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RENAL DISORDERS IN
PREGNANCY
DR SEEMA NISHAD
DNB
OBS AND GYNAE
• Normal changes during pregnancy
• Urinary tract infections- Asymptomatic bacteriuria
- Acute pyelonephritis
• Acute nephrolithiasis
• Acute renal failure
• Chronic renal failure
• Hemolytic-Uremic syndrome
• Renal cortical necrosis
• Nephrotic syndrome
• Renal transplant and pregnancy
NORMAL CHANGES DURING PREGNANCY
Anatomic
- 1 cm increase in length of kidneys due to
hypertrophy of glomeruli.
- Dilatation of the collecting system (calyces, renal
pelvis, ureters)
Physiologic
- Renal plasma flow - increase by 40-50%,
maximum at 16 wks, maintained until 34 wks,
then falls by 25%.
- 50% increase in GFR
- Increase clearance of creatinine, blood urea
nitrogen and uric acid from maternal blood.
- Decreased Tubular reabsorption of glucose, uric
acid, amino-acids and water soluble vitamins.
- Decreased afferent and efferent arteriolar
resistance
- Ureters – dilated due to pressure of gravid uterus
- Frequency of micturition in 1st and 3rd trimester
of pregnancy
- Creatinine clearance rises to 150-200ml/min and
average serum creatinine decreases to 0.5-0.6
mg/dl.
URINARY TRACT INFECTIONS
• Infections during gestation occur frequently.
• The bacteria, originally reside in the rectal or
anal area and from there colonize the
perineum, vaginal introitus, urethra, bladder
and eventually the pelvi-caliceal area and
kidney itself.
• Ascending bacterial infection affects only the
lower urinary tract (asymptomatic bacteriuria,
acute cystitis) but during pregnancy, 25-40%
may ascend to upper tract and may cause
acute pyelonephritis.
ASYMPTOMATIC BACTERIURIA
1. Incidence- 4 -10% of all pregnant women
2. Criteria for diagnosis-
• Urine analysis- > 10 leucocytes/ml,
• Dipstick test – reveals leucocyte esterase or nitrates.
High false positive and false negative results.
• > 105 colony forming units in single midstream catch
technique of sample collection
• >205 colony forming units/ml- diagnostic if sample by
catheterization
3. Complications- If untreated, 25-40% develop acute
pyelonephritis, preterm labor, low birth weight and
perinatal mortality.
3. Treatment- First episode by appropriate antibiotics
depending on prevalent resistance. 3 day course of
antibiotics is usually effective.
• Most effective oral regimen - Nitrofurantoin 100 mg
twice daily for 3-7 days (according to WHO)
• Amoxicilline 500 mg orally thrice daily x 3-7 days
• Amoxicilline-clavulanate 500 mg orally twice daily
3-7 days.
• Cephalexin 500 mg orally twice daily 3-7 days.
4. Success of treatment is confirmed by- urine
culture after 2 week of completion of
treatment.
5. If not cured or re-infection occurs, drugs
according to antibiotic sensitivity is used for
10 days.
6. In case of repeated infections, low daily dose
at night is continued till 4 weeks post-partum.
Nitrofurantoin 100 mg orally or Cephalexin
250 mg is given.
ACUTE PYELONEPHRITIS
• Incidence- 1-2% , > 50% cases occur in second
trimester.
• Symptoms- malaise ,fatigue, chills, fever ,
headache and back pain
• Signs- Fever, dehydration, costovertebral angle
tenderness (more on right side)
• Urinalysis - urine turbid or bloody, presence of
RBCs, WBCs, WBC cast, bacteria.
• RFT- elevated levels of S. Creatinine and BUN
• Investigations- Hemogram, renal function test,
serum electrolytes, urine culture and
sensitivity
• Histopathology- Infiltration of renal
interstitium and tubules with neutrophils
(formation of WBC cast)
• Cause – Ascending infections by bacteria
present in vagina or on perineum. Usually
caused by single species of bacteria. Most
common organism- Uropathogenic
Escherichia coli ( 70-95% of cases)
• Other causative organisms- Gram negative bacilli (as
Klebsiella pneumoniae, Proteus mirabilis),
enterococci, Staphylococcus saprophyticus.
• Treatment- Admission in hospital, hydration,
injectable antibiotics and careful monitoring of vitals
(Tachycardia and hypotension may indicate early
endotoxic shock), Pulse oxymetry, chest x-ray(to rule
out possibility of ARDS), uterine contraction and fetal
monitoring ( for preterm labor).
o Antibiotic of choice – Ampicillin 2 gms IV 4-6 hrly
o For Gram negative bacteria- best option- Cephazolin
2 gm IVPB 8 hrly
o Ceftrixone 1 gm IV 8 hrly
• When patient is afebrile for 24-48 hrs, switch to oral
drugs for 14 days.
• If patient do not respond within 72 hrs, or
relapse after discontinuation of therapy,
possibility of obstruction should be ruled out.
• Ureteral stents and percutaneous
nephrostomy may be needed in urinary
obstruction.
• Follow-up with urine culture is necessary.
• Complications – Hemolytic anemia,
Thrombocytopenia, ARDS, Preterm labor,
endotoxic shock, hypothalemic instability
ACUTE NEPHROLITHIASIS
• Incidence- 1 in 1500 deliveries, usually during second and
third trimester.
• Symptoms- severe flank pain which starts abruptly. (Site of
pain depends on site of stone), nausea, vomiting, dysuria.
• Urinalysis- presence of macroscopic or microscopic
hematuria, crystals (specific shape according to material of
stone)
• Renal ultrasound is test of choice. Transvaginal ultrasound
may detect distal ureteric stones. Limited IVP is a single flat
plate of abdomen, taken approximately 5 min after contrast
administration. This test has high sensitivity and minimal fetal
radiation exposure.
