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WELCOME TO 
SEMINAR 
Presented by 
Dr. Bipin Karki 
Dr. Amlendra Yadav 
Dr. Chandra shekhar
CASE 
Tuhin 7 yrs old male child from sylhet , admitted 
with a complain of oliguria for 2 days associated 
with respiratory distress for same duration. He had 
h/o bee sting all over body surface 7 days back 
when he was returning home from school. He was 
afebrile , puffy face, restless , mild pale , dyspenic , 
edema present. Abdomen was soft, distended, non-tender, 
no organomegaly , ascites present evidenced 
by shifting dullness.
INVESTIGATION 
 S creatinine: 8 mg/dl 
 Blood urea: 400 mg/dl 
 Urine R/E 
Pus cell – (4-6)/ HPF 
Epi. Cell – (2-4)/HPF 
RBC – Nil 
Protein – (++)
ACUTE KIDNEY 
INJURY
DEFINITION 
Rapid deteriotion of renal function resulting in 
retention of nitrogenous wastes and inability of 
kidney to regulate fluid and electrolyte 
homeostasis. 
In year 2004 the acute dialysis quality initiative 
(ADQI) proposed RIFLE criteria for defining 
AKI . 
Later, Acute Kidney Injury Network (AKIN) 
classified AKI based on the RIFLE system.
RIFLE CRITERIA 
R = risk for renal dysfunction 
I = injury to the kidney 
F = failure of kidney function 
L = loss of kidney function 
E = end-stage renal disease
> 3 months
INCIDENCE 
 The precise incidence of AKI in children is not well 
known. 
 Data from bangladesh is not available 
 A data from india . 
 4-6 % case of AKI seen in general ward and upto 
40% in PICU . 
 Affects childrens who have sepsis and multiorgan 
failure. 
 Children undergoing major cardiac surgery and organ 
transplantation are at considerable risk for developing 
AKI.
ETIOLOGY 
 Pre renal 
 Intrinsic or renal 
 Post renal
PRE RENAL 
 Acute gastroenteritis 
 Blood loss 
 Shock 
 Fulminant hepatic failure 
 Reye syndrome 
 Congestive cardiac failure 
 Nephrotic syndrome 
 Hepatorenal syndrome
INTRINSIC RENAL 
 Renal 
Major vessel obstruction 
- renal vein thrombosis , renal arterial obstruction, hemolytic uremic 
syndrome , HSP , polyarteritis and other vasculitis 
 Glomerular 
Acute glomerulonephritis ( poststreptococcal , other infections ), 
cresentic GN 
Acute tubulointerstitial nephritis 
Acute tubular necrosis 
Prolongation of pre-renal insult , intravascular hemolysis , sepsis , 
nephrotoxixc agents , multiorgan failure , rhabdomyolysis , snakebite 
, other envenomations , falciparum malaria , leptospirosis
POST RENAL 
Posterior urethral valves 
Ureteropelvic junction obstruction 
Ureterovesicular junction obstruction 
Ureterocele 
Tumor 
Urolithiasis 
Hemorrhagic cystitis 
Neurogenic bladder
PRE RENAL 
 Also called prerenal azotemia, is 
characterized by diminished effective 
circulating arterial volume, which leads to 
inadequate renal perfusion and a decreased 
GFR .
Mechanisms of Sodium and Water 
Conservation in Prerenal Azotemia 
Renin 
Angiotensin II 
Aldosterone 
Decreased Renal Perfusion 
Renal Tubular Na 
Reabsorption 
Vasopressin 
Renal Tubular H2O 
Reabsorption 
Urine Volume 
Concentrated Urine 
Urine Sodium
POST RENAL 
 It 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 AKI. 
 Relief of the obstruction usually results in 
recovery of renal function except in patients 
with associated renal dysplasia or prolonged 
urinary tract obstruction.
RENAL CAUSES 
 It includes a variety of disorders 
characterized by renal parenchymal damage, 
including sustained hypoperfusion , ischemia 
and nephrotoxins.
OBSTRUCTION OF RENAL ARTERIES AND VEINS 
 Bilateral renal arterial thrombosis may occur 
after umbilical artery catheterization in 
neonates. 
 Renal vein thrombosis may be a complication of 
infant of diabetic mother especially following 
dehydration. 
 In older children renal vein thrombosis may 
occur with nephrotic syndrome with anasarca 
and dehydration. 
 Gross hematuria, enlargement of kidney and 
azotemia are typical manifestation.
