Dr. Omnia Abdelazim lecture

1. Renal Disease and Pregnancy
:-By
Omnia Abd Elazim
:-Supervised by
prof:-Ahmed Fathy Elkoraie

2. :Agenda
 The normal kidney in Pregnancy.
 pregnancy-induced hypertension.
 Acute kidney injury in pregnancy.
 Chronic kidney disease and pregnancy.
 End-stage renal disease and pregnancy.
 Transplantation and pregnancy.

3. The normal kidney in
Pregnancy

4. Renal Function During Pregnancy
Renal plasma flow increases by 50-70% in pregnancy,
and this change occur mainly in the first two
trimesters. This is the factor that lead to an
increased glomerular filtration rate (GFR). The GFR
peaks around the 13th week of pregnancy and can
reach levels up to 150% of normal. So, both BUN
and creatinine levels, the plasma markers of GFR,
are decreased. This decrease has clinical
significance in that a normal BUN or creatinine level
in a pregnant female may actually indicate
.underlying renal disease

5. Similarly, in the initial part of pregnancy, increased
levels of progesterone enhance relaxation of the
arterial smooth muscles and thus decrease
peripheral vascular resistance.So, a blood pressure
fall of approximately 10 mm Hg occurs in the first 24
weeks of pregnancy. The blood pressure gradually
returns to a prepregnancy level by term; thus, a
consistent normal or prepregnancy blood pressure
may suggest the presence of a condition that
.hypertension predisposes patients to

6. The drop in blood pressure in normal
pregnancy occurs despite increased levels of
renin, angiotensin, and aldosterone. There is
resistance to the hypertensive effects of both
endogenously and exogenously administered
angiotensin. The resistance has been
attributed to production of prostacyclin by
placental endothelial cells as well as other
.vasodilators

7. Renal vasodilatation in pregnancy
EDRF; Endothelial Derived Relaxing Factor,
)(NO
Vasodilatory PG’s
Relaxin
ET;Endothelin
.All lead to increase RPF& GFR

8. Electrolytes & Acid Base Changes
Elevated progesterone levels stimulate
hyperventilation and result in a state of mild
respiratory alkalosis and a blood gas of
PH: 7.44
PCO2: 30
HCO3: 22

9. A reset in the osmostat occurs, resulting in
increased thirst and decreased serum
sodium levels (by approximately 5 mEq/L)
compared with nonpregnant females and
.also decreased osmolality

10. Hyponatremia during pregnancy parallels the
increased release of human chorionic
gonadotropin (HCG), which appears to
mediate these changes via the release of
relaxin. Serum potassium levels are normal
despite increased serum aldosterone,
perhaps due to the potassium-sparing effects
of elevated progesterone levels in
.pregnancy

11. Total serum calcium levels fall in pregnancy but ionized
calcium remains normal. Accelerated renal and
placental production of calcitriol leads to increased
gastrointestinal absorption of calcium and absorptive
hypercalciuria with urine calcium as high as 300
.mg/day
Serum parathyroid hormone (PTH) concentrations
are lower than normal, partly in response to higher
.serum levels of calcitriol

12. Increased urinary excretion of protein,amino
acids,uric acid,glucose and calcium occurs
as result of the elevated GFR.
Hence,proteinuria in pregnancy is considered
abnormal when it exceeds 300mg/day
compared with an upper limit of normal of
.150mg/day in the nonpregnant population

13. Pre-pregnancy pregnancy
S.Uric acid 4 3.2
Na 140 135
K Slight increase
BUN 12.7 9.3
Creatinine 0.8 0.5
Glucose glucosuria
Osmolality 285 275
Ca decrease
%Hct 41 33

14. The anatomic changes in
pregnancy
The anatomic changes are primarily in the collecting
system. A dilatation of the ureters and pelvis occurs
and it is secondary to the smooth muscle–relaxing
effect of progesterone. This dilatation is often more
on the right side secondary to dextrorotation of the
uterus and dilatation of the right ovarian venous
plexus. This can lead to urinary stasis and, an
increased risk of developing urinary tract infections
).(UTIs

15. There is also an increase in overall kidney size
. by about 1-1.5 cm
these changes may persist for up to 12 weeks
postpartum and should not be over-
.interpreted as obstructive uropathy