• 4 types of urinary stones- Calcium oxalate (80%), Magnesium
ammonium sulphate (15%), Uric acid stone(6%), cystein stone
(2%)
• When stone at renal
pelvis – pain occurs at
flank of respective side.
• When stone in ureter –
pain occur in lower
abdomen radiating to
groin and external
genitalia.
PHYSIOLOGICAL
HYDRONEPHROSIS
• Unilateral/ bilateral
• More marked on
right side
• Patient not severely
symptomatic
HYDRONEPHROSIS DUE
TO OBSTRUCTION
• Usually unilateral
• On side of patient’s
symptom
• Pain is relentless and
severe
• Treatment –
- 80% of pregnant women pass the stone
spontaneously and can be managed expectantly
with hydration and medication to relieve pain.
- High fluid intake to obtain minimum urinary
volume of 2 L/day.
- If no improvement after a reasonable period,
cystoscopic extraction can be done.
- In case of acute hydronephrosis due to
obstruction, cystoscopic passage of ureteral stent
and stone manipulation using retrograde ureteral
catheterization.
- If ureteral stent fails, per-cutaneous
nephrostomy should be done.
- Minimally invasive surgical procedures used
in post-partum period as shock wave
lithotripsy, percutaneous nephrolithotomy
and flexible ureteroscopy.
- Low calcium diet and thiazide diuretics –
beneficial for idiopathic hypercalciuria.
- Low purine diet for patient with uricosuria
and uric acid stone.
- Intensive treatment of chronic urinary tract
infections to prevent struvite stone.
ACUTE RENAL FAILURE
• Defined as –
 urine output < 400 ml in 24 hrs or <20 ml/ hr.
 Urine output < 0.5 ml/kg/hr for 6 hrs
 Increase of S Creatinine >0.3 mg/dL from base-line
 Increase of S. Creatinine > 1.5 times of the normal
• Incidence – decreased during recent years
significantly due to-
1. Diminished number of septic abortions
2. Judicious and early termination of severe pre-
eclampsia
3. Better management of shock
4. Appropriate management of abruptio placenta
5. Facilities of blood transfusion
CAUSES OF ARF IN PREGNANCY
PRE-RENAL CAUSES- due to renal hypoperfusion. Most
common form.
(A) Early pregnancy-
1) Acute and massive hemorrhage ( abortion, ectopic
pregnancy, hydatidiform mole)
2) Severe dehydration ( hyperemesis gravidarum)
3) Septic abortion (endotoxic shock, hypotension)
(B) Late pregnancy and labor-
1) Acute and massive hemorrhage ( PPH, Placenta
previa)
2) Abruptio placenta ( hypovolumia and DIC)
3) Severe pre-eclampsia and eclampsia, HELLP
syndrome
4) Acute fatty liver of pregnancy
5) severe infection ( chorioamnionitis, pyelonephritis)
(C)Other causes-
1. Mismatched blood transfusion
2. Thrombotic micro-angiopathy
3. Hemolytic uremic syndrome
RENAL CAUSES- Pre-existing renal disease- interstitial
nephritis, SLE, toxins, drugs ( NSAIDs,
aminoglycosides), obstetric pathology
superimposed on pre-existing renal pathology.
POST-RENAL CAUSES- Obstructive- accidental ligature
of ureters during caesarean section or
hysterectomy for rupture uterus.
ACUTE TUBULAR
NECROSIS
• Most common pathology in
obstetrics
• Less serious
• Reversible ( recovery in 1-2
weeks time)
• Associated with sepsis &
hypertension
• Kidney lesion- focal,
ischemic degeneration and
necrosis of renal tubules,
pigment and cast in lower
part of nephrons
RENAL CORTICAL
NECROSIS
• Relatively uncommon
• serious
• Irreversible
• Associated with obstetric
causes as abruptio
placentae and endotoxic
shock following Gram -
negative septicemia.
• Kidney lesion - focal, Patchy
/gross ischemic necrosis of
renal cortex resulting from
thrombosis of renal vascular
system
CLINICAL FEATURES- 4 phases-
1) Incipient phase - Marked diminution of urinary output.
2) Phase of anuria – Urinary output <100 ml in 24 hrs. Initially
patient looks well but gradually deteriorates if not treated
timely.
• Leucocytosis
• Scanty urine, protein in varying amount, presence of red cell
cast (s/o glomerular pathology)
URINALYSIS PRE-RENAL RENAL
URINARY Na < 20 mEq/L > 40 mEq/L
URINE OSMOLALITY >500 <350
FRACTIONAL
EXCRETION OF Na
< 1% >2%
• ECG- peak T wave, Absent P wave, prolonged QRS complex
( due to raised levels of potassium and magnesium)
3) (a) Phase of early diuresis - Favourable for recovery but S.
Creatinine, sodium, potassium, BUN, chloride levels are raised
continueously.
(b) Phase of late diuresis – Causes are-
• Osmotic diuresis due to high blood urea
• Functional inadequecy of tubular reabsorption
• Release of surplus fluid and electrolytes, mainly sodium and
potassium
4) Phase of recovery – Tubular epithelium regenerates, functions
re-established. May take about 1 yr for full recovery.
MANAGEMENT OF ARF –
1. To exclude post-renal cause (obstruction in ureters)
by USG.
2. Restore intravascular volume by appropriate fluid-
as by blood transfusion or PRBC transfusion in case
of massive haemorrhage, crystalloids and colloids
for mild and moderate haemorrhage.
