Helpful for better management of renal diseases in pregnancy

1. Dr. Shreyash Trived
Dr. (Prof.) V. Priyadarshi Unit

2. AGENDA
 Renal adaptation to pregnancy
 UTI and acute pyelonephritis
 Hypertensive disorders of pregnancy
 Acute kidney injury in pregnancy
 Chronic kidney disease and pregnancy

3. Renal adaptation to pregnancy
 Kidney length increases by 1-1.5 cm and volume by
30%.
 Physiological dilatation of the urinary collecting
system with hydronephrosis in 80% of women, more
pronounced on the right side
 Estrogen, progesterone and prostaglandins may also
affect ureteral structure and peristalsis

4. Contd..
 Renal plasma flow increases out of proportion to GFR.
 GFR increases by 40-65% as a result of an even larger
increase of renal blood flow.
 The increase in GFR results in a physiological decrease
in creatinine, urea and uric acid levels.
 Creatinine clearance rises to 150-200ml/min and
average serum creatinine decreases to 0.5-0.6 mg/dl.
 Thus a serum creatinine level of 1mg/dl which is
normal in nonpregnant state may reflect renal
impairment in the pregnant patients.

5. Contd..
 Blood urea nitrogen(BUN) decreases from an average
13 to 8-10 mg/dl
 A reset in the osmostat occurs, resulting in increased
thirst and decreased serum sodium levels (by
approximately 5 mEq/L) compared with non-pregnant
females and also decreased osmolality.

6. Contd..
 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 non-pregnant population.

8. UTI And Acute Pyelonephritis
 Most frequent renal problem encountered during
gestation.
 Asymptomatic bacteriuria in pregnancy
 Acute pyelonephritis in pregnancy

9. Asymptomatic bacteriuria in
pregnancy
 Needs to be treated more aggressively in the setting of
pregnancy.
 Untreated in pregnancy, can lead to overt cystitis and
pyelonephritis in up to 40% of patients.
 Increased risk of premature delivery and low birth
weight.

10. Screening
 Quantitative urine culture is preferred for screening.
 More than 1lakh bacteria/ml of a single species is
considered significant
 Screening is recommended during the first prenatal
visit and is repeated only in high risk women

11. Treatment
 If asymptomatic bacteriuria is found prompt
treatment is warranted, usually with a cephalosporin
for 3 to 7 days.
 A single dose of fosfomycin has also been used
successfully.
 A follow up culture two weeks after the therapy is
necessary to ensure eradication of bacteriuria.

12. Contd..
 Suppressive therapy with nitrofurantoin or cephalexin
is recommended for those patients with bacteriuria
that persists after two courses of therapy.

13. ACUTE PYELONEPHRITIS
 Pyelonephritis
 70% have asymptomatic bacteriuria
 Mostly in second trimester
 Symptoms – Pain, fever, dysuria
 Complication – Endotoxic Shock, DIC, ARF
 Treatment
 Hydration
 IV Antibiotics
 Change to oral antibiotics for 10-14 days

14. HYPERTENSIVE DISORDERS
IN PREGNANCY

16. GESTATIONAL HTN: WORKUP
 Determine the severity of HTN
 24 hour urinary protein
 Evaluate for the signs/symptoms of preeclampsia
 R/O end organ damage

17. GESTATIONAL HTN: MANAGEMENT
 MILD Gestational hypertension:
 Managed as outpatients
 No anti hypertensive therapy
 No antenatal steroids
 Regular monitoring of fetal well being with the help
of obstetrician.
 Deliver patients no later than EDD.

18. Contd…
 SEVERE Gestational hypertension:
1. SBP>/= 160 and DBP>/= 110 – treat with
antihypertensive agents.
2. >34 weeks – deliver.
3. <34 weeks– give steroids.

19. GESTATIONAL HTN
 15-25% risk of progression to preeclampsia.
 22-47% risk of recurrence in subsequent pregnancy.
 Associated with development of hypertension later in
life.

