‫هللا‬ ‫بسم‬
‫الرحمن‬
Acute Renal Failure
Islamic Republic of Afghanistan
Ministry of Public Health
Sardar. M. Dawood Khan Teaching Hospital
Presenter: Dr. Mohebullah Faqiri
Outline
1. Anatomy
2. physiology
3. Definitions.
4. Epidemiology.
5. Causes of ARF .
6. Pathogenesis.
7. Clinical features.
8. Laboratory investigations for Dx & Rx.
9. Complications.
10. Management.
11. Prognosis.
12. Prevention.
13. References.
Anatomy Of The Kidney
Cont….
 Bean Shape
 Retroperitoneal on each side of the
vertebral column
 Slightly above the level of umbilicus
 6cm length, 24 gram weight in a full
term newborn
 12 cm length, 150gram weight in adult
Con….
 Outer layer:
 Cortex (glomeruli ,proximal and distal convoluted tubules and
collecting duct)
 Inner layer:
 Medulla (straight portion of the tubules ,loop of henle, vasa recta &
terminal-collecting ducts)
• Excretion of metabolic waste products and foreign chemicals
• Regulation of water and electrolyte balances
• Regulation of body fluid osmolality and electrolyte concentrations
• Regulation of arterial pressure
• Regulation of acid-base balance
• Secretion, metabolism, and excretion of hormones
• Gluconeogenesis
Function of the kidney
Definitions
Acute renal failure (ARF) is a clinical syndrome in
which a sudden reduction in renal function results in
the inability of the kidneys to excrete nitrogenous
waste products and there is disturbance of water
and electrolyte balance.
Acute impairment of renal functions resulting
retention of nitrogenous wastes & other biochemical
derangements.
Epidemiology
 ARF causes 2-8 % admission of pediatrics hospital admissions.
 ARF causes 8-20% of ICU admissions.
Etiology
Pre renal
Renal
Post renal
1. Pre Renal
1. Dehydration(diarrhea,vomiting,DKA)
2. Blood loss.
3. Shock.
4. CHF.
5. Hepato renal syndrome.
6. Cutaneous loss
7. Burn.
8. Peritonitis,ascites, cirrhosis
9. Myocardial disease
2. Renal Cause.
1. Glomerular.
 PIGN.
 MPGN.
 RPGN.
 SLE.
 HSP.
2. Vascular.
 HUS.
 Renal vein thrombosis.
 Renal vasculitis.
 Kawasaki disease.
4. Acute tubular necrosis.
 Ischemic
 Nephrotoxic.
3. Interstitial nephritis.
 Drug induced.
 Infections
 Idiopathic.
3. Post renal:
Intra-luminal
•Stone,
•Blood clots,
•Papillary
necrosis
•Pelvic
malignan
cies
•Prolapse
d uterus
•Retroper
itoneal
fibrosis
Intra-mural
•Urethral stricture,
•BPH,
•Carcinoma
prostate,
• Bladder tumour,
• Radiation
fibrosis
Pathogenesis: Pre-renal failure:
↓ circulatory volume
a) Vasoconstriction.
b) H2o & salt re absorption.
Decrease renal perfusion
Activates neural and humoral response
1. Sympatic sys activation
2. Renin Ang-Ald syst activation.
3. Relaease of arginin vasopressin.
↑renal BF& GFR.
Activation of autoregatory sys
Stretch receptor stim in Aff art
PE2 secretion
and local myogenic reflex activation
Aff art dilatation
Inc secretion of
Ang2
Eff arteriol consriction
Intrinsic renal failure
Prolonged hypo perfusion.
Failure of compensatory mechanisms.
Tubular cell injury, necrosis, destruction.
Release of epethelial cast.
Obstrucain of glumerules.
Focal break against G.F.R.
Tubular contents shifts to interstitial space.
Interstitial edema.
Post Renal ARF
Its includes a variety of disorders characterized by
obstruction of the urinary tract. In a patient with 2
functioning kidneys, obstruction must be bilateral to
result in ARF. Relief of the obstruction usually results
in recovery of renal function except in patients with
associated renal dysplasia or prolonged urinary tract
obstruction.
Nephrotoxic Agents
 Exogenous
A. Antibiotic (amino glycoside ,sulfonamide,
amphotricin B , tetracycline , imipenum betalactum
antibiotic)
B. Chemotherapeutic agents ( cisplatin)
C. Radio contrast media
D. Other drugs ( NSAID , ACE inhibitor , acyclovir)
E. Snake bite
F. Chemical ( insecticide )
Con…..