3. Forced diuresis with use of Inj. Frusemide ( 80-120
mg) intravenously.
4. During phase of anuria, fluid balance is the goal.
Patient should not be overhydrated. Amount of fluid
to be transfused in calculated by-
Amount in vomitus + Gastric aspiration + Loss in
diarrhoea + Loss in sweating + 500 ml ( + 200 ml for
each degree of rise of temp. )
5. Protein and salt restricted diet, carbohydrate rich
diet. Glucose prevents protein catabolism and
production of urea and potassium is minimized.
( Prevention of complications)
6. Treatment of Hyperkalemia –
• Administration of insulin with infusion of 50%
Dextrose.
• Oral carbohydrate intake. Fruit juices must not be
given due to high content of potassium.
• Inj. Calcium gluconate 10 ml of 10% solution (
Reduces cardiotoxic effect of high potassium levels)
7. Treatment of Hyperphosphatemia – Restriction of
dietary intake of phosphate, phosphate binding
agents ( calcium carbonate, calcium oxalate)
8. Dialysis – Indication-
• Electrolyte abnormalities refractory to medical
treatment
• Volume overload with congestive heart failure and
pulmonary oedema refractory to standard therapy.
( Most common indication)
• Severe metabolic acidosis
• Uremia( BUN > 39 mg/dL or S. Creatinine > 5.65
mg/dl)
Continuous electronic fetal monitoring should be done
during dialysis. Hematocrit should be above 25%.
Risk of preterm labor is high, so parenteral
progesterone to be given. Placental abruption, sepsis
and heart failure can also occur.
9. Supportive therapy –
• Control of infections – Avoid nephrotoxic antibiotics.
• Intra-vascular volume overload – to be kept in check.
• Hemoglobin level to be maintained above 7 gm%, if
less, transfusion of PRBC should be done.
10. During phase of Diuresis – Fluid and electrolyte
balance to be maintained.
PROGNOSIS – Majority of patients recover without
sequelae. Prognosis of fetus is unfavourable, about
50% mortality.
CHRONIC RENAL FAILURE
• A linear relationship exists between the pre-
conceptional creatinine levels and risk of further
renal damage during pregnancy.
• Creatinine clearance is more accurate marker than
serum creatinine levels.
• Hypertension present at conception increases
perinatal mortality rates.
• Low sodium diet ( containing 1.5 gms), bed rest in
lateral position to improve GFR and small dose of
loop diuretics with caution should be given.
• Dialysis can be done as and when required during
expectant management.
• Antenatal visits at every 2 weeks and weekly after 32
weeks.
• Fetal growth assessed by USG and umbilical artery
Doppler studies. Bio-physical profile to be performed
weekly from 28 weeks onwards specially with
worsening renal failure, hypertension, proteinuria
and placental insufficiency.
• Delivery at term, if no deterioration. Caesarean
delivery only for obstetric indication.
• If deterioration in creatinine levels or creatinine
clearance of 25%, termination of pregnancy is
justified. Expectant management can be done if GA
between 24-31 weeks, normal well grown fetus and
blood pressure well controlled.
HEMOLYTIC UREMIC SYNDROME (HUS)
• HUS is a disease independent of pregnancy and closely
related to Thrombotic thrombocytopenic purpura.
• Thrombotic microangiopathy secondary to expoure to
enteropathic organisms, particularly E. Coli serotype
0157-H7.
• Characterized by sudden onset and rapid progression of
hemolytic anemia, thrombocytopenia and renal failure
usually in postpartum period, at any time from day 1 and
10 weeks after delivery.
• Pathophysiology – Damage to glomerular capillaries by
subendothelial deposits of fibrin, that separates the
endothelial cells from the basement membranes, leading
to reduced vascular lumen. Formation of microthrombi,
especially in afferent arterioles leads to renal ischemia.
• Microangiopathic hemolytic anemia and
thrombocytopenia occurs due to fragmentation of
RBCs and platelets during passage through affected
vessels.
• Most important D/D is HELLP syndrome.
• Persistence of symptoms and sign of HELLP
syndrome beyond postpartum day 3, raises the
probability of HUS. Diagnosis of HUS is more likely if
there is a symptom free period of several days after
delivery.
• Maternal mortality with HUS is 8 – 44%. Perinatal
mortality is also high, 30 -80 %.
CLINICAL
FINDINGS
HELLP
SYNDROME
TTP HUS
Onset After 28 weeks Median
23 weeks
Postpartum
Primary
menifestation
Hypertension,
Proteinuria
Neurologic
symptoms
Renal
failure
Fever Absent PRESENT Absent
Purpura Absent PRESENT Absent
VWF
multimers
Absent PRESENT PRESENT
RENAL CORTICAL NECROSIS
• This severe form of ARF is usually associated with
catastrophic obstetric complications such as
severe hypovolumia secondary to abruptio
placenta or placenta previa or amniotic fluid
embolism.
• Histology – Necrosis of all the elements of renal
cortex including extensive necrosis and
thrombosis of the renal vessels.
• Characterized by sudden onset of severe oliguria
or anuria with life threatening complications of
pregnancy.
• Prolonged oliguria and anuria with little or no
improvement of renal function is characterstic.
• Urine is frankly hematuric and urinary red cells are
dysmorphic and hypochromic with appearance of
collapsed empty sacs.
• Hematologic abnormalities characterstic of DIC.
• BUN and plasma Creatinine increase rapidly.
• Renal ultrasound demonstrates hypoechoic areas in
the renal cortex.
• Dialysis is required usually. Plasma exchange and
prednisolone to be continued even postpartum for 1
month. Delivery is advisable once diagnosis is
confirmed, as risk of maternal complication is high.