16. Renal Changes in Normal Pregnancy
 Anatomic
 1 cm incerased in length.
 Dilatation of the collecting system.
 Physiologic
 50% increased in GFR: normal BUN 9 mg/dL, creatinine 0.5mg/dL
 Respiratory alkalosis: normal PCO2 27 – 32 mm Hg, HCO- 3 18 – 22 mEq/L
 Decreased serum osmolality: normal 276 – 278 mOsm/L
 Doubling of uric acid clearance: normal 3 – 4 mg/dL
 Decreased Tubular reabsorption of glucose
 40% increased in renal blood flow
 Decreased afferent and efferent arteriolar resistance
 Decreased BP: normal < 125/75 mm Hg 2nd trimester, < 125/85 mm Hg 3rd trimester
 Increased Prostacyclin and thromboxane
 Increased Renin (8x), angiotensin (4x), aldosterone (10 – 20x)

17. pregnancy-induced
hypertension

18. Hypertension, the most common medical
complication of pregnancy, occurs in up to
10% of pregnancies; it is associated with a
significant increase in maternal and fetal
morbidity and mortality and is the leading
.cause of premature birth

19. hypertension in pregnancy is defined as a
systolic blood pressure of over 140 mm Hg
and a diastolic blood pressure greater than
.90 mm Hg

20. Types of pregnancy-induced
hypertension
Gestational hypertension) 1
de-novo hypertension occurring alone after
20/40 which
resolves post-partum. Risk factor for essential
.hypertension in later life

21. Chronic hypertension) 2
Pre-eclampsia) 3
Chronic hypertension with superimposed) 4
pre-eclampsia

22. Hypertension and adverse outcomes in
pregnancy
Progressive increase in perinatal mortality with each•
.5mmHg increased in MAP
MAP > 90mmHg during 2nd trimester correlates with•
.increased incidence of IUGR, pre-eclampsia
pregnant women with MAP> 90mmHg in 2nd 1/3•
. trimester progress to pre-eclampsia

23. Gestational hypertension( 1
Gestational hypertension is defined as
hypertension that appears after midterm, is
not associated with proteinuria, and resolves
after delivery. Women at risk for this
condition are those with a positive family
history of hypertension and patients with
obesity and multiparity. Women with
gestational hypertension are at risk for
.chronic hypertension

24. Chronic hypertension( 2
Chronic hypertension is defined as a prepregnancy
blood pressure of greater than 140/90 or as
hypertension occurring before 20 week's gestation.
The definition may also include some hypertensive
women with minimal proteinuria diagnosed during
pregnancy that does not resolve with delivery. Fisher
et al showed by renal biopsy that these women may
.have nephrosclerosis rather than preeclampsia

25. Chronic hypertension increases the risk of pre-
eclampsia, perinatal mortality, small for
gestational age (SGA) babies, premature
delivery,, gestational diabetes, intrauterine
growth retardation, and second-trimester
.fetal death

26. treatment
:-During pregnancy
Antihypertensive drugs*
methyldopa / labetalol = 1
.CCB / hydralazine = 2
 No ACE inhibitor/ARB after conception/1st trimester.
.Early delivery for severe hypertension*
.Bed rest*

27. treatment
:-During lactation
.Labetalol/propranolol/methyldopa
.Sustained release verapamil/nifedipine

28. :-treament of hypertensive urgency
Hydralazine: IV 5mg, then 5-10mg q30min
.or infusion 0.5-10mg/h
/Labetalol: IV 20mg then 20-80mg q20-30min
.max 300mg or infusion 1-2mg/min
Nifedipine: PO/SL 5-10mg PO, then 10-20mg every 2-
. 6 hrs
.Nitroprusside: IV 0.5-10mcg/kg/min

29. Common medications in hypertension
ACE inhibitors, ARBs. 1 Not safe to use Fetal oligohydramnios pulmonary
hypoplasia,skeletal deformities
Diuretics. 2 Not safe to use Maternal volume depletion; fetal
thrombocytopenia, hemolytic anemia,
jaundice
b-Blockers. 3 Not safe to use Fetal bradycardia, hypoglycemia,
respiratory distress
Labetalol. 4 Widely used Limited data
Methyldopa. -5 Safe to use Limited long-term follow-up shows no
developmental problem in children
Clonidine. 6 Not safe to use Limited data
Calcium channel. 7 Safe to use Potentiates the hypotensive effect of
blockers magnesium; limit use to refractory
hypertension
Hydralazine. 8 Safe to use Given intravenously for acute, severe
hypertension