 Endogenous
A. Pigments ( Hb , meth Hb , myoglubin )
B. Crystal ( uric acid , calcium , oxalate)
C. Tumor lysis syndrome
Clinical features
1. Usually anuria or oliguria.
2. Altered sensourim.
3. Convulsions.
4. Acidotic breathing.
5. Hypertension.
Causal:
PRE RENAL: vomiting, sunken eye, depressed fontanel, dry mucous membrane, loss of skin turgor, feeble
pulse.
G.N: hx of recent pharyngitis, hypertension, edema, hematurea,
HUS: petechia, pallor, dysentery, bleeding.
Acute Intravascular hemolysis: jaundice, pallor, sudden dark red urine,
Obs uropathy: interrupted urinary stream, palpable bladder and kidney.
U.T calculi: dysurea, hematurea, abdominal colic,
Obstruction: complete an urea,
ARF-on- CRF: Growth retardation, hypertensive retinopathy, osteodysrophy, severe anemia, hypocalcaemia.,
small contracted kidney.
Laboratory Investigations
1. Blood exam:
Anemia,
Leucositosis
Thrombocytopenia.
2. Serum electrolytes:
Hyponatremia.
Hyperkalemia.
hypocalcaemia.
Hyperphosphatemia
Metabolic acidosis.
Lab…
Blood urea and creatinine:
 Both are raised due to diminished renal blood flow.
Urine routine exam:
If glumerulonephrtiis:
hematurea.
Proteinurea.
RBC casts and granular cast.
If Tubulointerstitial .
WBC cast, low grade hematuria, proteinuria.
Indices for differentiating pre renal from established
RF.
Index Pre renal Intrinsic Renal
Urinary sodium
meq/L
<20 >40
Urinary osmolarity
mOsm/Kg
>500 <300
Blood urea to creat
ratio
>1:20 <1:20
Function excretion
of sodium
<1 >1
Specific gravity of
urine
>1,020 <1,010
Investigation con….
 Chest radography:
 cardiomegaly.
 Pulmonary congestion.
 Renal ultrasond.
 Vascularization of pelvicalyceal system.
 Assessment of renal size.
 Structure anomaly and calculi.
 Renal biopsy:
Indication of renal biopsy:
1. When etiology is not identified.
2. Un remitting RF lasting more than 2-3 weeks.
3. Suspected drug induced RF.
Complications of ARF
 Volume overload
 Heart failure
 Pulmonary odema
 Arrhythmia
 GI Bleeding
 Hyponatremia
 Hyperkalemia
 Hyperphosphatemia
 Hypermagnesemia
 Hypocalcemia
 Metabolic acidosis
 Infections
 Neurlogic complications
 ( seizers, insomnia, drawsness, coma)
 Anemia
Management
 Establish a secure IV line.
 Draw blood sample for necessary investigations
 Collect urine sample.
 Record BP.
 Catheterize.
 Carefully intake and output record
 Daily weight measurement.
 Urea and creatinine, s.electrolytes, estimated
daily base.
 Frequent E.C.G monitoring.
Daily Fluid Therapy.
daily fluid requirement:
300-400 cc/m2 /24h.
 insensible water loss + urine output of last
day+ extra renal loss.
 insensible loss should be replaced with G
5%. Urinary loss and extra renal loss should
be replaced with N/2 saline+glucose 5%.
Diet:
 Carbohydrates: 70 %.
 Lipid : 10-20 %.
 Protein: 0.5-0.8g/kg/D.
 Potassium and phosphorous should be restricted.
 Enough amount of multivitamin and micronutrient should
be given.
N.Saline or ringer
Give 20-30 ml/kg / 45-60 min
If urine output is
increased and but
CVP is still low,
Infusion of (N.S )
may be continued.
If no response e.g 2-4
ml/kg/2-3 hr urine,
Inj. Frusemide.2-3mg/kg
If no response e.g 2-4 ml/kg/2-3
hr urine: intrinsic renal failure
strongly suspected
Dopamin 1-3 µg
Mannitol
 Renal failure with dehydration:
N.Saline: 20ml/kg/30m.
If hydration and shock is improved, give, 90ml/kg/3h.
