1. Liver and Kidney diseases
in pregnancy
Prepared by: Rita Batta
Supervised by: Dr.
Molham Al.Sukhon

2. Liver diseases during
pregnancy
The liver diseases unique to
pregnancy include;
 Intrahepatic cholestasis of pregnancy
(ICP)
 Acute fatty liver of pregnancy (AFP)
 HELLP syndrome.

3. Intrahepatic cholestasis of
pregnancy (ICP)
 reversible type of hormonally influenced
cholestasis
 Is the most common pregnancy-related liver
disorder
 usually develops during the last third of
pregnancy, when hormone levels are highest
in approx. 1% of pregnant women.
 Risk factors include;
twins or triplets or oral CCPs, previous ICP,
sister or mother with ICP.
 ICP has no clear etiology, and it is believed to
be a multifactorial disorder with
environmental, hormonal, and genetic
contributions

4. symptoms
 Sudden onset of sever pruritus (without a rash)
that increase in intensity and characteristically
starts in the soles of the feet and palms of the
hands and progresses to the trunk and face and
worsen at night
 Loss of sleep, loss of appetite, and an inability to
perform normal daily tasks can be a result of the
intense itching.
 Less common symptoms (<10% of patients)
include dark urine and/or pale stools (greyish in
colour), jaundice abd. Pain and nausea.
 Steatorrhea and vitamin K deficiency may also
occur due to fat malabsorption
 If the vitamin K deficiency is not corrected by the
time of delivery, a postpartum hemorrhage may
ensue.

5. Lab. tests
1. The most specific and sensitive marker of ICP is total
serum bile acid (BA) levels >10 micromol/L
2. The elevation of aminotransferases associated with
ICP varies from a mild increase to a 10- to 25-fold
increase.
3. Elevated CA:CDCA
4. Total bilirubin levels are also increased but usually the
values are less than 5 mg/d
5. Alkaline phosphatase (AP) is elevated in ICP up to 4-
fold
6. alanine aminotransferase (ALT) is the most sensitive
of the conventional liver tests for diagnosis of ICP in the
presence of pruritus without a rash. (AST) values
greater than 40 IU/L as partial criteria for the diagnosis
of ICP.
7. Mild elevation of gamma glutamyltransferase (GGT) is

6. Impact on fetus
 increased risk for infant stillbirth
(intrauterine death of the baby)
 premature labour
 fetal distress.
 If vit-K is deficient – bleeding in both
mother and child

7. Management
 Antenatal testing (umbilical artery Doppler
studies, biophysical profile (BPP), and NST )
to reduce the risk of stillbirth.
 Delivery should be induced at 37 weeks’
without an amniocentesis for fetal lung
maturity due to increased risk of fetal
mortality, or after an amniocentesis for
delivery prior to 37 weeks’ gestation.
 If meconium is present at the time of
amniocentesis, delivery is indicated
regardless of the fetal lung maturity results.
 Delivery can proceed without an
amniocentesis if the fetal monitoring is
nonreassuring.

8. Medications
 Drug of choice is Ursodeoxycholic
acid (UDCA) at a daily dose ranging
from 600-2000 mg .
Others;
 phenobarbital (100 mg qd)
 hydroxyzine (25-50 mg qd)
 cholestyramine (8-16 g/d)
 dexamethasone (12 mg 4 times daily
for 7 days followed by a tapering
dose).

9. Acute fatty liver of pregnancy
 A serious complication unique to pregnancyby
characterized by microvesicular fatty infiltration of
hepatocytes
 It’s a rare condition (1 in 7000-20,000
deliveries).
 It is more common with multiple gestations and
possibly in women who are underweight.
 Acute fatty liver occurs typically in the third
trimester.
 The foremost cause of AFLP is thought to be due
to a mitochondrial dysfunction in the oxidation of
fatty acids leading to an accumulation in
hepatocytes
 The infiltration of fatty acids causes acute liver
insufficiency

10. Presentation
Clinical presentation of acute fatty liver of
pregnancy (AFLP) is nonspecific, and the
patient can present with the following
complaints:
 Malaise
 Nausea and vomiting (70%); this may present for
the first time in the third trimester
 RUQ and epigastric pain (50-80%)
 Upper GI hemorrhage
 Acute renal failure
 Infection
 Pancreatitis
 Hypoglycemia
 Fulminant liver failure with hepatic encephalopathy

11. Lab. Tests
 Elevated AST and ALT >300 IU/L
 Decreased blood glucose levels .
 Liver detoxification is also affected, resulting in
elevated levels of blood ammonia
 In addition, laboratory findings may be consistent
with disseminated intravascular coagulation
(DIC)
 Bilirubin levels are elevated. This elevation is
primarily the conjugated form, with levels
exceeding 5 mg/dL. This can result in jaundice,
which is rarely seen in patients with other forms
of pregnancy-related hepatic injury, including
preeclampsia.
 As the maternal kidneys become affected,
blood creatine and uric acid can become
elevated, leading to metabolic acidosis.