30. Pre-eclampsia( 3
Pre-eclampsia is characterized by the triad
of edema, hypertension, and proteinuria, in
previously normotensive women that typically
occurs after 20 weeks' gestation and
.resolves with delivery
Eclampsia :is defined as the occurrence of
.seizures in women with pre-eclampsia

31. :-Cause
.unknown–
.Abnormal placentation–
.Maternal endothelial dysfunction–
.Genetic factors–
.Increased maternal inflammatory response–
.Immunologic factors–
.Infectious diseases–
.Predicting pre-eclampsia – no good markers•

32. Risk Factors for Preeclampsia
 – Primigravida.
 – Different father in pregnancy for multigravida.
 – Diabetes.
 – Preexisting hypertension.
 – Renal disease.
 – Twin gestation.
 – Hydatidiform mole.
 – Fetal hydrops.
 – Family history.

33. ;-Clinically
preeclampsia usually begins after 20 weeks of
:-pregnancy.it manifested by
. De novo hypertension
.New onset proteinuria

34. Severe Pre-eclampsia
:-Preeclampsia with one or more of the following
Systolic BP ≥160 mm Hg or diastolic BP ≥110 mm Hg on two occasions*
.at least 6 hr apart while on bedrest
Proteinuria >5 g in a 24-hr urine specimen or dipstick proteinuria ≥3+*
.on two random urine samples at least 4 hr apart
).Oliguria (<500 mL urine output over 24 hr*
disturbances *Severe headache, mental status changes, visual .

35. Hepatocellular injury (transaminase elevation *
). to at least twofold over normal level
). Thrombocytopenia (<100,000*
*growth restriction. Fetal
.Cerebrovascular accident*
.pulmonary edema or cyanosis*

36. Pathology
The characteristic pathologic changes in the kidney of women with
preeclampsia include swelling of the endothelial cells
(glomerular endotheliosis), ballooning of capillary loops
into the tubule, fibrinogen and lipid in endothelial cells, and
.occasional foam cells
Rarely, changes similar to focal sclerosis occur, with reversal
postpartum. Ischemic changes are less marked than in other
.organs
.The renal pathologic changes resolve 2 – 4 weeks postpartum

37. Prevention of Preeclampsia
Two interventions have been extensively
investigated to determine whether they
prevent preeclampsia: low-dose aspirin and
calcium supplementation. Despite initial
promise, the effects of these two treatments
.have been disappointing in large trials

38. :-Management
Delivery if viable / termination if remote from
.term
Temporizing measures if stable
maternal/fetal unit and benefit of increased
.fetal maturity outweight risk
Antihypertensive therapy: PO or IV (not
).diuretics
.Seizure control – magnesium sulfate

39. Indications for delivery
 ≥ 36 weeks gestation.
 BP ≥ 160/110 after 24 hours of hospitalization.
 HELLP syndrome.
 ≥ 3 g of protein in 24 hours.
 Rising serum creatinine.
 Headache, blurred vision, scotomata, right upper
quadrant pain, clonus.

40. Chronic hypertension with( 4
superimposed pre-eclampsia
If the systolic blood pressure exceeds 200 mm
Hg, pre-eclampsia superimposed on chronic
hypertension is suggested. In this setting,
pulmonary capillary permeability may be
increased, resulting in pulmonary edema,
central nervous system excitability may
occur, causing hyper-reflexia and cerebral
.hemorrhage

41. Diagnosis of pre-eclampsia
superimposed on chronic
hypertension
:If proteinuria prior to 20 wk is absent
New-onset proteinuria in a woman with *
. chronic hypertension

42. If proteinuria prior to 20 wk is present, any of
the following raise concern for superimposed
:preeclampsia
. A sudden increase in proteinuria
.A sudden increase in hypertension
. Thrombocytopenia
. Increased in liver enzymes

43. HELLP Syndrome
HELLP, a syndrome characterized by
hemolysis, elevated liver enzyme
levels and a low platelet count, is an
obstetric complication that is frequently
misdiagnosed at initial presentation. Many
investigators consider the syndrome to be a
variant of pre-eclampsia.