INVOLVEMENT OF RENAL MICROVASCULATURE 
 Hemolytic uremic sundrome is a common 
cause in children developing AKI . 
 Following dysentry shigela-toxin enters the 
circulation and lead to endothelial injury in 
microvasculature . 
 Localized coagulation and deposition of 
platelet thrombi and fibrin in glomeruli 
causing decrease in GFR.
ACUTE INTERSTITIAL NEPHRITIS 
 Allergic: antibiotics (β-lactams, sulfonamides, 
quinolones, rifampin), nonsteroidal anti-inflammatory 
drugs, diuretics, other drugs 
 Infection: pyelonephritis (if bilateral) 
 Infiltration: lymphoma, leukemia, sarcoidosis 
 Inflammatory, nonvascular: Sjögren’s syndrome, 
tubulointerstitial nephritis with uveitis 
 The patient may have fever , arthralgia , rash 
and eosinophilia : urine often shows eosinophils 
.
Etiology of AIN
ACUTE TUBULAR NECROSIS 
 Occurs most often in critically ill infants and children 
who have been exposed to nephrotoxic and/or 
perfusion insults. 
 Common causes of ATN include renal hypoperfusion 
following volume contraction , severe renal 
vasoconstriction , nephrotoxic agents , sepsis , shock 
and hypotension. 
 The mechanisms of injury in ATN can include 
alterations in intrarenal hemodynamics, tubular 
obstruction, and passive backleak of the glomerular 
filtrate across injured tubular cells into the peritubular 
capillaries.
CLINICAL PRESENTATION 
Pre renal 
There may be history of volume loss from 
vomiting, diarrhea, or blood loss and may 
present with dehydration , hypotension , 
tachycardia , pallor , and decreased urine 
output .
RENAL 
 Hematuria, edema, and hypertension indicates 
a glomerular etiology for AKI. 
 Dysentry, patechie and pallor- HUS 
 Sudden passage of dark red urine, pallor and 
jaundice- acute intravascular hemolysis 
 Presence of rash, arthritis might suggest SLE or 
HSP. 
 History of prolong hypotension or with exposure 
to nephrotoxic medication most likely have ATN.
 Allergic interstitial nephritis should be 
suspected with fevers, rash, arthralgias, and 
exposure to certain medications, including 
NSAIDs and antibiotics.
POST RENAL 
 History of interrupted urinary stream and 
palpable bladder or kidney suggest 
obstructive uropathy. 
 Abdominal colic hematuria and dysuria 
suggest urinary tract calculi.
DIAGNOSIS 
Physical examination 
Obtaining a thorough physical examination is extremely 
important when collecting evidence about the etiology of 
AKI. Clues may be found in any of the following 
 Skin 
 Eyes 
 Ears 
 Cardiovascular system 
 Abdomen 
 Pulmonary system
Skin :- Palpable purpura - Systemic vasculitis 
Maculopapular rash - Allergic interstitial nephritis 
Eye :- Evidence of uveitis may indicate interstitial nephritis 
and necrotizing vasculitis. Ocular palsy may indicate 
ethylene glycol poisoning or necrotizing vasculitis 
Ear :- Hearing loss - Alport disease and aminoglycoside 
toxicity 
Mucosal or cartilaginous ulcerations - Wegener 
granulomatosis 
Pulmonary system :- Respiratory rate , pattern 
On Auscultation of lungs basal crepts
CARDIOVASCULAR EXAMINATION 
 Pulse rate and blood pressure recordings 
 Close inspection of the jugulovenous pulse 
 Careful examination of the heart and lungs 
 Assessment for peripheral edema 
Cardiovascular examination may reveal the 
following: 
 Murmurs - Endocarditis 
 Pericardial friction rub - Uremic pericarditis 
 Increased jugulovenous distention, rales, S3 - 
Heart failure
Abdomen 
 Abdominal or costovertebral angle tenderness - 
Nephrolithiasis, papillary necrosis, renal artery 
thrombosis, renal vein thrombosis 
 distended bladder – Urinary obstruction 
 The presence of tense ascites can indicate 
elevated intra-abdominal pressure that can retard 
renal venous return and result in AKI.
CONT……. 
 Urine R/E 
 CBC with PBF 
 24 hour urinary protien 
 Blood urea and S. creatinine level 
 Serum electrolyte 
 ASO titer 
 C3 level 
 Serum calcium 
 Serum phosphate 
 Serum uric acid 
 ANA 
 ABG
IMAGING 
 Ultrasound of KUB - evaluates renal size, 
able to detect masses, obstruction, stones 
 Chest x-ray 
 DTPA 
 DMSA
RENAL BIOPSY 
Indicated in 
 Patient in whom the etiology is not identified. 