12. Impact on fetus
 The toxic products accumulate in the
mitochondria and can cause degeneration
and fatty infiltration of muscle fibres. This
affects both skeletal and cardiac muscle
development. The liver becomes enlarged
with lipid depositions within the hepatocytes.
There may be progressive jaundice
associated with impaired bilirubin
metabolism.
 At the time of diagnosis, infants frequently
have severe liver failure, severe
cardiomyopathy and hypoketotic
hypoglycemic hepato-encephalopathy

13. Management
 Delivery of the fetus, regardless of gestational age,
is the only treatment for acute fatty liver of
pregnancy (AFLP) once the diagnosis has been
made. And the mode of delivery depends on :
 Fetal status: Many fetuses demonstrate evidence
of asphyxia and hypoxia; therefore, close
monitoring of fetal status is necessary, along with
the ability to expedite delivery should fetal
compromise be evident.
 Maternal coagulation status: Due to coagulation
abnormalities that can accompany AFLP, patients
may need to have replacement of their coagulation
factors should cesarean delivery be necessary.
 Likelihood of success with IOL : If delivery cannot
be safely accomplished within 24 hours from the
time of diagnosis, then cesarean delivery may be
optimal.

14.  Management of sever hypoglycemia
(5% dextrose)
 Fluid replacement (hemorrhage affect
Renal- ATN)
 using postpartum plasma exchange (
plasmapheresis) to treat severe cases
of AFLP in the postpartum period (esp.
encephalopathy or multi-irgan
damage)

15. Renal disease during
pregnancy Renal disease can affect the outcome of pregnancy,
pregnancy can affect the progression of pre-existing
renal disease, and pregnancy can itself cause renal
impairment
 Physiologic changes on renal system:
◦ Anatomical;
o increase in overall kidney size by about 1-1.5 cm
o dilation of the urinary collecting system ; stasis
◦ Renal plasma flow increases by 50-70%
◦ Increased GFR by 50%.
◦ Therefore, both urea and creatinine levels are decreased.
◦ A change in tubular function with increased glycosuria.
◦ Increase urine pH
 In general, the physiological changes peak by the end
of the second trimester and then start to return to pre-
pregnancy levels; anatomical changes generally take
up to three months postpartum to subside.

16. Generally; UTIs incidence increases in
pregnant women due to the physiologic
changes mentioned earlier, in addition
to the difficulty with hygiene due to a
distended pregnant belly the already
short urethra
 untreated asymptomatic bacteriuria
(15%) is an important risk factor for
pyelonephritis (25-30%).

17. Acute pyelonephritis
 An inflammation of the
renal parenchyma ,calyces,
and pelvis.
 It is commonly caused by bacterial
infection (ascending or descending).
 It’s an upper UTI
 one of the most common medical
complications of pregnancy (1-2)%

18. Pathogenes:
a. E.coli (75-90)%
b. Klebsiella (10-15)%
c. Proteaus species (5%)
d. Others; Pseudomonas, staph. and strep.
groups B and D
Clinical Findings:
 Fever, chills, malaise, dysuria, frequency
 CVA pain/tenderness
 50% unilateral right sided flank pain
 25% bilateral or unilateral left sided flank pain
Laboratory Findings:
 Pyuria, bacteriuria
 White blood cell casts highly predictive
 Positive urine culture
 10 – 20% bacteremic

20. Pyelonephritis in Pregnancy
Complications
 Multi-organ system involvement in 20%
 Anemia due to hemolysis in up to 66%
 DIC with severe sepsis
 Transient renal dysfunction in 20%
 ARDS in 2 – 8%, especially with:
• Tachycardia >110 BPM
• Fever >38.5 in first 24 hours
• Fluid overload
• Tocolytic therapy
 Preterm Labor

