestation. In general, as kidney disease progresses and function
Impact of pregnancy on renal disease
Impact of renal disease on pregnancy
deteriorates, the ability to sustain a healthy pregnancy decreases. The
presence of hypertension greatly increases the likelihood of renal
Hemodynamic changes → hyperfiltration
Increased risk of preeclampsia
deterioration [2]. Although hyperfiltration (increased glomerular
Increased proteinuria
Increased incidence of prematurity,
filtration rate) is a feature of normal pregnancy, increased intra-
Intercurrent pregnancy-related illness,
intrauterine growth retardation
glomerular pressure is not a major concern because the filtration
eg, preeclampsia
fraction decreases. Possible factors related to the pregnancy-related
Possibility of permanent loss
of renal function
deterioration in renal function include the gestational increase in
proteinuria and intercurrent pregnancy-related illnesses, such as
preeclampsia, that might cause irreversible loss of renal function.
Women with renal disease are at greater risk for complications
related to pregnancy such as preeclampsia, premature delivery,
and intrauterine growth retardation.
Diabetes Mellitus and Pregnancy
FIGURE 10-7
RENAL DISEASE CAUSED
Diabetes mellitus is a common disorder in pregnant women. Patients with overt nephropathy
BY SYSTEMIC ILLNESS
are likely to develop increased proteinuria and mild but usually reversible deteriorations in
renal function during pregnancy. Hypertension is common, and preeclampsia occurs in
35% of women. (From Reece and coworkers [9]; with permission.)
Gestation in pregnant women with diabetic
nephropathy is complicated by the following:
Increased proteinuria, 70%
Decreased creatinine clearance, 40%
Increased blood pressure, 70%
Preeclampsia, 35%
Fetal developmental problems, 20%
Fetal demise, 6%

10.6
Systemic Diseases and the Kidney
Pregnancy and Systemic Lupus Erythematosus
FIGURE 10-8
Patients with systemic lupus erythematosus
RENAL DISEASE ASSOCIATED WITH SYSTEMIC ILLNESS
(SLE) often are women in their childbearing
years. Pregnancies in women with evidence
of nephritis are potentially hazardous, partic-
Pregnancy and SLE*
Antiphospholipid antibody syndrome in pregnancy
ularly if active disease is present at the time
Poor outcome is associated with the following:
Increased fetal loss
of conception or if the disease first develops
Active disease at conception
Arterial and venous thromboses
during pregnancy. When hypertension and
Disease first appearing during pregnancy
Renal vasculitis, thrombotic microangiopathy
azotemia are present at the time of concep-
Hypertension, azotemia in the first trimester
Preeclampsia
tion the risk of complications increases, as it
High titers of antiphospholipid antibodies or
Treatment: heparin and aspirin?
does with other nephropathies [10–14]. The
lupus anticoagulant
presence of high titers of antiphospholipid
antibodies also is associated with poor preg-
nancy outcome [15]. The presence of anti-
*Systemic lupus erythematosus (SLE) is unpredictable during pregnancy.
phospholipid antibodies or the lupus anti-
coagulant is associated with increased fetal
loss, particularly in the second trimester;
increased risk of arterial and venous throm-
bosis; manifestations of vasculitis such as
thrombotic microangiopathy; and an
increased risk of preeclampsia. Treatment
consists of anticoagulation with heparin
and aspirin.
Lupus Versus Preeclampsia
FIGURE 10-9
In the second or third trimester of pregnancy a clinical flare-up of
LUPUS FLARE-UP VERSUS PREECLAMPSIA
lupus may be difficult to distinguish from preeclampsia. Treatment
of a lupus flare-up might involve increased immunosuppression,
whereas the appropriate treatment of preeclampsia is delivery. Thus,
SLE
PE
it is important to accurately distinguish these entities. Preeclampsia
Proteinuria
+
+
is rare before 24 weeks’ gestation. Erythrocyte casts and hypocom-
Hypertension
+
+
plementemia are more likely to be a manifestation of lupus, whereas
Erythrocyte casts
+
-
abnormal liver function test results are seen in preeclampsia and not
Azotemia
+
+
usually in lupus.
Low C3, C4
+
-
Abnormal liver function test results
-
+/-
Low platelet count
+
+/-
Low leukocyte count
+
-
C—complement; minus sign—absent; plus sign—present; PE—preeclampsia;
SLE—systemic lupus erythematosus.