After 3h: if no urine out put but hydration is impvoved, give
frusemide 2mg/kg,
after 2-3 h, if No urine output, second dose of frusemide should be
given.
if hydration is good and BP is low: start Dopamine 2-3µg/kg/min.
Renal failure with fluid overload ( pul.edema)
 No IV fluid are given.
 Give frusemide 2mg/kg.
 Assess after 2-3 hr. if no improve in diuresis, repeat
the above dose.
 If no diuresis, give mannitol: 0.5-1g/kg/3o m.
 dopamine 5µg/kg/min may be given if there is no
hypertension.
If all the above measures failed, dialyses is indicated.
Mangement Of Compilcation
 Hyperkalemia:
Metabolic acidosis
Infection
Hemolysis
Tissue damage
 ECG changes (peak T wave , wide QRS complex ,ST depression ,
Prolong PR interval
Management of Hyperkalemia
If hyperkalemia (> 6meq/dl)
1. Avoidance of fluids , medication , and food
containing potassium
2. Sodium poly styrene sulfonate resin (kayexalat)
1gr/kg/day oral or per rectum
Con…..
If Hyperkalemia (>7mEq/dl)
1. Calcium gluconate 10% solution 1ml/kg given 3-5
minutes
2. Sodium bicarbonate 1-2 mEq/kg IV over 5-10 minutes
3. Regular insulin 0,5-1 unit /kg with 0.5 gr glucose over
90 minutes
4. Beta 2 agonist drugs ( salbutamol)
Metabolic Acidosis
Moderate -common no specific treatment
Severe acidosis (arterial PH less than 7,15 and serum
bicarbonate less than 8mEq/L) or acidosis combined
with hyperkalemia requires treatment
Sodium bicarbonate 1-2 mEq/kg aiming to raise the
serum bicarbonate level to 15-17 mEq .
Hypocalcaemia
Hypocalcemia
is primarily treated by lowering the serum phosphorus level.
Calcium should not be given intravenously, except in cases
of tetany, to avoid deposition of calcium salts into tissues.
Patients should be instructed to follow a low phosphorus
diet, and phosphate binders should be orally administered to
bind any ingested phosphate and increase gastrointestinal
phosphate excretion.
 Common agents include sevelamer (Renagel), calcium
carbonate (Tums tablets or Titralac suspension), and calcium
acetate (PhosLo).
Con…..
Hyponatremia
is most commonly a dilutional disturbance that
must be corrected by fluid restriction rather than
sodium chloride administration. Administration
of hypertonic (3%) saline should be limited to
those patients with symptomatic hyponatremia
(seizures, lethargy) or those with a serum sodium
level <120 mEq/L.
Con…..
Acute correction of the serum sodium to 125
mEq/L (mmol/L) should be accomplished
using the following formula:
mEq/L NaCL required=0.6xweight(kg)x(125-
serum sodium, mEq/L)
Hypertension
 Symptomatic hypertension (decreased gradually )
1. Sodium nitropersid 0.5-1µg /kg/minute by continues infusion
2. Labetolol 0,25-0,3 mg/kg/h
3. Esmolol 150-300µg/kg/minute
4. If there is feature of fluid excess ferusamid 1-2 mg /kg
 Asymptomatic hypertension
1. Calcium channel blocker ( nefidepin and amlodepin)
2. Betablocker ( atenolol)
3. Vasodilator (Hydralazine )
Con….
 Neurologic symptoms
may include headache, seizures, lethargy, and confusion. Potential
etiologic factors include hyponatremia, hypocalcemia,
hypertension, cerebral hemorrhage, cerebral vasculitis, and the
uremic state. Diazepam is the most effective agent in controlling
seizures, and therapy should be directed toward the precipitating
cause.
 Anemia
If Hb less than 7gr/dl packed RBC transfusion 5-10 cc /kg
Indication Of Dialysis
 Volume over load with evidence of hypertension ,
pulmonary edema and CHF refractory to diuretic
therapy
 Persistent hyperkalemia ( 6,5mEq/L)
 Severe metabolic acidosis ( PH less than 7,2 )
 Neurological symptoms ( altered sensorium , seizure)
 blood urea nitrogen greater than 100-150mg/dl
 Ca/phasphate imbalance with hypocalcaemia tetany
Prognosis
 Optimal management and dialysis can reavarse the derangement
cause by ARF.