21. Pyelonephritis in Pregnancy
Disease Categorization
Outpatient management after
inpatient observation and initial
parenteral Rx. can be considered
with 14 day oral antibiotic therapy
(Amoxicillin/Clavulanat )
Inpatient management is required
IV fluids and parentral;
Ceftriaxone, Cefotetan,
Cefotaxime, Gentamicin,
Ampicillin/Sulbactam,
Piperacillin/Tazobactam.
Mild / Moderate
• Low-grade Fever
• Normal or slightly
elevated white blood cell
count
• Absence of Nausea or
Vomiting
Severe
• High Fever
• Respiratory Insufficiency
• Poor urine output
• Sepsis
• Unable to tolerate oral intake or
antibiotics
• No improvement during initial /
observational phase

22. ACUTE RENAL FAILURE

23. The underlying causative
factors may be;
 prerenal :
a history of blood or fluid
loss.
 Renal:
direct damage to kidney by
inflammation, toxins, drugs
or infections
 Postrenal:
urologic obstructive
conditions.
Acute renal failure
Pro

24. Acute renal failure in
pregnancy
challenging clinical problem that requires understanding normal physiology
of the kidney in pregnancy and the natural history of different underlying
renal diseases
 prerenal
hyperemesis gravidarum and uterine hemorrhage, as in abruptio
placentae , hemorrhage folloing spontaneous abortion
 Renal
causes in the pregnant woman include acute pyelonephritis and
septic abortion. Renal cortical necrosis, hypercoagulable state, such
as TTP or HUS. Prolonged hypotension can lead to acute cortical
necrosis or ATN.
 Post-renal
The most likely causes are the gravid uterus, polyhydramnios,
kidney stones, and enlarged uterine fibroids. Obstructive uropathy
usually resolves with delivery, although ureteral stenting may be
required preterm.

25.  Those conditions that cause renal
failure unique to pregnancy must
always be considered when renal
function deteriorates in the last
trimester or the postpartum period.
 Severe preeclampsia, acute fatty liver
of pregnancy, and idiopathic
postpartum acute renal failure may all
present similar complications.
Impact on fetus :

26. classification
 Early pregnancy
Prerenal azotemia, ATN, RCN,
pyelonephritis,TTP, HUS.
 Late pregnancy
Sever pre-eclampsia, HELLP, ATN,
acute fatty liver disease.
 Post partum
Days to wks. Retained placental
fragments

27. symptoms
 bloody stools
 breath odor
 slow, sluggish
movements
 swelling - generalized
(fluid retention)
 fatigue
 pain between ribs and
hips
 hand tremor
• prolonged bleeding
• seizures
• nausea
• vomiting
• elevated blood pressure
• metallic taste
•decreased sensation,
especially in your hands
or feet
Lab. Tests:
 BUN
 Creatinine clearance
 Serum creatinine
 Serum potassium
 Urinalysis (WBCs,RBCs or hyaline
casts) tubular cells.

31. CHRONIC RENAL FAILURE
 The outcome of pregnancies
complicated by chronic renal disease
is less favorable.
 High fetal/maternal morbidity and
mortality
 Low liklihood of successful outcome
 Pregnancy is discouraged
 Poor prognosis

32. Pregnancy in patients
receiving dialysis
 Although fertility is significantly impaired in
women with end-stage renal disease,
pregnancy may still occur.
 Most women on dialysis are anovulatory, with
either irregular or no menses, which can
result in significant delays in the diagnosis of
pregnancy in those who do conceive.
 In addition, the spontaneous abortion rate for
pregnant women who require dialysis is
approximately 50%.
 For pregnancies that continue, however, the
fetal survival rate is as high as 71%.

33. Pregnancy in women with
kidney transplants
 Pregnancy in women following renal
transplantation has become
commonplace.
 Transplantation restores fertility, and
although most women with kidney
transplants can deliver successfully,
there is a higher risk of miscarriage,
therapeutic abortion, stillbirth, ectopic
pregnancy, preterm birth, low
birthweight babies, and neonatal
death.

34. Guidelines for pregnancy in kidney
transplant recipients include the following:
 Good general health for 2 years post-
transplantation, with serum creatinine levels
below 2.0 mg/dL (preferably < 1.5 mg/dL)
 No recent acute rejection or ongoing rejection
 Normotension, or hypertension controlled
with minimal antihypertensive agents
 No or minimal proteinuria
 No evidence of pelvicaliceal dilatation on
renal ultrasonogram

35. The following are complication risks in
kidney transplant recipients:
 Immunosuppressive agents increase the risk
of hypertension during pregnancy
 Preeclampsia occurs in approximately one
third of kidney-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
cytomegalovirus, toxoplasmosis, and herpes
infections, which raise concern for the fetus