Kidney Disease and Hypertension in Pregnancy
10.7
Chronic Primary Renal Disease in Pregnancy
FIGURE 10-10
CAUSES OF CHRONIC PRIMARY
Primary renal disease in pregnancy that is chronic (ie, preceded pregnancy) may result
RENAL DISEASE IN PREGNANCY
from any of the causes of renal disease in premenopausal women. Overall, the outcome in
pregnancy is favorable when the serum creatinine level is less than 1.5 mg/dL and blood
pressure levels are normal in early pregnancy.
Anatomic, congenital
Glomerulonephritis
Interstitial nephritis
Polycystic kidney disease
Advanced Renal Disease Caused by
Polycystic Kidney Disease
FIGURE 10-11
POLYCYSTIC KIDNEY DISEASE
Although advanced renal disease caused by polycystic kidney disease (PKD) usually devel-
AND PREGNANCY
ops after childbearing, women with this condition may have hypertension or mild
azotemia. Certain considerations are relevant to pregnancy. Pregnancy is associated with
an increased incidence of asymptomatic bacteriuria and urinary infection that may be
more severe in women with PKD. The presence of maternal hypertension has been shown
Increased incidence of urinary tract infection
to be associated with adverse pregnancy outcomes [16]. Pregnancy has been reported to be
Maternal hypertension associated with poor outcome
associated with increased size and number of liver cysts owing to estrogen stimulation.
Extrarenal complications: subarachnoid hemorrhage,
liver cysts
Women with intracranial aneurysms may be at increased risk of subarachnoid hemorrhage
during labor.
Management of Chronic Renal Disease During Pregnancy
FIGURE 10-12
MANAGEMENT OF CHRONIC RENAL
Management of chronic renal disease during pregnancy is best
DISEASE DURING PREGNANCY
accomplished with a multidisciplinary team of specialists.
Preconception counseling permits the explanation of risks involved
with pregnancy. Patients should understand the need for frequent
monitoring of blood pressure and renal function. Protein restriction
Preconception counseling
is not advisable during gestation. Salt intake should not be severely
Multidisciplinary approach
restricted. When renal function is impaired, modest salt restriction
Frequent monitoring of blood pressure (every 1–2 wk) and renal function (every mo)
may help control blood pressure. Blood pressure should be main-
Balanced diet (moderate sodium, protein)
tained at a level at which the risk of maternal complications owing
Maintain blood pressure at 120–140/80–90 mm Hg
to elevated blood pressure is low. Patients should be monitored
Monitor for signs of preeclampsia
closely for signs of preeclampsia, particularly in the third trimester.

10.8
Systemic Diseases and the Kidney
Renal Disease During Pregnancy
FIGURE 10-13
MOST COMMON CAUSES OF DE NOVO
Renal disease may develop de novo during pregnancy. The usual
RENAL DISEASE IN PREGNANCY
causes are new-onset glomerulonephritis or interstitial nephritis,
lupus nephritis, or acute renal failure. Rarely, obstructive uropathy
develops as a result of stone disease or large myomas that have
increased in size during pregnancy.
Glomerulonephritis
Interstitial nephritis
Lupus nephritis
Obstructive uropathy
Acute renal failure
Investigation of the Cause of Renal Disease During Pregnancy
FIGURE 10-14
RENAL EVALUATION
Investigation of the cause of renal disease during pregnancy can be conducted with serolog-
DURING PREGNANCY
ic, functional, and ultrasonographic testing. Renal biopsy is rarely performed during gesta-
tion. Renal biopsy usually is reserved for situations in which renal function suddenly deteri-
orates without apparent cause or when symptomatic nephrotic syndrome occurs, particular-
ly when azotemia is present. Almost no role exists for renal biopsy after gestational week
Serology
32 because at this stage the fetus will likely be delivered, independent of biopsy results [17].
Function
Ultrasonography
Biopsy: <32 wk
Deteriorating function
Morbid nephrotic syndrome
New-Onset Azotemia, Proteinuria, and Hypertension
Occurring in the Second Half of Pregnancy
FIGURE 10-15
INTRINSIC RENAL DISEASE VERSUS PREECLAMPSIA
New-onset azotemia, proteinuria, and hypertension occurring in
the second half of pregnancy should be distinguished from pre-
eclampsia. Most cases of preeclampsia are associated with only
mild azotemia; significant azotemia is more suggestive of renal dis-
Renal disease
Preeclampsia
ease. Azotemia in the absence of proteinuria or hypertension would
Serum creatinine
>1.0 mg/dL
0.8–1.2 mg/dL
be unusual in preeclampsia, and thus, would be more suggestive of
Urinary protein
Variable
>300 mg/d
intrinsic renal disease. Thrombocytopenia, elevated liver function
Uric acid
Variable
>5.5 mg/dL
test results, and significant anemia are not typical features of renal
Blood pressure
Variable
>140/90 mm Hg
disease (except for thrombotic microangiopathic syndromes) and
Liver function test results
Normal
May be increased
are features of the variant of preeclampsia known as the hemolysis,
Platelet count
Normal
May be decreased
elevated liver enzymes, and low platelet count (HELLP) syndrome.
Urine analysis
Variable
Protein, with or without
erythrocytes, leukocytes