• Prognosis – poor, majority do not recover and
require chronic dialysis. Only 20 – 40% with partial
recovery and can live without dialysis.
NEPHROTIC SYNDROME
• Characterized by –
 Presence of proteinuria > 3 gms/24 hr
 S. Albumin < 3 gm/dL
 Edema
 Hypercholesterolemia
• Etiology –
1) pre-eclampsia
2) Diabetic nephropathy
3) Lupus nephritis
4) Primary glomerular disease
Etiology is strongly suggested by clinical history
DIFFERENTIAL DIAGNOSIS OF CAUSES OF NEPHROTIC
SYNDROME DURING PREGNANCY
HYPERTENSION
NO YES PRE-ECLAMPSIA
COMPLIMENTS
NORMAL LOW LUPUS NEPHRITIS
SELECTIVITY OF PROTEINURIA
LACK OF
SELECTIVITY
HIGHLY SELECTIVE MINIMAL CHANGE
URINE
SEDIMENT
NEPHROTIC
NEPHRITIC
DIABETES
IgA GLOMERULONEPHRITIS
• Complications – Hypertension, fetal growth
restriction, preterm birth, fetal distress.
• Management –
1) General measures –
o Moderate physical activity, avoid prolonged
periods of standing up or sitting.
o Increased periods of bed rest in left lateral
position,
o diet rich in high quality protein,
o Sodium intake adjustment if patient is
hypertensive or excessive accumulation of
sodium and water.
2) Antihypertensive treatment
3) Monitoring of renal function –
o S. Creatinine every 4-6 weeks
o Daily qualitative determination of urine
protein
o If significant change in urine protein with
albustix strips, quantitative protein
determination of 24 hr urine is done.
o Renal function tests at least twice every week
by measuring BUN, S. Creatinine, uric acid and
electrolytes. Urine protein creatinine ratio
(normal < 0.15) becomes > 3.5.
4) Prophylactic antibiotics – as there is high risk of
development of infections, particularly UTI.
5) Prophylactic anticoagulants- for risk of thrombo-
embolism.
5) Fetal evaluation – Serial USG at every 3-4 weeks
to follow fetal growth, Doppler study every week.
NST and amniotic fluid evaluation twice weekly.
6) Delivery –
o If patient is stable- delivery at term with
development of spontaneous labor.
o If unstable, delivery as soon as fetal lung maturity
is reached.
o If patient is severely ill, immediate delivery is
indicated even without fetal lung maturity.
DIABETIC NEPHROPATHY
• Most common chronic renal disorder in pregnancy.
• History of insulin dependent diabetes of long
duration.
• Pre-eclampsia is present in more than 50% cases.
• Managed by adequate glycemic control and control
of BP < 150/90 mmHg.
• In case of severe renal failure, early delivery is
considered.
PREGNANCY IN WOMEN ON CHRONIC
DIALYSIS
• Women having end stage renal disease are less likely
to conceive, but with hemodialysis, there is a
possibility of spontaneous conception.
• Dialysis regimen should mimic physiological changes
in renal system during pregnancy.
• After completion of first trimester, dialysis should be
done daily (20-24 hrs/week).
• Pre-dialysis BUN <50 mg/dL and S. Creatinine < 4.5
mg/dL and fluid removal < 400ml/session should be
maintained.
• Follow-up –
1. Hb, serum iron, serum ferritin – assessed monthly
2. If Hb < 8gm/Dl, IV iron or IV/SC Erythropoitin should
be given.
Erythropoitin
• contraindicated with uncontrolled hypertension.
• Does not cross placenta
• Dose should be reduced if Hb rise > 1 gm/Dl in 2
weeks due to increased risk of hypertension.
3. Fetal monitoring after each dialysis session due to
acute fluid shift.
4. Fetal growth scans and doppler – to follow the
growth.
• Complications – Preterm labor, IUGR, fetal loss
• Delivery – planned at GA 34 – 36 weeks.
Caesarean section rates- 50%
• Post-partum – Peritoneal dialysis can be
resumed with smaller (1 L) exchange fluid
after 24 hr of Ceasarean. If there is leakage,
hemodialysis is used.
• Perinatal complications –
Osmotic diuresis at birth.
Hypocalcemia and tetany afterwards.
Monitoring and appropriate management of
Electrolyte imbalance is needed.
PREGNANCY IN WOMEN WITH RENAL
TRANSPLANT
• Pregnancy can be safely undertaken one year
after renal transplant if –
1) No rejection
2) Allograft function is adequate
3) S. Creatinine < 1.5 mg/dL and urinary protein
excretion <500 mg/ 24 hr.
4) Immunosuppressive medications are
responsive and well tolerated
5) No infection.
• If S. Creatinine >2.3 mg/dL, progression of renal
failure and need of renal replacement therapy
within next 2 yrs of delivery. Hence , pregnancy
should be contraindicated in such patients.
• Maternal complication – worsening of renal
function, pre-eclampsia, infectious morbidity,
preterm delivery(50%)
• Fetal survival is good (95%), once the
pregnancy is beyond first trimester.
• Immunosuppression should be maintained
similar to pre-pregnancy levels. Cyclosporin is
well tolerated. Side effects may present as low
birth weight, preterm births and midline facial
defects (with prolonged use of steroids).
Follow-up during pregnancy-
1. BUN, S. Creatinine and electrolytes- every 10 days
2. Allograft function assessment – monthly by USG
3. Technetium scan – at least in each trimester
4. Urine culture – monthly ( UTI – most common infection)
5. Fetal USG and doppler- to evaluate interval growth.
During labor - Prophylactic antibiotics and stress dose of
corticosteroids should be given.