 Dispite advance dialysis mortality rate is 30-40% are reported .
 Prognosis is good in ATN , intravascular Hemolysis and pre renal
failure when complicated factor is absent .
 Factors associated with high mortality include sepsis , cardiac
surgery delayed referral and MOF.
Prevention
Several condition that cause ARF may be prevented.
important measure include.
1. Oral rehydration therapy in diarrhea
2. Avoidance and judicious use of drugs that are nephrotoxic .
3. Care full observation of patients who receiving anti malarial drugs .
4. Good hydration of the patient under going diagnostic procedure
with radio contrast media.
5. Force diuresis and use of allopurinol is effective in preventing ARF
ARF In Newborn
Causes:
 prenatal asphyxia.
 Shock.
 septicemia.
 respiratory distress syndrome.
 Intravascular volume depletion.
 following surgery.
 bilateral renal artery thrombosis( umbilical artery catheterization).
 Renal vein thrombosis( asphyxiated, dehydrated or polycythemia),
hematurea, enlarged flank mass, and azeothemia, Thrombocytopenia.
 renal failure may occasionally, be the first manifestation of congenital
anomaly of the urinary tract.
Ranal failure is suspected in pressence of the following.
1. Oliguria( 1ml/kg/hr).
2. Blood creatinine is 1.2 mg/dl ).
Management
 Principle of management is similar to that of the
older children:
 Fluid given should be limited to:
 Insensible( 30ml/kg/D for full term).
5o-100 ml/kg/D for preterm
 Extremely premature neonates nursed in radiant
warmer, requires extra fluid.
 Systolic BP>95-100 mmHg: may need treatment.
Dialysis
 Some exceptin in neonatal dialysis:
 Perotoneal dialysis is preffered for neonates.
 PD may cause respiratory embarrasment or apnea.
 Hypothermia should be avoided by the careful
warming of the dialysis fluid.
Prognosis
 Mortality rate:
Mortality rate for oliguric renal failure are
about 40-50 %.
Nonoliguric patient has better prognosis.
 Outcome is related to underlying condition.
Indicatins for transplantations
When no systemic disease is present.
When GFR is less than 3oml /1.73m2 .
Thanks For Your
Kind Attention

Acute renal failure

  • 1.
  • 2.
    Acute Renal Failure IslamicRepublic of Afghanistan Ministry of Public Health Sardar. M. Dawood Khan Teaching Hospital Presenter: Dr. Mohebullah Faqiri
  • 3.
    Outline 1. Anatomy 2. physiology 3.Definitions. 4. Epidemiology. 5. Causes of ARF . 6. Pathogenesis. 7. Clinical features. 8. Laboratory investigations for Dx & Rx. 9. Complications. 10. Management. 11. Prognosis. 12. Prevention. 13. References.
  • 4.
    Anatomy Of TheKidney Cont….  Bean Shape  Retroperitoneal on each side of the vertebral column  Slightly above the level of umbilicus  6cm length, 24 gram weight in a full term newborn  12 cm length, 150gram weight in adult
  • 5.
    Con….  Outer layer: Cortex (glomeruli ,proximal and distal convoluted tubules and collecting duct)  Inner layer:  Medulla (straight portion of the tubules ,loop of henle, vasa recta & terminal-collecting ducts)
  • 7.
    • Excretion ofmetabolic waste products and foreign chemicals • Regulation of water and electrolyte balances • Regulation of body fluid osmolality and electrolyte concentrations • Regulation of arterial pressure • Regulation of acid-base balance • Secretion, metabolism, and excretion of hormones • Gluconeogenesis Function of the kidney
  • 8.
    Definitions Acute renal failure(ARF) is a clinical syndrome in which a sudden reduction in renal function results in the inability of the kidneys to excrete nitrogenous waste products and there is disturbance of water and electrolyte balance. Acute impairment of renal functions resulting retention of nitrogenous wastes & other biochemical derangements.
  • 9.
    Epidemiology  ARF causes2-8 % admission of pediatrics hospital admissions.  ARF causes 8-20% of ICU admissions.
  • 10.
  • 11.
    1. Pre Renal 1.Dehydration(diarrhea,vomiting,DKA) 2. Blood loss. 3. Shock. 4. CHF. 5. Hepato renal syndrome. 6. Cutaneous loss 7. Burn. 8. Peritonitis,ascites, cirrhosis 9. Myocardial disease
  • 12.