Kidney Disease and Hypertension in Pregnancy
10.9
Acute Tubular Necrosis and Pregnancy
FIGURE 10-16
ACUTE RENAL FAILURE
Most pregnant women with acute renal failure have acute tubular necrosis secondary to
IN PREGNANCY
either hemodynamic factors, toxins, or serious infection. Occasionally, glomerulonephritis
or obstructive nephropathy may be seen. Acute cortical necrosis may complicate severe
obstetric hemorrhage. Acute renal failure may be a complication of the rare syndrome of
acute fatty liver of pregnancy, a disorder that occurs late in gestation characterized by
Acute tubular necrosis; hemodynamic factors, toxins,
serious infection, and so on
jaundice and severe hepatic dysfunction. This syndrome has features that overlap with the
Acute interstitial nephritis
hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome variant of
Acute fatty liver of pregnancy
preeclampsia as well as microangiopathic syndromes (eg, hemolytic uremic syndrome and
thrombotic thrombocytopenic purpura).
Preeclampsia-HELLP syndrome
Microangiopathic syndromes
Acute cortical necrosis: obstetric hemorrhage
HELLP—hemolysis, elevated liver enzymes, and low
platelet count.
HELLP Syndrome, AFLP, TTP, and HUS
FIGURE 10-17
Hemolysis, elevated liver enzymes, and low
DIFFERENTIAL DIAGNOSIS OF MICROANGIOPATHIC
platelet count (HELLP) syndrome; acute
SYNDROMES DURING PREGNANCY
fatty liver of pregnancy (AFLP); thrombotic
thrombocytopenic purpura (TTP); and
hemolytic uremic syndrome (HUS) have sim-
HELLP
AFLP
TTP
HUS
ilar clinical and laboratory features [18,19].
Hypertension
80%
25–50%
Occasional
Present
The subtle differences are summarized.
Renal insufficiency
Mild to moderate
Moderate
Mild to moderate
Severe
(Adapted from Saltiel and coworkers [18].)
Fever, neurologic
0
0
++
0
symptoms
Onset
3rd trimester
3rd trimester
Any time
Postpartum
Platelet count
Low to very low
Low to very low
Low to very low
Low to very low
Liver function test
High to very high
High to extremely
Usually normal
Usually normal
results
high
Partial thromboplastin
Normal to high
High
Normal
Normal
time
Antithrombin III
Low
Low
Normal
Normal
AFLP—acute fatty liver of pregnancy; HELLP—hemolysis, elevated liver enzymes, and low platelet count;
HUS–hemolytic uremic syndrome; TTP—thrombotic thrombocytopenic purpura.
Adapted from Saltiel et al. [18].

10.10
Systemic Diseases and the Kidney
Fertility in Women in End-Stage Renal Disease
FIGURE 10-18
DIALYSIS AND PREGNANCY
Because fertility is decreased in end-stage renal disease, pregnancy is uncommon in women
on chronic dialysis. When pregnancies occur, however, only about 20% to 30% are suc-
cessful, with the chances of success increasing when residual renal function exists [20]. The
overall strategy should be to maintain blood chemistry levels as close as possible to normal
Successful outcome, 20–30%
by increasing the number of hours of dialysis to 20 or more. Erythropoietin may be used
High incidence of prematurity
in pregnancy. Blood pressure control is important, and low doses of heparin should be
Outcome related to residual maternal renal function
used to prevent bleeding. There are no apparent advantages of chronic ambulatory peri-
Management:
toneal dialysis compared with hemodialysis. The incidence of worsening maternal hyper-
Increased hours on dialysis
tension and subsequent premature delivery is high.
Erythropoietin therapy
Blood pressure control
Therapy with low doses of heparin
Continuous ambulatory peritoneal dialysis versus
hemodialysis ?
Fertility and Renal Transplantation
FIGURE 10-19
RENAL TRANSPLANTATION AND PREGNANCY
Fertility is restored after successful renal transplantation.
Pregnancy outcome is improved if renal function is normal and
hypertension is absent. It is advisable to wait 2 years after trans-
plantation before pregnancy so that renal function is stable and
Prognosis depends on blood pressure and baseline renal function
(<1.5–2 mg/dL; normal blood pressure)
doses of immunosuppressants are lowest [21]. Cyclosporine, pred-
Controversy over whether pregnancy accelerates graft loss
nisone, and azathioprine are safe during pregnancy and are not
Patients are advised to wait 2 y after transplantation before pregnancy
associated with fetal abnormalities. Limited experience exists with
mycophenolate mofetil during pregnancy.
Hypertensive Disorders in Pregnancy
FIGURE 10-20
Developing nations
Developed nations
Mortality and hypertension. Worldwide, hypertensive disorders are a
Sepsis
major cause of maternal mortality, accounting for almost 20% of mater-
8%
nal deaths. Most deaths occur in women with eclampsia and severe
Hemorrhage
20%
hypertension (HTN) and are due to intracerebral hemorrhage [22].
Embolism
Sepsis
20%
Other
40%
HTN
25%
Abortion
15%
17%
Other
HTN
25%
17%
Hemorrhage
13%
100–800/100,000
12/100,000
(deaths, births)
(deaths, births)

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