20. PRE ECLAMPSIA
 It is a multisystem disorder of unknown etiology.
 In normal pregnancy the interaction between
vasodilator and vasoconstrictor systems stabilizes the
BP.
 In preeclampsia this balance is lost due to endothelial
dysfunction which is preceded by decreased uterine
blood flow and placental ischemia.
 Resulting vasospasm affects almost all the vessels,
most importantly uterus, kidney and brain.

21. PRE -ECLAMPSIA

22. BASIC MECHANISM OF MULTIPLE
ORGAN DAMAGE
 Increased vasoconstriction.
 Decreased organ perfusion.
 Increased endothelial dysfunction– capillary leak-
edema, pulmonary edema, proteinuria.
 Activation of coagulation: DIC, reduced platelets.
 Hemoconcentration.

23. RENAL SYSTEM INVOLVEMENT
 Decreased renal perfusion d/t decreased blood volume
and increased afferent arteriolar pressure .
 Decreased GFR d/t:
1. Glomerular capillary endotheliosis.
2. Endothelial damage.
3. Mesangial swelling and disruption of basement
membrane.

24. SCREENING
 Adequate antenatal care.
 Risk assessment– nulliparous women or women with
other risk factors should be assessed more frequently
during the third trimester.
 Uterine artery Doppler ultrasound may detect
abnormal uterine artery waveform– this is presently
the most promising screening procedure.
 Biomarkers for pre eclampsia– Placental protein
13(PP13),Sflt1, PIGF.

25. PREVENTION
 Many strategies have been studied, unfortunately none
have proven unequivovally effective.
1. Aspirin (75mg OD)– is only recommended in high
risk pregnancies.
2. Calcium supplementation– should be considered in
women with low baseline calcium intake and high
risk.

26. MANAGEMENT AND TREATMENT
 OBJECTIVES:--
1. Prevention of complications.
2. Prevention of eclampsia.
3. To ensure minimal fetal and maternal morbidity.

27. HOSPITALISATION
 Ideally every patient should be hospitalised for
detailed evaluation.
 Mild uncomplicated preeclampsia – rest, high protein
diet and sedatives are prescribed– patient is
investigated and checked after one week or earlier– if
treatment fails pt is to be admitted.
 She should be warned against ominous symptoms–
headache, visual disturbance, vomiting , epigastric
pain, scanty urine.

28. INVESTIGATIONS BP check– 4 times per day.
 Platelet count
 Coagulation profile
 Uric acid
 Creatinine
 LFT.
 24 hour urinary protein
 Ophthalmoscopy

29. Treament modalities Restricted physical activity.
 Diet– adequate amt of protein(100gm), calorie
Sedatives– Diazepam 5mg at bed time.
 Antihypertensives:--
Methyl dopa- 250-500 mg tid to qid
Labetalol- 200 mg tid
Nifedipine- 10-20 mg bid
Hydralazine- 10-25 mg bid
 Diuretics are avoided
 ACEI and ARBs are contraindicated

31. TIMING OF DELIVERY
 The definitive treatment of preeclampsia is delivery.
 Timing of delivery depends upon:
1. Severity
2. Duration of pregnancy
3. Response to treatment

32. Contd..
 Depending upon the response to treatment, pts are
grouped into:
A. Preeclamptic features completely subside.
B. Partial control– BP at steady high level.
C. Severely increased BP with ominous signs.

33. Contd..
 Group A– 1. Remote from term pt is discharged with
advice to follow up after one week. 2.Near term she
should be kept till completion of 37th week.
 Group B-- >37 weeks– termination without delay.<37
weeks– expectant treatment upto 34 weeks with
continuous monitoring.
 Group C– termination is considered irrespective of the
duration of pregnancy.

34. Contd..
 Magnesium and seizure prophylaxis—
used in severe preeclampsia—
loading dose– 4-6 gm i.v over 15-20 minutes
maintenance dose– 1-2 gm/hr i.v infusion
With continuous monitoring for toxicity.