Delivery – should be attempted at birth, if no complication.
• Vaginal delivery is route of choice.
• Delivery without delay if PROM.
• Caesarean delivery only for obstetric indications but
preferred in combined pancreas-kidney transplant.
Breast feeding - Not contraindicated.
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Renal disorders in pregnancy

  • 1. RENAL DISORDERS IN PREGNANCY DR SEEMA NISHAD DNB OBS AND GYNAE
  • 2. • Normal changes during pregnancy • Urinary tract infections- Asymptomatic bacteriuria - Acute pyelonephritis • Acute nephrolithiasis • Acute renal failure • Chronic renal failure • Hemolytic-Uremic syndrome • Renal cortical necrosis • Nephrotic syndrome • Renal transplant and pregnancy
  • 3. NORMAL CHANGES DURING PREGNANCY Anatomic - 1 cm increase in length of kidneys due to hypertrophy of glomeruli. - Dilatation of the collecting system (calyces, renal pelvis, ureters) Physiologic - Renal plasma flow - increase by 40-50%, maximum at 16 wks, maintained until 34 wks, then falls by 25%. - 50% increase in GFR - Increase clearance of creatinine, blood urea nitrogen and uric acid from maternal blood.
  • 4. - Decreased Tubular reabsorption of glucose, uric acid, amino-acids and water soluble vitamins. - Decreased afferent and efferent arteriolar resistance - Ureters – dilated due to pressure of gravid uterus - Frequency of micturition in 1st and 3rd trimester of pregnancy - Creatinine clearance rises to 150-200ml/min and average serum creatinine decreases to 0.5-0.6 mg/dl.
  • 5. URINARY TRACT INFECTIONS • Infections during gestation occur frequently. • The bacteria, originally reside in the rectal or anal area and from there colonize the perineum, vaginal introitus, urethra, bladder and eventually the pelvi-caliceal area and kidney itself. • Ascending bacterial infection affects only the lower urinary tract (asymptomatic bacteriuria, acute cystitis) but during pregnancy, 25-40% may ascend to upper tract and may cause acute pyelonephritis.
  • 6. ASYMPTOMATIC BACTERIURIA 1. Incidence- 4 -10% of all pregnant women 2. Criteria for diagnosis- • Urine analysis- > 10 leucocytes/ml, • Dipstick test – reveals leucocyte esterase or nitrates. High false positive and false negative results. • > 105 colony forming units in single midstream catch technique of sample collection • >205 colony forming units/ml- diagnostic if sample by catheterization 3. Complications- If untreated, 25-40% develop acute pyelonephritis, preterm labor, low birth weight and perinatal mortality.
  • 7. 3. Treatment- First episode by appropriate antibiotics depending on prevalent resistance. 3 day course of antibiotics is usually effective. • Most effective oral regimen - Nitrofurantoin 100 mg twice daily for 3-7 days (according to WHO) • Amoxicilline 500 mg orally thrice daily x 3-7 days • Amoxicilline-clavulanate 500 mg orally twice daily 3-7 days. • Cephalexin 500 mg orally twice daily 3-7 days.
  • 8. 4. Success of treatment is confirmed by- urine culture after 2 week of completion of treatment. 5. If not cured or re-infection occurs, drugs according to antibiotic sensitivity is used for 10 days. 6. In case of repeated infections, low daily dose at night is continued till 4 weeks post-partum. Nitrofurantoin 100 mg orally or Cephalexin 250 mg is given.
  • 9. ACUTE PYELONEPHRITIS • Incidence- 1-2% , > 50% cases occur in second trimester. • Symptoms- malaise ,fatigue, chills, fever , headache and back pain • Signs- Fever, dehydration, costovertebral angle tenderness (more on right side) • Urinalysis - urine turbid or bloody, presence of RBCs, WBCs, WBC cast, bacteria. • RFT- elevated levels of S. Creatinine and BUN
  • 10. • Investigations- Hemogram, renal function test, serum electrolytes, urine culture and sensitivity • Histopathology- Infiltration of renal interstitium and tubules with neutrophils (formation of WBC cast) • Cause – Ascending infections by bacteria present in vagina or on perineum. Usually caused by single species of bacteria. Most common organism- Uropathogenic Escherichia coli ( 70-95% of cases)
  • 11. • Other causative organisms- Gram negative bacilli (as Klebsiella pneumoniae, Proteus mirabilis), enterococci, Staphylococcus saprophyticus. • Treatment- Admission in hospital, hydration, injectable antibiotics and careful monitoring of vitals (Tachycardia and hypotension may indicate early endotoxic shock), Pulse oxymetry, chest x-ray(to rule out possibility of ARDS), uterine contraction and fetal monitoring ( for preterm labor). o Antibiotic of choice – Ampicillin 2 gms IV 4-6 hrly o For Gram negative bacteria- best option- Cephazolin 2 gm IVPB 8 hrly o Ceftrixone 1 gm IV 8 hrly • When patient is afebrile for 24-48 hrs, switch to oral drugs for 14 days.