44. Clinical Presentation
 90%of patients present with generalized
malaise,
 65 % with epigastric pain,
 30 % with nausea and vomiting,
 31 percent with headache.

45. 90
90
80
70 65
60 general malase
50 epigastric pain
40 vomiting
30 31
30 haedache
20
10
0
symptoms

46. The physical examination may be normal in
patients with HELLP syndrome.
%.right upper quadrant tenderness 90- 1
. Edema is not a useful marker- 2
Hypertension and proteinuria may be- 3
. absent or mild

47. 90
90
80
70
60
Rt.hypochond.pain
50
40 edema
30 30
30
hypertention + proteinuria
20
10
0
signs

48. Diagnosis
Haemolysis
Abnormal peripheral smear : spherocytes, schistocytes,
triangular cells and burr cells
Total Bilirubin level > 1.2 mg/dL
Lactate dehydrogenase level > 600U/L
Elevated liver function test result
Serum aspartate amino transferase level > 70U/L
Lactate dehydrogenase level >600 U/L
Low platelet count
Platelet count < 150 000/mm3

49. Complications
 The mortality rate for women with HELLP
syndrome is approximately 1.1 %
 From 1 to 25 % of affected women develop
serious complications such as DIC, placental
abruption, adult respiratory distress syndrome,
hepatorenal failure, pulmonary edema,
subcapsular hematoma and hepatic rupture.
 A significant percentage of patients receive
blood products.

50.  Infant morbidity and mortality rates range
from 10 to 60 %, depending on the
severity of maternal disease.
 Infants affected by HELLP syndrome are
more likely to experience intrauterine
growth retardation and respiratory
distress syndrome.

51. 60%
60.00%
50.00%
40.00%
25%
30.00%
20.00%
10.00% 1.10%
0.00%
matern.mort. maternal fetal
complication complication

52. Management
Delivery.
Corticosteroids.
Magnesium sulphate.
Hypotensive drugs.
Blood products.

53. :-Corticosteroids-1
 The antenatal administration of dexamethasone in a high
dosage of 10 mg intravenously every 12 hours has been
shown to markedly improve the laboratory abnormalities
associated with HELLP syndrome.
 Steroids given antenatally do not prevent the
typical worsening of laboratory abnormalities
after delivery. However, laboratory abnormalities
resolve more quickly in patients who continue to
receive steroids postpartum.

54. :-Magnesium sulphate-2
Patients with HELLP syndrome
should be treated
prophylactically with
magnesium sulfate to
prevent seizures, whether
hypertension is present or
not.

55. Antihypertensive therapy-3
should be initiated if blood
pressure is consistently greater
than 160/110 mm hg despite the
use of magnesium sulfate. The
goal is to maintain diastolic
blood pressure between 90 and
100 mm hg.

56. :-Blood products-4
 Patients who undergo cesarean section
should be transfused if their platelet count is
less than 50,000 per mm3.
 Prophylactic transfusion of platelets at
delivery does not reduce the incidence of
postpartum hemorrhage or hasten
normalization of the platelet count.
 Patients with DIC should be given fresh
frozen plasma and packed red blood cells.

57. Acute kidney injury in
pregnancy

58. Classification
 Renal failure in early pregnancy.
 Renal failure in late pregnancy.
 Postpartum renal failure .

59. Renal failure in early
pregnancy

60. Renal failure in early pregnancy
:-prerenal azotemia-1
Causes
associated with Hyperemesis gravidarum--
metabolic alkalosis; diagnosis is made by
history. Treatment requires the
.administration of intravenous fluids
Hemorrhage associated with spontaneous-
.abortion

61. Renal failure in early pregnancy
:-Acute tubular necrosis-2
Causes
Severe volume depletion associated with
hyperemesis gravidarum, hemorrhage from
spontaneous abortion, or shock secondary to
.septic abortion
Septic abortion, most commonly due to
Escherichia coli; in some cases, however,
Clostridium, which can cause myonecrosis of the
.uterus and myoglobinuria, is responsible

