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Dr. Shreyash Trived
Dr. (Prof.) V. Priyadarshi Unit
AGENDA
 Renal adaptation to pregnancy
 UTI and acute pyelonephritis
 Hypertensive disorders of pregnancy
 Acute kidney injury in pregnancy
 Chronic kidney disease and pregnancy
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
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.
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.
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.
UTI And Acute Pyelonephritis
 Most frequent renal problem encountered during
gestation.
 Asymptomatic bacteriuria in pregnancy
 Acute pyelonephritis in pregnancy
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.
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
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.
Contd..
 Suppressive therapy with nitrofurantoin or cephalexin
is recommended for those patients with bacteriuria
that persists after two courses of therapy.
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
HYPERTENSIVE DISORDERS
IN PREGNANCY
GESTATIONAL HTN: WORKUP
 Determine the severity of HTN
 24 hour urinary protein
 Evaluate for the signs/symptoms of preeclampsia
 R/O end organ damage
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.
Contd…
 SEVERE Gestational hypertension:
1. SBP>/= 160 and DBP>/= 110 – treat with
antihypertensive agents.
2. >34 weeks – deliver.
3. <34 weeks– give steroids.
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.
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.
PRE -ECLAMPSIA
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.
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.
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.
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.
MANAGEMENT AND TREATMENT
 OBJECTIVES:--
1. Prevention of complications.
2. Prevention of eclampsia.
3. To ensure minimal fetal and maternal morbidity.
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.
INVESTIGATIONS BP check– 4 times per day.
 Platelet count
 Coagulation profile
 Uric acid
 Creatinine
 LFT.
 24 hour urinary protein
 Ophthalmoscopy
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
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
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.
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.
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.
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.
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.
ACUTE KIDNEY INJURY IN
PREGNANCY
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
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
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
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
_
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.
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
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
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
Chronic kidney disease and
pregnancy
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.
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
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
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.
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.
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
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.
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.
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
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.
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,
 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
Thankyou
for kind attention

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Renal diseases and 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.
  • 7.
  • 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
  • 15.
  • 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.
  • 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
  • 30.
  • 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