    2. Renal Cause. 1.Glomerular.  PIGN.  MPGN.  RPGN.  SLE.  HSP. 2. Vascular.  HUS.  Renal vein thrombosis.  Renal vasculitis.  Kawasaki disease. 4. Acute tubular necrosis.  Ischemic  Nephrotoxic. 3. Interstitial nephritis.  Drug induced.  Infections  Idiopathic.
  • 13.
    3. Post renal: Intra-luminal •Stone, •Bloodclots, •Papillary necrosis •Pelvic malignan cies •Prolapse d uterus •Retroper itoneal fibrosis Intra-mural •Urethral stricture, •BPH, •Carcinoma prostate, • Bladder tumour, • Radiation fibrosis
  • 14.
    Pathogenesis: Pre-renal failure: ↓circulatory volume a) Vasoconstriction. b) H2o & salt re absorption. Decrease renal perfusion Activates neural and humoral response 1. Sympatic sys activation 2. Renin Ang-Ald syst activation. 3. Relaease of arginin vasopressin. ↑renal BF& GFR. Activation of autoregatory sys Stretch receptor stim in Aff art PE2 secretion and local myogenic reflex activation Aff art dilatation Inc secretion of Ang2 Eff arteriol consriction
  • 15.
    Intrinsic renal failure Prolongedhypo perfusion. Failure of compensatory mechanisms. Tubular cell injury, necrosis, destruction. Release of epethelial cast. Obstrucain of glumerules. Focal break against G.F.R. Tubular contents shifts to interstitial space. Interstitial edema.
  • 16.
    Post Renal ARF Itsincludes a variety of disorders characterized by obstruction of the urinary tract. In a patient with 2 functioning kidneys, obstruction must be bilateral to result in ARF. Relief of the obstruction usually results in recovery of renal function except in patients with associated renal dysplasia or prolonged urinary tract obstruction.
  • 17.
    Nephrotoxic Agents  Exogenous A.Antibiotic (amino glycoside ,sulfonamide, amphotricin B , tetracycline , imipenum betalactum antibiotic) B. Chemotherapeutic agents ( cisplatin) C. Radio contrast media D. Other drugs ( NSAID , ACE inhibitor , acyclovir) E. Snake bite F. Chemical ( insecticide )
  • 18.
    Con…..  Endogenous A. Pigments( Hb , meth Hb , myoglubin ) B. Crystal ( uric acid , calcium , oxalate) C. Tumor lysis syndrome
  • 19.
    Clinical features 1. Usuallyanuria or oliguria. 2. Altered sensourim. 3. Convulsions. 4. Acidotic breathing. 5. Hypertension. Causal: PRE RENAL: vomiting, sunken eye, depressed fontanel, dry mucous membrane, loss of skin turgor, feeble pulse. G.N: hx of recent pharyngitis, hypertension, edema, hematurea, HUS: petechia, pallor, dysentery, bleeding. Acute Intravascular hemolysis: jaundice, pallor, sudden dark red urine, Obs uropathy: interrupted urinary stream, palpable bladder and kidney. U.T calculi: dysurea, hematurea, abdominal colic, Obstruction: complete an urea, ARF-on- CRF: Growth retardation, hypertensive retinopathy, osteodysrophy, severe anemia, hypocalcaemia., small contracted kidney.
  • 20.
    Laboratory Investigations 1. Bloodexam: Anemia, Leucositosis Thrombocytopenia. 2. Serum electrolytes: Hyponatremia. Hyperkalemia. hypocalcaemia. Hyperphosphatemia Metabolic acidosis.
  • 21.
    Lab… Blood urea andcreatinine:  Both are raised due to diminished renal blood flow. Urine routine exam: If glumerulonephrtiis: hematurea. Proteinurea. RBC casts and granular cast. If Tubulointerstitial . WBC cast, low grade hematuria, proteinuria.
  • 22.
    Indices for differentiatingpre renal from established RF. Index Pre renal Intrinsic Renal Urinary sodium meq/L <20 >40 Urinary osmolarity mOsm/Kg >500 <300 Blood urea to creat ratio >1:20 <1:20 Function excretion of sodium <1 >1 Specific gravity of urine >1,020 <1,010
  • 23.