62. The diagnosis of acute tubular necrosis can be
established via the clinical setting, urinalysis,
.and urinary indices
Treatment includes fluids, antibiotics and, if
.necessary, dialysis

63. Renal failure in early pregnancy
:-Renal cortical necrosis-3
;Cause
The disorder is most likely initiated by
primary disseminated intravascular
coagulation in the setting of severe renal
.ischemia
This is a rare cause of severe acute renal
failure; it is more commonly associated
.with pregnancy

64. Renal cortical necrosis presents with gross
hematuria, flank pain, and severe
oliguria/anuria following an obstetric
:catastrophe
septic abortion, retained fetus, amniotic fluid (
).embolism

65. Laboratory Studies
check for hyperkalemia, hypocalcemia, metabolic*
.acidosis, and elevated creatinine levels
A CBC count may reveal hemolytic anemia and*
.thrombocytopenia
Coagulation studies detect low fibrinogen levels *
.and increased fibrin-degradation products
Urinalysis detects hematuria, proteinuria, RBC*
.casts, and granular casts

66. Imaging Studies
Ultrasonography*
The sonogram initially shows enlarged
.kidneys with reduced blood flow
Cortical tissue becomes shrunken later in
.disease progression

67. Imaging Studies
*Contrast-enhanced CT scanning
CT scanning with contrast are the most sensitive
.imaging modality
Diagnostic features include absent opacification of
the renal cortex and enhancement of
subcapsular and juxtamedullary areas and of the
.medulla without excretion of contrast medium
Initiating hemodialysis immediately after the
procedure may be necessary to minimize further
.contrast-mediated renal damage

68. Histologic Findings
Renal cortical necrosis is classified into 5 pathologic forms, depending on
severity, as shown below. Renal cortical necrosis classifications are as
:follows
Focal pathologic form: Kidneys show focally necrotic glomeruli
.without thrombosis and patchy necrosis of tubules
Minor pathologic form: Larger foci of necrosis are evident with
.vascular and glomerular thrombi
Patchy pathologic form: Patches of necrosis may occupy two thirds
.of the cortex
Gross pathologic form: Almost all cortex is involved. Thrombosis of
.the arteries is more widespread
Confluent pathologic form: Kidneys show widespread glomerular
.and tubular necrosis with no arterial involvement

69. Recovery typically requires months, and renal
.functional recovery is usually incomplete

70. Renal failure in early pregnancy
:-pyelonephritis-4
Acute pyelonephritis is associated with a GFR -
reduction that can be reversed with treatment
.of the underlying infection

71. Renal failure in early pregnancy
TTP&HUS-5-:
represent a spectrum that includes
microangiopathic hemolytic anemia,
thrombocytopenia, and renal failure, TTP is more
likely to occur in the first trimester and generally
.does not cause severe renal failure
Patients may have a severe deficiency of ADAMTS-
.13
.Plasma exchange is the primary treatment

72. Renal failure in late
pregnancy

73. Renal failure in late pregnancy
.Pre-eclampsia &eclampsia- 1
.HELLP syndrome-2
.Acute tubular necrosis-3
.Acute fatty liver of pregnancy-4

74. Acute fatty liver of pregnancy
Acute fatty liver of pregnancy (or hepatic
lipidosis of pregnancy) usually manifests in
the third trimester of pregnancy, but may
occur any time in the second half of
pregnancy or in the the period immediately
.after delivery

75. :-Causes
It is thought to be caused by a disordered
metabolism of fatty acids by mitochondria in
the mother, caused by deficiency in the
LCHAD((long-chain 3-hydroxyacyl-coenzyme
. A dehydrogenase) enzyme

76. Clinical manifestations
The usual symptoms in the mother are non-.
specific including nausea ,vomiting , anorexia
.and abdominal pain
Jaundice and fever may occur in 70% of
.patients
In patients with more severe disease pre-
.eclampsia may occur

77. This may progress to involvement of additional
systems, including acute renal failure,hepatic
.encephalopathy and pancreatitis
There have also been reports of diabetes
.insipidus complicating this condition