 Unremitting AKI lasting longer then 2-3 wks 
or in accessing the extent of renal damage 
and out come. 
 Suspected drug induced AKI in a patient 
receiving therapy with a potentially 
nephrotoxic drugs.
INDICES FOR DIFFERENTIATING PRE-RENAL FROM RENAL AKI 
PRE-RENAL INTRINSIC 
URINARY SODIUM (mEq/l) < 20 > 40 
Urinary osmolality (mOsm/kg) > 500 < 300 
Blood urea to creatinine ratio >20:1 < 20:1 
Urine to plasma osmolality ratio >1.5 < 0.8 – 1.2 
Fractional excretion of sodium < 1 > 1
MANAGEMENT 
The basic principles of management include 
 Treatment of life-threatening complications 
 Maintenance of fluid and electrolyte balance 
 Nutritional support. 
 Specific management of underlying disorder
LIFE THREATENING COMPLICATIONS 
 Hyperkalemia 
 Fluid overload with heart failure 
 Severe hypertension with encephalopathy 
 Profound acidosis 
 Severe anemia
MANAGEMENT OF COMPLICATION 
Hperkalemia : 
 Calcium gluconate 0.5-1 ml/kg over 5 to 10 
minute 
 Salbutamol nebulization 
 Glucose 0.5-1 gm/kg with 0.1-0.2 unit/kg 
insulin 
 Sodium bicarbonate 1-2 ml/kg
Fluid overload : 
 fluid restriction (insensible loss + POD) 
Pulmonary Edema 
 Oxygen 
 Dopamine (5-10) mcg /kg /min infusion 
 Frusemide (2-4)mg /kg
 Hypertension 
 Nitroprusside 1-8 mcg/kg/min 
 Frusemide 2-4 mg/kg 
 Nifedipine 0.3-0.5 mg/kg
 Acidosis 
Sodium bicarbonate 
Anemia 
Pack red cell 3-5 ml/kg
SUPPORTIVE CARE 
 Fluids: amount given equals insensible loss 
plus urine volume 
 Nutrition: protein intake of 1 gm/kg 
 Prevent infection and treat with appropriate 
antibiotics. 
 Avoid nephrotoxic drugs 
 Measure Weight daily, Prevent weight gain 
 Monitor urine output
DIALYSIS 
Indication: 
 Uremia: altered sensorium abnormal 
behavior seizure 
 Hyperkalemia: k+ > 6.5 meq/l, k+ 5.5-6.5 
meq/l with ECG changes 
 Hyponatremia: Na+ < 120 meq/l if 
symptomtic 
 Fluid overload: resistant to diuretics, 
CCF,HTN 
 Metabolic acidosis: PH< 7.2 despite 
sodium bicarbonate therapy.
MANAGEMENT OF COMMON CONDITION 
CAUSING AKI 
 Prerenal AKI: administer crystalloids, stop 
diuretics, NSAIDs, ACE inhibitors. 
 ATN: supportive care, discontinue drugs or 
toxin, treat cause of circulatory failure. 
 Glomerulonephritis: supportive care If post-infectious, 
antibiotic for endocarditis, shunt 
infection, immunosuppressive medication.
 HUS: supportive care, plasma infusion, plasma 
exchange 
 Vasculitis: immunosuppressive medication, plasma 
exchange 
 Interstital nephritis: discontinue offending drugs, 
consider steroid therapy. 
 Renal artery , vein occlusion: anticoagulation, 
thrombolysis or surgery. 
 Intrarenal obstruction: discontinue offending drugs, 
alkaline diuresis for rhabdomyolysis , haemoglobinuria 
or urate crystal. 
 Urinary tract obstruction: bladder cathaterization or 
nephrostomy, surgical treatment of obstruction.
OUTCOME 
 Mortality rates from 30-50% have been reported from 
developing countries. But the results have markedly 
improved at tertiary centers with proper experties and 
modern facilities. 
 Outcome depend upon underlying cause. 
 Prognosis is favourable in ATN from volume 
depletion, intravascular hemolysis, acute interstial 
nephritis and drugs or toxin related AKI especially 
when complicating factor are absent . 
 In cresentic GN, atypical HUS, and AKI associated 
with sepsis, multi organ failure the prognosis is less 
satisfactory .