  • 12. • If patient do not respond within 72 hrs, or relapse after discontinuation of therapy, possibility of obstruction should be ruled out. • Ureteral stents and percutaneous nephrostomy may be needed in urinary obstruction. • Follow-up with urine culture is necessary. • Complications – Hemolytic anemia, Thrombocytopenia, ARDS, Preterm labor, endotoxic shock, hypothalemic instability
  • 13. ACUTE NEPHROLITHIASIS • Incidence- 1 in 1500 deliveries, usually during second and third trimester. • Symptoms- severe flank pain which starts abruptly. (Site of pain depends on site of stone), nausea, vomiting, dysuria. • Urinalysis- presence of macroscopic or microscopic hematuria, crystals (specific shape according to material of stone) • Renal ultrasound is test of choice. Transvaginal ultrasound may detect distal ureteric stones. Limited IVP is a single flat plate of abdomen, taken approximately 5 min after contrast administration. This test has high sensitivity and minimal fetal radiation exposure. • 4 types of urinary stones- Calcium oxalate (80%), Magnesium ammonium sulphate (15%), Uric acid stone(6%), cystein stone (2%)
  • 14. • When stone at renal pelvis – pain occurs at flank of respective side. • When stone in ureter – pain occur in lower abdomen radiating to groin and external genitalia.
  • 15. PHYSIOLOGICAL HYDRONEPHROSIS • Unilateral/ bilateral • More marked on right side • Patient not severely symptomatic HYDRONEPHROSIS DUE TO OBSTRUCTION • Usually unilateral • On side of patient’s symptom • Pain is relentless and severe
  • 16. • Treatment – - 80% of pregnant women pass the stone spontaneously and can be managed expectantly with hydration and medication to relieve pain. - High fluid intake to obtain minimum urinary volume of 2 L/day. - If no improvement after a reasonable period, cystoscopic extraction can be done. - In case of acute hydronephrosis due to obstruction, cystoscopic passage of ureteral stent and stone manipulation using retrograde ureteral catheterization. - If ureteral stent fails, per-cutaneous nephrostomy should be done.
  • 17. - Minimally invasive surgical procedures used in post-partum period as shock wave lithotripsy, percutaneous nephrolithotomy and flexible ureteroscopy. - Low calcium diet and thiazide diuretics – beneficial for idiopathic hypercalciuria. - Low purine diet for patient with uricosuria and uric acid stone. - Intensive treatment of chronic urinary tract infections to prevent struvite stone.
  • 18. ACUTE RENAL FAILURE • Defined as –  urine output < 400 ml in 24 hrs or <20 ml/ hr.  Urine output < 0.5 ml/kg/hr for 6 hrs  Increase of S Creatinine >0.3 mg/dL from base-line  Increase of S. Creatinine > 1.5 times of the normal • Incidence – decreased during recent years significantly due to- 1. Diminished number of septic abortions 2. Judicious and early termination of severe pre- eclampsia 3. Better management of shock 4. Appropriate management of abruptio placenta 5. Facilities of blood transfusion
  • 19.
  • 20. CAUSES OF ARF IN PREGNANCY PRE-RENAL CAUSES- due to renal hypoperfusion. Most common form. (A) Early pregnancy- 1) Acute and massive hemorrhage ( abortion, ectopic pregnancy, hydatidiform mole) 2) Severe dehydration ( hyperemesis gravidarum) 3) Septic abortion (endotoxic shock, hypotension) (B) Late pregnancy and labor- 1) Acute and massive hemorrhage ( PPH, Placenta previa) 2) Abruptio placenta ( hypovolumia and DIC) 3) Severe pre-eclampsia and eclampsia, HELLP syndrome 4) Acute fatty liver of pregnancy 5) severe infection ( chorioamnionitis, pyelonephritis)
  • 21. (C)Other causes- 1. Mismatched blood transfusion 2. Thrombotic micro-angiopathy 3. Hemolytic uremic syndrome RENAL CAUSES- Pre-existing renal disease- interstitial nephritis, SLE, toxins, drugs ( NSAIDs, aminoglycosides), obstetric pathology superimposed on pre-existing renal pathology. POST-RENAL CAUSES- Obstructive- accidental ligature of ureters during caesarean section or hysterectomy for rupture uterus.
  • 22. ACUTE TUBULAR NECROSIS • Most common pathology in obstetrics • Less serious • Reversible ( recovery in 1-2 weeks time) • Associated with sepsis & hypertension • Kidney lesion- focal, ischemic degeneration and necrosis of renal tubules, pigment and cast in lower part of nephrons RENAL CORTICAL NECROSIS • Relatively uncommon • serious • Irreversible • Associated with obstetric causes as abruptio placentae and endotoxic shock following Gram - negative septicemia. • Kidney lesion - focal, Patchy /gross ischemic necrosis of renal cortex resulting from thrombosis of renal vascular system
  • 23. CLINICAL FEATURES- 4 phases- 1) Incipient phase - Marked diminution of urinary output. 2) Phase of anuria – Urinary output <100 ml in 24 hrs. Initially patient looks well but gradually deteriorates if not treated timely. • Leucocytosis • Scanty urine, protein in varying amount, presence of red cell cast (s/o glomerular pathology) URINALYSIS PRE-RENAL RENAL URINARY Na < 20 mEq/L > 40 mEq/L URINE OSMOLALITY >500 <350 FRACTIONAL EXCRETION OF Na < 1% >2%
  • 24. • ECG- peak T wave, Absent P wave, prolonged QRS complex ( due to raised levels of potassium and magnesium) 3) (a) Phase of early diuresis - Favourable for recovery but S. Creatinine, sodium, potassium, BUN, chloride levels are raised continueously. (b) Phase of late diuresis – Causes are- • Osmotic diuresis due to high blood urea • Functional inadequecy of tubular reabsorption • Release of surplus fluid and electrolytes, mainly sodium and potassium 4) Phase of recovery – Tubular epithelium regenerates, functions re-established. May take about 1 yr for full recovery.