    Investigation con….  Chestradography:  cardiomegaly.  Pulmonary congestion.  Renal ultrasond.  Vascularization of pelvicalyceal system.  Assessment of renal size.  Structure anomaly and calculi.  Renal biopsy: Indication of renal biopsy: 1. When etiology is not identified. 2. Un remitting RF lasting more than 2-3 weeks. 3. Suspected drug induced RF.
  • 24.
    Complications of ARF Volume overload  Heart failure  Pulmonary odema  Arrhythmia  GI Bleeding  Hyponatremia  Hyperkalemia  Hyperphosphatemia  Hypermagnesemia  Hypocalcemia  Metabolic acidosis  Infections  Neurlogic complications  ( seizers, insomnia, drawsness, coma)  Anemia
  • 25.
    Management  Establish asecure IV line.  Draw blood sample for necessary investigations  Collect urine sample.  Record BP.  Catheterize.  Carefully intake and output record  Daily weight measurement.  Urea and creatinine, s.electrolytes, estimated daily base.  Frequent E.C.G monitoring.
  • 26.
    Daily Fluid Therapy. dailyfluid requirement: 300-400 cc/m2 /24h.  insensible water loss + urine output of last day+ extra renal loss.  insensible loss should be replaced with G 5%. Urinary loss and extra renal loss should be replaced with N/2 saline+glucose 5%.
  • 27.
    Diet:  Carbohydrates: 70%.  Lipid : 10-20 %.  Protein: 0.5-0.8g/kg/D.  Potassium and phosphorous should be restricted.  Enough amount of multivitamin and micronutrient should be given.
  • 28.
    N.Saline or ringer Give20-30 ml/kg / 45-60 min If urine output is increased and but CVP is still low, Infusion of (N.S ) may be continued. If no response e.g 2-4 ml/kg/2-3 hr urine, Inj. Frusemide.2-3mg/kg If no response e.g 2-4 ml/kg/2-3 hr urine: intrinsic renal failure strongly suspected Dopamin 1-3 µg Mannitol
  • 29.
     Renal failurewith dehydration: N.Saline: 20ml/kg/30m. If hydration and shock is improved, give, 90ml/kg/3h. After 3h: if no urine out put but hydration is impvoved, give frusemide 2mg/kg, after 2-3 h, if No urine output, second dose of frusemide should be given. if hydration is good and BP is low: start Dopamine 2-3µg/kg/min.
  • 30.
    Renal failure withfluid overload ( pul.edema)  No IV fluid are given.  Give frusemide 2mg/kg.  Assess after 2-3 hr. if no improve in diuresis, repeat the above dose.  If no diuresis, give mannitol: 0.5-1g/kg/3o m.  dopamine 5µg/kg/min may be given if there is no hypertension. If all the above measures failed, dialyses is indicated.
  • 31.
    Mangement Of Compilcation Hyperkalemia: Metabolic acidosis Infection Hemolysis Tissue damage  ECG changes (peak T wave , wide QRS complex ,ST depression , Prolong PR interval
  • 32.
    Management of Hyperkalemia Ifhyperkalemia (> 6meq/dl) 1. Avoidance of fluids , medication , and food containing potassium 2. Sodium poly styrene sulfonate resin (kayexalat) 1gr/kg/day oral or per rectum
  • 33.
    Con….. If Hyperkalemia (>7mEq/dl) 1.Calcium gluconate 10% solution 1ml/kg given 3-5 minutes 2. Sodium bicarbonate 1-2 mEq/kg IV over 5-10 minutes 3. Regular insulin 0,5-1 unit /kg with 0.5 gr glucose over 90 minutes 4. Beta 2 agonist drugs ( salbutamol)
  • 34.
    Metabolic Acidosis Moderate -commonno specific treatment Severe acidosis (arterial PH less than 7,15 and serum bicarbonate less than 8mEq/L) or acidosis combined with hyperkalemia requires treatment Sodium bicarbonate 1-2 mEq/kg aiming to raise the serum bicarbonate level to 15-17 mEq .
  • 35.
    Hypocalcaemia Hypocalcemia is primarily treatedby lowering the serum phosphorus level. Calcium should not be given intravenously, except in cases of tetany, to avoid deposition of calcium salts into tissues. Patients should be instructed to follow a low phosphorus diet, and phosphate binders should be orally administered to bind any ingested phosphate and increase gastrointestinal phosphate excretion.  Common agents include sevelamer (Renagel), calcium carbonate (Tums tablets or Titralac suspension), and calcium acetate (PhosLo).