35. MANAGEMENT OF ECLAMPSIA
 Resuscitation – maintain airways.
 Oxygen inhalation.
 Anti convulsants– MgSO4 is the agent of choice.
 Hemodynamic stabilisation– fluids
 Deliver by 6-8 hrs.
 Postpartum care.

36. MANAGEMENT OF CHRONIC
HYPERTENSION IN PREGNANCY There is little evidence that treatment of mild to
moderate hypertension has a clear benefit for either
mother or fetus.
 Aggressive treatment of mild to moderate
hypertension may adversely affect fetal growth.
 Current guidelines suggest that treatment should be
initiated only if there is evidence of end organ damage
or BP exceeds 150-160/100-110.
 In those receiving therapy prior to pregnancy, tapering
or discontinuing therapy should be considered unless
BP exceeds these levels.

37. ACUTE KIDNEY INJURY IN
PREGNANCY

38. AKI in Pregnancy
 Incidence of ARF in pregnancy is 1:20000
 Causes of renal failure in pregnancy can be divided
into :
 Early pregnancy:- 1. Hyperemesis gravidarum, 2. Septic
abortion.
 Late pregnancy:-PIH and its complications, HELLP,
Post- partum HUS, Acute fatty liver of pregnancy, Vol
loss-APH, PPH, sepsis

39. Causes of AKI
 The most common cause of AKI during pregnancy is
prerenal azotemia due to hyperemesis gravidarum or
vomiting from acute pyelonephritis
 Pregnancy-specific conditions- preeclampsia, HELLP
syndrome, and acute fatty liver of pregnancy are
complicated by acute renal failure.
 Obstetric complications- septic abortion and placental
abruption are associated with severe acute tubular
necrosis and bilateral cortical necrosis
 Obstructive uropathy

40. TYPES OF ACUTE RENAL FAILURE
ACUTE TUBULAR
NECROSIS
RENAL CORTICAL
NECROSIS
Less serious serious
Reversible Irreversible
a/w sepsis & htn a/w obstetric causes&
pre-eclampsia
Kidney lesion- focal,
dilatation & flattening of
epethelium of
DCT,pigmented cast in
lower part of nephrons
Kidney lesion-
focal,patchy
confluent/gross resulting
from thrombosis of renal
vascular system

41. TYPES OF ACUTE RENAL FAILURE
ACUTE TUBULAR
NECROSIS
RENAL CORTICAL
NECROSIS
Patint have high grade
temperature, vomiting,
diarhoea
Oliguria which can lead to
anuria, azotoemia
&consumptive
coagulopathy
Shock occurs rapidly &
may have mild jaundice,
pallor& cyanosis
Extra-renal manifestations
like cardic dilatation, CHF,
lethargy, convulsions
Most patient respond to
volume resuscitation
&vigorous antibiotics in
ICU
_

42. Treatment of AKI in pregnancy
 Supportive—prompt restoration of volume deficits,
antibiotics and in later pregnancy expedient delivery.
 Acute cortical necrosis– no specific therapy; dialysis
when needed.

43. TTP/HUS
 Pregnancy appears to be a/w increased risk of TTP (
usually before 24 weeks of gestation) and HUS ( near
term or post partum).
 HUS/TTP is characterized by thrombocytopenia,
hemolysis, and variable organ dysfunction including
acute renal failure.
 Patients are thought to have TTP when neurological
symptoms dominate, and HUS when renal failure is
the dominant presenting feature

44. ACUTE FATTY LIVER OF
PREGNANCY
 c/f- abdominal pain and jaundice, typically occurring after
week 34 of gestation.
 Bilirubin is elevated, with mild elevations of aspartate
aminotransferase and alanine aminotransferase levels also.
Severe cases can present with fulminant hepatic failure.
 The disorder is commonly associated with acute renal failure.
 Noninvasive imaging can also provide evidence of fatty liver.
 Pathogenesis- microvesicular fatty infiltration of
hepatocytes, which may related to defective mitochondrial
beta-oxidation of fatty acid
 Rx- Immediate delivery and supportive care. Most patients
fully recover