  • 25. MANAGEMENT OF ARF – 1. To exclude post-renal cause (obstruction in ureters) by USG. 2. Restore intravascular volume by appropriate fluid- as by blood transfusion or PRBC transfusion in case of massive haemorrhage, crystalloids and colloids for mild and moderate haemorrhage. 3. Forced diuresis with use of Inj. Frusemide ( 80-120 mg) intravenously. 4. During phase of anuria, fluid balance is the goal. Patient should not be overhydrated. Amount of fluid to be transfused in calculated by- Amount in vomitus + Gastric aspiration + Loss in diarrhoea + Loss in sweating + 500 ml ( + 200 ml for each degree of rise of temp. )
  • 26. 5. Protein and salt restricted diet, carbohydrate rich diet. Glucose prevents protein catabolism and production of urea and potassium is minimized. ( Prevention of complications) 6. Treatment of Hyperkalemia – • Administration of insulin with infusion of 50% Dextrose. • Oral carbohydrate intake. Fruit juices must not be given due to high content of potassium. • Inj. Calcium gluconate 10 ml of 10% solution ( Reduces cardiotoxic effect of high potassium levels) 7. Treatment of Hyperphosphatemia – Restriction of dietary intake of phosphate, phosphate binding agents ( calcium carbonate, calcium oxalate)
  • 27. 8. Dialysis – Indication- • Electrolyte abnormalities refractory to medical treatment • Volume overload with congestive heart failure and pulmonary oedema refractory to standard therapy. ( Most common indication) • Severe metabolic acidosis • Uremia( BUN > 39 mg/dL or S. Creatinine > 5.65 mg/dl) Continuous electronic fetal monitoring should be done during dialysis. Hematocrit should be above 25%. Risk of preterm labor is high, so parenteral progesterone to be given. Placental abruption, sepsis and heart failure can also occur.
  • 28. 9. Supportive therapy – • Control of infections – Avoid nephrotoxic antibiotics. • Intra-vascular volume overload – to be kept in check. • Hemoglobin level to be maintained above 7 gm%, if less, transfusion of PRBC should be done. 10. During phase of Diuresis – Fluid and electrolyte balance to be maintained. PROGNOSIS – Majority of patients recover without sequelae. Prognosis of fetus is unfavourable, about 50% mortality.
  • 29. CHRONIC RENAL FAILURE • A linear relationship exists between the pre- conceptional creatinine levels and risk of further renal damage during pregnancy. • Creatinine clearance is more accurate marker than serum creatinine levels. • Hypertension present at conception increases perinatal mortality rates. • Low sodium diet ( containing 1.5 gms), bed rest in lateral position to improve GFR and small dose of loop diuretics with caution should be given. • Dialysis can be done as and when required during expectant management.
  • 30. • Antenatal visits at every 2 weeks and weekly after 32 weeks. • Fetal growth assessed by USG and umbilical artery Doppler studies. Bio-physical profile to be performed weekly from 28 weeks onwards specially with worsening renal failure, hypertension, proteinuria and placental insufficiency. • Delivery at term, if no deterioration. Caesarean delivery only for obstetric indication. • If deterioration in creatinine levels or creatinine clearance of 25%, termination of pregnancy is justified. Expectant management can be done if GA between 24-31 weeks, normal well grown fetus and blood pressure well controlled.
  • 31. HEMOLYTIC UREMIC SYNDROME (HUS) • HUS is a disease independent of pregnancy and closely related to Thrombotic thrombocytopenic purpura. • Thrombotic microangiopathy secondary to expoure to enteropathic organisms, particularly E. Coli serotype 0157-H7. • Characterized by sudden onset and rapid progression of hemolytic anemia, thrombocytopenia and renal failure usually in postpartum period, at any time from day 1 and 10 weeks after delivery. • Pathophysiology – Damage to glomerular capillaries by subendothelial deposits of fibrin, that separates the endothelial cells from the basement membranes, leading to reduced vascular lumen. Formation of microthrombi, especially in afferent arterioles leads to renal ischemia.
  • 32. • Microangiopathic hemolytic anemia and thrombocytopenia occurs due to fragmentation of RBCs and platelets during passage through affected vessels. • Most important D/D is HELLP syndrome. • Persistence of symptoms and sign of HELLP syndrome beyond postpartum day 3, raises the probability of HUS. Diagnosis of HUS is more likely if there is a symptom free period of several days after delivery. • Maternal mortality with HUS is 8 – 44%. Perinatal mortality is also high, 30 -80 %.
  • 33. CLINICAL FINDINGS HELLP SYNDROME TTP HUS Onset After 28 weeks Median 23 weeks Postpartum Primary menifestation Hypertension, Proteinuria Neurologic symptoms Renal failure Fever Absent PRESENT Absent Purpura Absent PRESENT Absent VWF multimers Absent PRESENT PRESENT
  • 34. RENAL CORTICAL NECROSIS • This severe form of ARF is usually associated with catastrophic obstetric complications such as severe hypovolumia secondary to abruptio placenta or placenta previa or amniotic fluid embolism. • Histology – Necrosis of all the elements of renal cortex including extensive necrosis and thrombosis of the renal vessels. • Characterized by sudden onset of severe oliguria or anuria with life threatening complications of pregnancy. • Prolonged oliguria and anuria with little or no improvement of renal function is characterstic.
  • 35. • Urine is frankly hematuric and urinary red cells are dysmorphic and hypochromic with appearance of collapsed empty sacs. • Hematologic abnormalities characterstic of DIC. • BUN and plasma Creatinine increase rapidly. • Renal ultrasound demonstrates hypoechoic areas in the renal cortex. • Dialysis is required usually. Plasma exchange and prednisolone to be continued even postpartum for 1 month. Delivery is advisable once diagnosis is confirmed, as risk of maternal complication is high. • Prognosis – poor, majority do not recover and require chronic dialysis. Only 20 – 40% with partial recovery and can live without dialysis.