  • 36.
    Con….. Hyponatremia is most commonlya dilutional disturbance that must be corrected by fluid restriction rather than sodium chloride administration. Administration of hypertonic (3%) saline should be limited to those patients with symptomatic hyponatremia (seizures, lethargy) or those with a serum sodium level <120 mEq/L.
  • 37.
    Con….. Acute correction ofthe serum sodium to 125 mEq/L (mmol/L) should be accomplished using the following formula: mEq/L NaCL required=0.6xweight(kg)x(125- serum sodium, mEq/L)
  • 38.
    Hypertension  Symptomatic hypertension(decreased gradually ) 1. Sodium nitropersid 0.5-1µg /kg/minute by continues infusion 2. Labetolol 0,25-0,3 mg/kg/h 3. Esmolol 150-300µg/kg/minute 4. If there is feature of fluid excess ferusamid 1-2 mg /kg  Asymptomatic hypertension 1. Calcium channel blocker ( nefidepin and amlodepin) 2. Betablocker ( atenolol) 3. Vasodilator (Hydralazine )
  • 39.
    Con….  Neurologic symptoms mayinclude headache, seizures, lethargy, and confusion. Potential etiologic factors include hyponatremia, hypocalcemia, hypertension, cerebral hemorrhage, cerebral vasculitis, and the uremic state. Diazepam is the most effective agent in controlling seizures, and therapy should be directed toward the precipitating cause.  Anemia If Hb less than 7gr/dl packed RBC transfusion 5-10 cc /kg
  • 40.
    Indication Of Dialysis Volume over load with evidence of hypertension , pulmonary edema and CHF refractory to diuretic therapy  Persistent hyperkalemia ( 6,5mEq/L)  Severe metabolic acidosis ( PH less than 7,2 )  Neurological symptoms ( altered sensorium , seizure)  blood urea nitrogen greater than 100-150mg/dl  Ca/phasphate imbalance with hypocalcaemia tetany
  • 41.
    Prognosis  Optimal managementand dialysis can reavarse the derangement cause by ARF.  Dispite advance dialysis mortality rate is 30-40% are reported .  Prognosis is good in ATN , intravascular Hemolysis and pre renal failure when complicated factor is absent .  Factors associated with high mortality include sepsis , cardiac surgery delayed referral and MOF.
  • 42.
    Prevention Several condition thatcause ARF may be prevented. important measure include. 1. Oral rehydration therapy in diarrhea 2. Avoidance and judicious use of drugs that are nephrotoxic . 3. Care full observation of patients who receiving anti malarial drugs . 4. Good hydration of the patient under going diagnostic procedure with radio contrast media. 5. Force diuresis and use of allopurinol is effective in preventing ARF
  • 43.
    ARF In Newborn Causes: prenatal asphyxia.  Shock.  septicemia.  respiratory distress syndrome.  Intravascular volume depletion.  following surgery.  bilateral renal artery thrombosis( umbilical artery catheterization).  Renal vein thrombosis( asphyxiated, dehydrated or polycythemia), hematurea, enlarged flank mass, and azeothemia, Thrombocytopenia.  renal failure may occasionally, be the first manifestation of congenital anomaly of the urinary tract.
  • 44.
    Ranal failure issuspected in pressence of the following. 1. Oliguria( 1ml/kg/hr). 2. Blood creatinine is 1.2 mg/dl ).
  • 45.
    Management  Principle ofmanagement is similar to that of the older children:  Fluid given should be limited to:  Insensible( 30ml/kg/D for full term). 5o-100 ml/kg/D for preterm  Extremely premature neonates nursed in radiant warmer, requires extra fluid.  Systolic BP>95-100 mmHg: may need treatment.
  • 46.
    Dialysis  Some exceptinin neonatal dialysis:  Perotoneal dialysis is preffered for neonates.  PD may cause respiratory embarrasment or apnea.  Hypothermia should be avoided by the careful warming of the dialysis fluid.
  • 47.
    Prognosis  Mortality rate: Mortalityrate for oliguric renal failure are about 40-50 %. Nonoliguric patient has better prognosis.  Outcome is related to underlying condition.
  • 48.
    Indicatins for transplantations Whenno systemic disease is present. When GFR is less than 3oml /1.73m2 .
  • 49.