45. CLINICAL
FEATURES
HUS/TTP HELLP AFLP
Hemolytic anemia +++ ++ +/-
Thrombocytopeni
a
+++ ++ +/-
Coagulopathy - +/- +
CNS symptoms ++ +/- +/-
Renal failure +++ + ++
Hypertension +/- +++ +/-
Proteinuria +/- ++ +/-
Elevated AST +/- ++ +++
Elevated bilirubin ++ + +++
Anemia ++ + +/-
Ammonia Normal Normal High
Effect of delivery
on disease
None Recovery Recovery
Management Plasma Exchange Supportive care,
Delivery
Supportive care,
Delivery

46. Chronic kidney disease and
pregnancy

47. CKD AND PREGNANCY
 Women who enter pregnancy with chronic renal
disease are at increased risk for adverse maternal and
fetal outcomes, including rapid decline of renal
function and perinatal mortality.
 Frequency of live births now exceeds 90% in these
women, the risk for preterm delivery, IUGR, perinatal
mortality, and preeclampsia are significantly elevated.

48. Contd..
 Overall maternal and fetal prognosis correlates with
the degree of hypertension, proteinuria, and renal
insufficiency prior to conception.
 Current consensus suggests the degree of renal
insufficiency, rather than the underlying renal
diagnosis, is the primary determinant of outcome

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

50. Contd..
1. Preserved/mildly reduced renal function, Cr < 1.4
– good outcome for pregnancy and renal disease
2. Initiating pregnancy with S. creatinine >2mg/dl
– >30% risk for accelerated decline in renal function
3. Severe renal insufficiency, Cr > 2.5
– >70% preterm labour and >40% experience
preeclampsia.

51. Diabetic nephropathy
 Pregnant women with diabetic nephropathy may also
develop worsening proteinuria and hypertension.
 Complications- preeclampsia
still birth
 Good control of blood glucose & blood pressure
before and during pregnancy improves perinatal &
maternal out come.

52. LUPUS NEPHRITIS AND
PREGNANCY
 SLE increases the risk of adverse pregnancy outcomes.
 Superimposed renal disease increases the risk even
further.
 Specific subsets of women with SLE are at especially
high risk—
-- women with SLE and antiphospholipid
antibody.
-- proliferative lupus nehritis

53. Contd..
 Women with lupus should postpone pregnancy until
lupus activity is quiescent and immunosuppressives
are minimized.
 Prophylactic therapy with steroids does not appear to
prevent a lupus flare during pregnancy
 Immunosuppressive (e.g., steroids, azathioprine) have
been used to manage lupus flares during pregnancy.

54. LUPUS FLARE AND PREECLAMPSIA
 Unfortunately, both syndromes share the common
presenting symptoms of hypertension and proteinuria,
hence distinguishing the two can be a clinical
challenge.

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

56. Pregnancy in Renal Transplant
Patients
 Successful renal transplantation results in return to
normal hormonal level and fertility within 6 months
of in approx. 90% women of child bearing age.
 There is substantial risk of low birth weight, pre term
delivery and ectopic pregnancy.
 American Society of Transplantation currently
suggests that for women on stable, low doses of
immunosuppressive agents, with normal renal
function, and with no prior rejection episodes,
conception could be safely considered as early as 1 year
post transplant.

57. Contd..
 Pregnancy itself does not appear to adversely affect
graft function in transplant recipients, provided
baseline graft function is normal and significant
hypertension is not present.
 The most common complication of pregnancy in
transplant recipients is hypertension, which affects
between 30% and 75% of pregnancies among
transplant recipients.
 Preeclampsia complicates 25% to 30% of pregnancies
in renal transplant patients,

58.  Antihypertensive agents of choice include methyldopa,
nonselective β-adrenergic antagonists (i.e., labetalol),
and calcium channel blockers.
 Cyclosporine (or tacrolimus) and steroids, with or
without azathioprine, form the basis of
immunosuppression during pregnancy
 Although high-dose steroids have been associated with
fetal malformations and maternal infections, this
remains a mainstay of treatment of acute rejection
during pregnancy

59. Thankyou
for kind attention