78. Diagnosis
.Elevation of liver enzymes*
Bilirubin is elevated *
Alkaline phosphatase is often elevated in *
pregnancy due to production from the
.placenta
Elevated white blood cell count. *
.*disseminated intravascular coagulation
.Hypoglycemia*

79. Diagnosis
Abdominal ultrasound may show fat deposition
in the liver but, as the hallmark of this
condition is microvesicular steatosis this may
not be seen on ultrasound Rarely, the
condition can be complicated by rupture or
necrosis of the liver, which may be identified
by ultrasound

80. Treatment
Initial treatment involves supportive management with
intravenous fluids, intravenous glucose and blood
products, including fresh frozen plasma and
.cryoprecipitate to correct DIC
The fetous should be monitored with cardiotocography.
After the mother is stabilized, arrangements are
usually made for delivery. This may occur vaginally,
but, in cases of severe bleeding or compromise of
the mother's status, a caesarian section may be
. needed

81. Liver transplantation is rarely required for
treatment of the condition, but may be
needed for mothers with severe DIC, those
with rupture of the liver, or those with severe
.encephalopathy

82. Postpartum renal failure

83. Postpartum renal failure
Postpartum acute renal failure usually presents
days to weeks following a normal delivery
and may be related to retained placental
.fragments

84. DIFFERENTIAL DIAGNOSIS OF MICROANGIOPATHIC
:-SYNDROMES DURING PREGNANCY
HELLP AFLP TTP HUS
Hypertension
80% 25-50% occasional present
Renal Mild to Moderate Mild to Severe
insufficiency moderate moderate
Fever, neurologic
symptoms 0 0 ++ 0
onest 3rd trimester 3rd trimester Any time Postpartum
Plt count Low to very low Low to very low Low to very low Low to very low
PTT Normal to high High Normal Normal
Liver function test High to very high High to extremely Usually normal Usually normal
Antithrombin III
Low Low Normal Normal

85. Chronic kidney disease and
pregnancy

86. Relationship between pregnancy and
.kidney disease
 Effects of pregnancy  Effects of kidney
on kidney disease disease on pregnancy
 Worsening proteinuria  Infertility
 Loss of kidney function  Preterm delivery
 Hypertension and  IUGR
preeclampsia  Decreased fetal survival
 Preeclampsia

87. preserved/mildly reduced renal function, Cr < 1.4*1
good outcome for pregnancy and renal disease–
Moderately impaired renal function, Cr 1.4 – 2.8* 2
risk progression of renal failure, increased fetal risk–
Severe renal insufficiency, Cr > 2.8* 3
high fetal/maternal morbidity/mortality, low likelihood–
.of successful outcome, pregnancy discouraged

88. High grade proteinuria and severe*4
hypertension
also important risk factors for progression of –
.renal disease in pregnancy, worse outcomes

89. CKD and pregnancy – diabetic
nephropathy
of pregnant women with type I DM have overt 6%
diabetic nephropathy (<20/40: U prot>300mg/d,
macroalbuminuria >300mg/d, alb/creat. ratio
)>0.3mg/mg
Microalbuminuria also associated with an increased•
risk of adverse fetal-maternal outcomes
Effect of nephropathy on pregnancy:•
.prematurity(22%), IUGR(15%), pre-eclampsia

90. Effect of pregnancy on nephropathy:•
.exacerbation of proteinuria and hypertension
Return to baseline post-partum with well
.preserved renal function
Pre-eclampsia is the most frequent*
complication of pregnancy in women with
.diabetic nephropathy

91. CKD and pregnancy - ADPKD
Exacerbation of HTN, increased risk of pre-
.eclampsia
Prenatal genetic testing for PKD1 disease
.(C16) – available
No increased incidence of simple UTI during
.pregnancy

92. CKD and pregnancy - Lupus
 Rate of relapse not different between pregnant
women and concurrent controls (9-60%).
 Major factor determining a pregnancy related
exacerbation is the stability of the disease before
conception
 If in remission for >6mths pre-conception, low
incidence of clinical flare during pregnancy.
 Women with intracranial aneurysms may be at
increased risk of subarachnoid hemorrhage
. during labor

93. the frequency of exacerbations during
pregnancy was higher for women with
membranous nephropathy than for those
.with diffuse proliferative glomerulonephritis

