HAI FRDS I HAVE WORKED HARD AND DID THIS SEMINAR FOR U,,,,

1. THE RENAL DISEASES
IN THE KIDNEY
BY
PRAYTHIESH BRUCE(CRRI)
DEPT OF OBG,SMIMS
KULASEKHARAM

2. OVER VIEW
 Introduction
 Urinary tract infection
 Acute pyelonephritis
 Chronic pyelonephritis
 Acute renal failure
 Pregnancy in renal transplant patient
 Hypertension and renal disease

3. INTRODUCTION
 Diseases of urinary tract is common in
pregnancy-structural and functional changes
are normally seen in pregnancy
 STRUCTURAL CHANGES:
 Dilatation of urinary tract-iii trimester
Stasis,hydronephrosis occur- due to gravid
uterus and dilatation of right side ureter
occur-due to dextrorotation uterus
 Progesterone-relaxant-smooth muscle

4. FUNCTIONAL CHANGES IN
PREGNANCY
 Renal blood flow-increases by 80%
 Gfr,creatinine,creatinine clearance-increases
by 50%
 >0.9%mg/dl s.creatinine suggest renal
disease
 Glycosuria-lowering of renal threshold
 Sodium and water retention
 Fall in osmolality

5. URINARY TRACT INFECTION
 Commonest infection
 Causative organism;
 Ecoli
 Klebsiella
 Pseudomonas aeroginosa
 TYPES
 A)asymptomatic bacteruria
 B)cystitis
 C)acute pyelonephritis

6. ASYMPTOMATIC BACTERURIA
 Occur in 5%pregnancy
 Must be treated as 30%can cause
symptomatic infection
 Diagnosis:
 First visit:screening by urine culture and
microscopy
 Routine mid stream urine culture of
>1,00,000organisms per 1 ml
 (Len)leucocyte esterase nitrate dip stick test
can be used if prevalence is low in the
population

7. TREATMENT OF ASYMPTOMATIC
BACTERURIA
 Treatment required to prevent
pyelonephritis/preterm delivery
 It is associated with risk of
hypertension,preeclampsia,anaemia in
mother and lbw in children
 Treatment depend on culture sensitivity
report

8. TREATMENT OF ASYMPTOMATIC
BACTERURIA(3-5)DAYS
 Oral antibiotics:
 Ampicillin 500mg qid
 Amoxycillin 5oomg tds
 Cephalexin 250mg tds
 Nitrofurantoin 100mg qid
 Iv antibiotics:
 Cefuroxime 750 mg tds
 Coamoxyclav 1.2g tds

9. CYSTITIS
 Infection
of lower urinary tract
 Characterised by burning micturition( dysuria)
 Frequency
 Urgency
 Complicate in 1% pregnancy

10. CYSTITIS CAUSATIVE ORGANISM
 Ecoli
 Klebsiella
 Pseudomonas aeroginosa
 DIAGNOSIS:
 Urine analysis shows
 Bacteriuria,pyuria,hematuria
 Urine culture and sensitivity

11. TREATMENT FOR CYSTITIS
 Depend on culture sensitivity report
 Oral antibiotics:
 Nitrofurantoin 100mg qid
 Ampicillin 500mg qid
 Amoxycillin 500mg tds
 Cephalexin 250mg tds

12. ACUTE PYELONEPHRITIS
 Infection of upper urinary tract involving both
renal pelvis and parenchyma
 Incidence- 1-2%
 Causative organism;
 Ecoli
 Klebsiella
 Pseudomonas aeroginosa

13. CLINICAL FEATURES OF
ACUTE PYELONEPHRITIS
 Onset is acute, 2nd &3rd trimester of pregnancy
 Symptoms:
 Anorexia, back pain , chills & rigor with fever,
dysuria, nausea & vomiting
 Signs:
 Increased temprature(101of)
 Urine turbid
 Tachycardia

14. INVESTIGATIONS FOR ACUTE
PYELONEPHRITIS
 Urine examination:
 High specific gravity, acid reaction,
proteinuria, leucocytes, red cells, white cell
cast,bacteria
 Urine culture & sensitivity test:
 Blood examination: sign of renal dysfunction,
elevated bun, creatinine & creatinine
clearance

15. COMPLICATIONS OF ACUTE
PYELONEPHRITIS
 Septic shock due to endo-toxins
 Pulmonary injury
 Chronic renal infections
 Adult respiratory distress syndrome
 Abortion, fetal growth restriction,intra-uterine
fetal death
 Premature labour