  • 36. NEPHROTIC SYNDROME • Characterized by –  Presence of proteinuria > 3 gms/24 hr  S. Albumin < 3 gm/dL  Edema  Hypercholesterolemia • Etiology – 1) pre-eclampsia 2) Diabetic nephropathy 3) Lupus nephritis 4) Primary glomerular disease Etiology is strongly suggested by clinical history
  • 37. DIFFERENTIAL DIAGNOSIS OF CAUSES OF NEPHROTIC SYNDROME DURING PREGNANCY HYPERTENSION NO YES PRE-ECLAMPSIA COMPLIMENTS NORMAL LOW LUPUS NEPHRITIS SELECTIVITY OF PROTEINURIA LACK OF SELECTIVITY HIGHLY SELECTIVE MINIMAL CHANGE URINE SEDIMENT NEPHROTIC NEPHRITIC DIABETES IgA GLOMERULONEPHRITIS
  • 38. • Complications – Hypertension, fetal growth restriction, preterm birth, fetal distress. • Management – 1) General measures – o Moderate physical activity, avoid prolonged periods of standing up or sitting. o Increased periods of bed rest in left lateral position, o diet rich in high quality protein, o Sodium intake adjustment if patient is hypertensive or excessive accumulation of sodium and water.
  • 39. 2) Antihypertensive treatment 3) Monitoring of renal function – o S. Creatinine every 4-6 weeks o Daily qualitative determination of urine protein o If significant change in urine protein with albustix strips, quantitative protein determination of 24 hr urine is done. o Renal function tests at least twice every week by measuring BUN, S. Creatinine, uric acid and electrolytes. Urine protein creatinine ratio (normal < 0.15) becomes > 3.5.
  • 40. 4) Prophylactic antibiotics – as there is high risk of development of infections, particularly UTI. 5) Prophylactic anticoagulants- for risk of thrombo- embolism. 5) Fetal evaluation – Serial USG at every 3-4 weeks to follow fetal growth, Doppler study every week. NST and amniotic fluid evaluation twice weekly. 6) Delivery – o If patient is stable- delivery at term with development of spontaneous labor. o If unstable, delivery as soon as fetal lung maturity is reached. o If patient is severely ill, immediate delivery is indicated even without fetal lung maturity.
  • 41. DIABETIC NEPHROPATHY • Most common chronic renal disorder in pregnancy. • History of insulin dependent diabetes of long duration. • Pre-eclampsia is present in more than 50% cases. • Managed by adequate glycemic control and control of BP < 150/90 mmHg. • In case of severe renal failure, early delivery is considered.
  • 42. PREGNANCY IN WOMEN ON CHRONIC DIALYSIS • Women having end stage renal disease are less likely to conceive, but with hemodialysis, there is a possibility of spontaneous conception. • Dialysis regimen should mimic physiological changes in renal system during pregnancy. • After completion of first trimester, dialysis should be done daily (20-24 hrs/week). • Pre-dialysis BUN <50 mg/dL and S. Creatinine < 4.5 mg/dL and fluid removal < 400ml/session should be maintained.
  • 43. • Follow-up – 1. Hb, serum iron, serum ferritin – assessed monthly 2. If Hb < 8gm/Dl, IV iron or IV/SC Erythropoitin should be given. Erythropoitin • contraindicated with uncontrolled hypertension. • Does not cross placenta • Dose should be reduced if Hb rise > 1 gm/Dl in 2 weeks due to increased risk of hypertension. 3. Fetal monitoring after each dialysis session due to acute fluid shift. 4. Fetal growth scans and doppler – to follow the growth.
  • 44. • Complications – Preterm labor, IUGR, fetal loss • Delivery – planned at GA 34 – 36 weeks. Caesarean section rates- 50% • Post-partum – Peritoneal dialysis can be resumed with smaller (1 L) exchange fluid after 24 hr of Ceasarean. If there is leakage, hemodialysis is used. • Perinatal complications – Osmotic diuresis at birth. Hypocalcemia and tetany afterwards. Monitoring and appropriate management of Electrolyte imbalance is needed.
  • 45. PREGNANCY IN WOMEN WITH RENAL TRANSPLANT • Pregnancy can be safely undertaken one year after renal transplant if – 1) No rejection 2) Allograft function is adequate 3) S. Creatinine < 1.5 mg/dL and urinary protein excretion <500 mg/ 24 hr. 4) Immunosuppressive medications are responsive and well tolerated 5) No infection. • If S. Creatinine >2.3 mg/dL, progression of renal failure and need of renal replacement therapy within next 2 yrs of delivery. Hence , pregnancy should be contraindicated in such patients.
  • 46. • Maternal complication – worsening of renal function, pre-eclampsia, infectious morbidity, preterm delivery(50%) • Fetal survival is good (95%), once the pregnancy is beyond first trimester. • Immunosuppression should be maintained similar to pre-pregnancy levels. Cyclosporin is well tolerated. Side effects may present as low birth weight, preterm births and midline facial defects (with prolonged use of steroids).
  • 47. Follow-up during pregnancy- 1. BUN, S. Creatinine and electrolytes- every 10 days 2. Allograft function assessment – monthly by USG 3. Technetium scan – at least in each trimester 4. Urine culture – monthly ( UTI – most common infection) 5. Fetal USG and doppler- to evaluate interval growth. During labor - Prophylactic antibiotics and stress dose of corticosteroids should be given. Delivery – should be attempted at birth, if no complication. • Vaginal delivery is route of choice. • Delivery without delay if PROM. • Caesarean delivery only for obstetric indications but preferred in combined pancreas-kidney transplant. Breast feeding - Not contraindicated.