94. Antiphospholipid antibody syndrome in
:-pregnancy
The presence of antiphospholipid antibodies or the
lupus anticoagulant is associated with increased fetal
;loss, particularly in the second trimester
;increased risk of arterial and venous thrombosis
manifestations of vasculitis such as thrombotic
microangiopathy; and an increased risk of
. preeclampsia
Treatment consists of anticoagulation with heparin and
.aspirin

95. LUPUS FLARE-UP VERSUS
PREECLAMPSIA
SLE PE
Proteinuria + +
Hypertension + +
RBCs cast + -
Azotemia + +
Low C3, C4 + -
Abnormal liver function - +/-
test results
Low platelet count + +/-
Low leukocyte count + -

96. End-stage renal disease
and pregnancy

97. ESRD requiring dialysis is associated with a
marked decrease in fertility. Pregnancy,
however, occurs in approximately 1% of
patients, usually within the first few years of
.starting dialysis

98. The fetal outcome is quite poor. Only 23-55% of
pregnancies result in surviving infants, and a large
number of second-trimester spontaneous abortions
occur. In addition, surviving infants have significant
morbidities. Approximately 85% of surviving infants
are born premature, and 28% are born SGA.
Maternal complications occur as well. Several
maternal deaths have been reported. Hypertension
worsens in more than 80% of pregnant females on
.dialysis and is a major concern

99. :-Recommendations
Some general recommendations apply to patients who become pregnant
while receiving dialysis. Place the patient on a transplant list (if not on
already) because outcomes with allograft transplant patients are
markedly better. During hemodialysis, uterine and fetal monitoring and
make every attempt to avoid dialysis-induced hypotension. Some
evidence indicates that the use of erythropoietin may improve fetal
survival; however, no findings from randomized studies supports this.
Erythropoietin can also increase hypertension and must be used
cautiously. Increased frequency of dialysis may improve mortality and
morbidity. Aggressive dialysis to keep BUN levels less than 50 mg/dL
may be need daily dialysis. Controlling uremia in this fashion may
avoid polyhydramnios, control hypertension, and improve the mother's
.nutritional status

100. Medications
Common Safety issues Comments
medications in
CKD/ESRD
Erythropoietin. 1 Safe to use .Limited data
Iron. 2 Safe to use Low dose
intravenous iron
recommended
Vitamin D. 3 Widely used .Limited data
Heparin. 4 Safe to use Minimize dose of
heparin

101. Transplantation and
pregnancy

102. Guidelines for pregnancy in kidney
:-transplant recipient
 Two years post-transplant, with good general
health and serum creatinine less than 2.0 mg/dL
(preferably <1.5 mg/dL(.
 No recent or ongoing rejection .
 Normotension, or minimal antihypertensives
 Absent or minimal proteinuria
 No evidence of pelvicalyceal dilation on renal
ultrasonogram

103. :-Immunosuppression
 Prednisone - Less than 15 mg per day
 Azathioprine - Less than or equal to 2 mg/kg/d
 Calcineurin inhibitor–based therapy -
Therapeutic levels
 Mycophenolate mofetil and sirolimus -
Discontinue 6 weeks prior to conception
 Methylprednisolone - The preferred agent for
treatment of rejection during pregnancy

104. Common medications in kidney
transplantation
Prednisone. 1 Safe to use Fetal adrenal insuffi ciency
Cyclosporine. 2 Safe to use IUGR
Tacrolimus. 3 Not safe to use Severe IUGR, renal
failure, hyperkalemia
Mycophenolate.4 Not safe to use Teratogenic in animals
mofetil
Azathioprine. 5 Widely used Fetal neutropenia,
teratogenic in high doses
Polyclonal. 6 Not safe to use Very limited data
antibodies

105. :-Complication Risks
 Immunosuppressive agents increase the risk of
hypertension during pregnancy.
 Preeclampsia occurs in approximately one-third of
transplant recipients.
 Almost 50% of pregnancies in these women end in preterm
delivery due to hypertension.
 Blood levels of calcineurin inhibitors need to be frequently
monitored due to changes in volumes of distribution of
extracellular volume.
 There is an increased risk of infection included
cytomegalovirus, toxoplasmosis, and herpes infections,
and bacterial infection which arouse concern for the fetus.