16. TREATMENT OF ACUTE
PYELONEPHRITIS
 Hospitalisation, bed rest, plenty of fluids, easily
digestable diet, pulse oximetry
 4th hrly TPR & B.P monitoring
 Uterine contractions, fetal monitoring,
 I.V.F for dehydrated & oliguric patients
(crystalloids,dextrose, D.saline)
 I/V antibiotics
 Ampicillin 500mg iv 6th hrly
 Co amoxyclav 1.2g iv 12 hrly after patient is afebrile
for 24-48 hrs oral antibiotics started

17. CHRONIC PYELONEPHRITIS
 Chronic diseases charecterised by severe
scarring of the kidneys resulting from
persistent/ recurrent infections in patients
with vesico-urethral reflux
 Complications :
 Chronic hypertension
 Acute pyelonephritis
 Chronic microcytic anaemia
 Pre-eclampsia, hyponatraemia, glycosuria

18. TREATMENT OF CHRONIC
PYELONEPHRITIS
 Maternal & fetal prognosis depends on the
extent of the renal damage
 Cap. Ampicillin 500mg/tab.nitrofurantoin
100mg/cap. Cephalexin 500mg -1cap. Every
night for the duration of pregnancy

19. ACUTE RENAL FAILURE
 Rare complication in pregnancy in which
sudden decrease in renal function with
oliguria over a period of hours or days
 Diagnosis:
 Oliguria, hyperkalemia, metabolic
acidosis,rising blood urea &creatinine

20. CAUSES OF ACUTE RENAL
FAILURE
 Obstetric haemorrhage
 Infection
 Septic abortion
 Pre eclampsia
 Drugs-nsaids
 Renal diseases
 Post renal(obstructive uropathy)

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

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

23. CLINICAL FEATURES OF
ACUTE RENAL FAILURE
 Oliguria- sign of acute impaired renal function
 Input /output chart
 Patient is warm to touch, thirsty, irritable,
lethargic
 Rise in blood urea &serum potassium level
which causes muscular & ECG changes
 In diuretic phase there is excess of passage
of urine, but blood urea remains high

24. MANAGEMENT OF ACUTE RENAL FAILURE
 Early diagnosis is important
 Blood volume replacement is required for hemorrhage,
control of B.P& delivery for pre- eclampsia, stoppage of
nephro-toxic drugs
 Patient needs intensive care with hydration
 Assessment of fluid balance by C.V.P line is important
 Liberal fluids given in hemorrhagic shock
 Infection should be controlled by antibiotics in septic
abortion & puerperal sepsis
 Blood levels of electrolytes, urea, creatinine should be
checked daily
 Help of nephrologist is sought
 Peritoneal/hemodialysis is performed to keep BUN to
50mg/dl
 If not already delivered, delivery should be expedited
after stabilising her general condition

25. PREGNANCY IN RENAL
TRANSPLANT PATIENT
 More women are expected to come for pregnancy
with more liberal use of renal transplant
 They should delay pregnancy for 1-2 years after
transplantation to allow the graft function to stabilise
&immunosupperession reach maintenance level
 Cyclosporine, azathioprine, prednisolone are
considered safe in pregnancy
 Women on Cyclosporine should not breast feed

26. CHRONIC RENAL DISEASE IN
PREGNANCY
 Incidence: 0.2%
 Effect of pregnancy on kidney disease:
Mild Moderate Severe
Risk of renal Risk of renal Risk of renal
failure is low failure is 10% failure is 50%
(<5%)
Serum creatinine Serum creatinine Serum creatinine
<125 micromol/lit 125-250 >250 micromol/lit
micromol/lit

27.  Super-imposed pre-eclampsia prognosis is
worse
 Primary glomerulo-nephritis has better
prognosis
 Focal glomerulo sclerosis, immune
nephropathy, membrano-proliferative
glomerulo-nephritis has poor prognosis

28. Effect of kidney disease on
pregnancy
 Effect of pregnancy depends upon the severity of
renal diseases, serum creatinine levels,
hypertension & proteinuria
 Super-imposed pre-eclampsia- perinatal mortality is
50%
 In severe kidney disease risk of abortion, IUGR, pre-
term labour
 Careful pregnancy surveillance, proper treatment,
improved neonatal care& colaboration with
nephrologist has improved prognosis of mother &
newborn

29. TREATMENT OF CHRONIC RENAL
DISEASE IN PREGNANCY
 Pre-conceptional counselling
 Mild to moderate kidney disease- regular
assessment of kidney function
 Women with severe kidney disease adviced against
contraception
 Therapeutic abortion justified in early pregnancy
 Anti-hypertensive drugs given for hypertension
 Fetal monitoring performed each visit
 Management of labour is like pre-eclampsia with the
aim of vaginal delivery

30. RENAL DISEASE AND
HYPERENSION
 DEFINITION-blood pressure of more
than140/90mmhg or greater or an increase of
30 mm hg sysolic or 15 mm hg diastolic over
the baseline value on atleast two occations

31. TYPES OF HYPERTENSIVE DISEASE IN
PREGNANCY
 1-Gestationalhypertension/pregnancy
induced hypertension
 2-pre eclampsia
 3-Eclampsia
 4-preclampsia superimposed on chronic
hypertension
 5-chronic hypetension

32. ** INCIDENCE: 5-10% 0f all pregnancies . 20% recurrence
This is the third most important cause of maternal mortality worldwide
** DEFINITION OF HYPERTENSION:
 D.B.P. > 90 mmHg or
 S.B.P. > 140 mmHg along with
** PROTIENUREA:
Proteinurea is defined as urinary excretion
0.3 g protein or greater in a 24-hour
30 mg/dl (+1 or greater on urine dip specimen)
+/-
** OEDEMA: 90% pregnancy. progressive

33. INCIDENCE 6-8%RISK FACTORS
Pre eclampsia occurs in
& of all
live birth
RISK FACTORS  Multiple pregnancy  twins 13
 Extremes of reproductive age vs 6%
15 < & >35 Y  Hydatidiform mole
 Nulliparity  Nonimmune hydrops fetalis
 Black race  Obesity  4.3%  BMI < 19.8
 Hx of PET in a 1st degree female kg/m²
relative  13.3%  BMI ≥ 35
 Hx of PET in prior pregnancy kg/m²
 DM  Smoking  ↓ risk of HPT
 Chronic renal disease
 Ch HPT

34. •Abnormal trophoblast invasion…
first 12 weeks, the decidual segments of the spiral arteries are invaded…
elastic and muscular wall replaced by fibinoid walls
… by 20 weeks trophoblast invades intramyometrial segment of spiral
arteries(high resistance low flow-low resistanc high flow) increase in utero
placental flow
In pre eclampsia- trophoblast invasion is patchy & spiral arteries retain
their muscular walls….

36. PATHOGENESIS
 Endothelial cell injury ↓ ↓ prostacyclin & ↑ thromboxaneA2
 Vasospasm and endothelial cell dysfunction>>> platelet
activation and micro aggregate formation Rejection
phenomenon (inadequate matenal Ab response)
 Compromised placental perfusion
 Altered vascular reactivity  ↑sensitivity to vasopressin
EPN, NEPN & angiotensin
 ↓ GFR with retention of salt & water
 ↓ intravascular volume
 ↑ CNS irritability
 DIC
 Uterine muscle stretch & ischemia
 Dietary factors
 Genetic factors

37. PATHOGENESIS
Summary of current hypothesis:
 Immunological disturbance  abnormal placental
implantation ↓ placental perfusion  production of
substances that activate or injure endothelial cells of the
blood vessels  multiple organ system involvement

39. SYMPTOMS & SIGNS
↑ BP
 Proteinuria
 Edema of the face & hands ( but it has been
dropped of the definition due to poor
predictive value)
 Headache
 Visual disturbance
 Epigastric pain
 Exaggerated reflexes

40. CLASSIFICATION OF PE
ECLAMPSIA
SEVERE PRE ECLAMPSIA-Systolic BP >160 mmHg or
diastolic >110 mmHg on two occasions at least 6 hrs
apart
 Proteinuria ≥ 5 g/24 hrs
 Oliguria < 500 cc /24 hrs
 Cerebral or visual symptoms
 Epigastric or Rt upper quadrant pain
 Pulmonary edema or cyanosis
 Low PLt
 IUGR
 MILD PRE ECLAMPSIA  any pre eclampsia that is
not considered severe

41. •Why screening
•Accuracy. Uterine artery doppler at 24 weeks, notching on both uterine
arteries identifies 80% who will develop pre clampsia,,, 5% false positive

42. Management of pre eclampsia
OBJECTIVES
 Birth of an infant who subsequently thrives
 Complete restoration of health to the mother
 terminaton of pregnancy with the least possible trauma
to the mother & fetus
1- Hospitalization
 Women with new onset BP ≥ 140/90
 Worsening BP
 Development of proteinuria in addition to existing BP

43. INITIAL HOSPITAL
MANAGEMENT
 Observe for headache , visual disturbance, epigastric
pain & rapid wt gain
 Wt daily
 Analysis for proteinuria every 2 days / daily
 BP in sitting position every 4 hrs except during sleep
 Blood investigations  Hct, Plt, S creatinine, liver
enzymes
 Frequent evaluation of fetal size & AF
 Reduced physical activity but not absolute bed rest
 N diet & fluid intake

44. FURTHER MANAGEMENT
Depends on:
 Severity of pre eclampsia
 Duration of gestation
 Condition of the Cervix
 Complete resolution of the signs & symptoms does not
occur till after delivery
Lines of management
 Termination of pregnancy
 Antihypertensive therapy Anticonvulsant therapy
 Home health care if BP improved within few days Pt
can be managed as outpatient Home BP & urine
protein monitoring . Instruction to come to hospital if she
has waning symptoms . Rest at home

45. Termination of pregnancy
Indications
 Term pregnancy with mild or severe Pre eclampsia
 Severe Pre eclampsia regardless of the gestational age
Warning signs  headache , visual disturbance, epigastric pain,
oliguria
 Eclampsia Pt must be stabilized & delivered immediately
Preterm with mild Pre eclampsia  Assess fetal wellbeing by NST,
BPP, Doppler
Methods of termination
 IOL with prostaglandines to ripen the Cx followed by IV oxytocin
 Elective CS  Severe Pre eclampsia with unfavorable
cervix

46. Antihypertensive therapy for
severe pre eclampsia
 Hydralazine
 IV infusion or IV 5-10 mg bolus at 15-20 min interval
 when diastolic BP ≥100-110 mm Hg or systolic BP ≥
160 mmHg
 Nifedipine 10 mg po repeated in 30 min
 Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after
10min/80 mg (not to exceed 220 mg)
 Nitroprusside used only in PT not responding to other
drugs
 Diuretics not recommended because intravascular
volume depletion already exists in Pre eclampsia

47. Antihypertensive therapy
Mild pre eclampsia-There is no benefit of antihypertensive
therapy
 Reduction in the maternal BP with labetalol or nifedipine
IUGR
 ACI contraindicated  IUGR, boney malformations,
limb contracture, PDA, pulmonary hypoplasia, RDS,
hypotension &death
Severe pre eclampsia-
Antihypertensive therapy is used to control BP untill the Pt
delivers or in preterm for 48 48 hrs to allow time for
glucocorticoid administration for fetal lung maturity then
delivery

48. Fluid therapy
 Hyperosmoticagents not recommended
because intravascular influx of fluid
subsequent escape of fluid to vital organs
pulmonary edema & cerebral edema
 LR60-120 ml/hr Excessive fluid
administration pulmonary edema &
cerebral edema

49. Definitions
 Chronic hypertension:
 A sustained BP > 140/90 that can antecedes
pregnancy or persists postpartum (beyond 6
weeks). HTN that is present before the 20th week
of pregnancy may also be included as CHTN.

50. Chronic Hypertension
 Oftenseen in patients who have other
medical complications: obesity, diabetes,
hyperlipidemia, cigarette smoking.
 Essential HTN – majority will have normal
pregnancies.
 Secondary HTN – parenchymal renal disease,
pheochromocytoma, Cushing’s syndrome,
hyperthyroidism, etc.

51. Chronic Hypertension
 Ifend-organ disease is present (renal,
cardiac, cerebrovascular), there is an
increased risk of morbidity and mortality.
 Maternal – superimposed preeclampsia, placental
abruption, congestive heart failure
 Fetal – intrauterine growth restriction, prematurity
and fetal death

52. Preconception Care of CHTN
 Review the medical history: diagnosis and
duration of hypertension, ongoing
pharmacological treatment, known existence
of organ damage or other compounding
illnesses.
 Review obstetrical history.

53. Preconception Care of CHTN
 Physical exam and laboratory evaluation
 Urine analysis, urine culture/sensitivity, 24 hour urine
for total protein and creatinine clearance
 CBC
 Diabetes screening
 If the patient has severe hypertension, significant
proteinuria or prior poor obstetric outcome more
extensive tests may be offered.

54. Preconception Care of CHTN
 Optimize control with recommended
medications.
 Methyldopa (Aldomet): extensively studied in
pregnant women, treatment of choice if needed.
Central adrenergic inhibitor
 Hydralazine: potent vasodilator, which acts
directly on vascular smooth muscle.
 Calcium channel blockers (Nifedipine): inhibits
transmembrane calcium ion influx which causes
vasodilation.

55. Antihypertensives
 B-Adrenoreceptor blockers (e.g. atenolol,
propranolol): possible fetal IUGR, neonatal
respiratory depression, bradycardia and
hypoglycemia
 Angiotensin-converting enzyme inhibitors: not
recommended for use in pregnancy
 Thiazides diuretics: not recommended for use in
pregnancy.

56. THANK YOU