PREVENTION OF AKI 
 Important measures includes prompt 
rehydration therapy in acute diarrhea, 
avoidance or judicious use of nephrotoxic 
drugs. 
 Maintenance of proper hydration for patients 
undergoing diagnostic procedures with radio 
contrast media. 
 Force diuresis along with the use of 
allopurinol is effective preventing AKI in 
patient with TLS.
Seminar on Acute Kidney Injury in Children

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Seminar on Acute Kidney Injury in Children

  • 1. WELCOME TO SEMINAR Presented by Dr. Bipin Karki Dr. Amlendra Yadav Dr. Chandra shekhar
  • 2. CASE Tuhin 7 yrs old male child from sylhet , admitted with a complain of oliguria for 2 days associated with respiratory distress for same duration. He had h/o bee sting all over body surface 7 days back when he was returning home from school. He was afebrile , puffy face, restless , mild pale , dyspenic , edema present. Abdomen was soft, distended, non-tender, no organomegaly , ascites present evidenced by shifting dullness.
  • 3. INVESTIGATION  S creatinine: 8 mg/dl  Blood urea: 400 mg/dl  Urine R/E Pus cell – (4-6)/ HPF Epi. Cell – (2-4)/HPF RBC – Nil Protein – (++)
  • 5. DEFINITION Rapid deteriotion of renal function resulting in retention of nitrogenous wastes and inability of kidney to regulate fluid and electrolyte homeostasis. In year 2004 the acute dialysis quality initiative (ADQI) proposed RIFLE criteria for defining AKI . Later, Acute Kidney Injury Network (AKIN) classified AKI based on the RIFLE system.
  • 6. RIFLE CRITERIA R = risk for renal dysfunction I = injury to the kidney F = failure of kidney function L = loss of kidney function E = end-stage renal disease
  • 8. INCIDENCE  The precise incidence of AKI in children is not well known.  Data from bangladesh is not available  A data from india .  4-6 % case of AKI seen in general ward and upto 40% in PICU .  Affects childrens who have sepsis and multiorgan failure.  Children undergoing major cardiac surgery and organ transplantation are at considerable risk for developing AKI.
  • 9. ETIOLOGY  Pre renal  Intrinsic or renal  Post renal
  • 10. PRE RENAL  Acute gastroenteritis  Blood loss  Shock  Fulminant hepatic failure  Reye syndrome  Congestive cardiac failure  Nephrotic syndrome  Hepatorenal syndrome
  • 11. INTRINSIC RENAL  Renal Major vessel obstruction - renal vein thrombosis , renal arterial obstruction, hemolytic uremic syndrome , HSP , polyarteritis and other vasculitis  Glomerular Acute glomerulonephritis ( poststreptococcal , other infections ), cresentic GN Acute tubulointerstitial nephritis Acute tubular necrosis Prolongation of pre-renal insult , intravascular hemolysis , sepsis , nephrotoxixc agents , multiorgan failure , rhabdomyolysis , snakebite , other envenomations , falciparum malaria , leptospirosis
  • 12. POST RENAL Posterior urethral valves Ureteropelvic junction obstruction Ureterovesicular junction obstruction Ureterocele Tumor Urolithiasis Hemorrhagic cystitis Neurogenic bladder
  • 13.
  • 14. PRE RENAL  Also called prerenal azotemia, is characterized by diminished effective circulating arterial volume, which leads to inadequate renal perfusion and a decreased GFR .
  • 15. Mechanisms of Sodium and Water Conservation in Prerenal Azotemia Renin Angiotensin II Aldosterone Decreased Renal Perfusion Renal Tubular Na Reabsorption Vasopressin Renal Tubular H2O Reabsorption Urine Volume Concentrated Urine Urine Sodium
  • 16. POST RENAL  It 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 AKI.  Relief of the obstruction usually results in recovery of renal function except in patients with associated renal dysplasia or prolonged urinary tract obstruction.
  • 17. RENAL CAUSES  It includes a variety of disorders characterized by renal parenchymal damage, including sustained hypoperfusion , ischemia and nephrotoxins.
  • 18. OBSTRUCTION OF RENAL ARTERIES AND VEINS  Bilateral renal arterial thrombosis may occur after umbilical artery catheterization in neonates.  Renal vein thrombosis may be a complication of infant of diabetic mother especially following dehydration.  In older children renal vein thrombosis may occur with nephrotic syndrome with anasarca and dehydration.  Gross hematuria, enlargement of kidney and azotemia are typical manifestation.
  • 19. INVOLVEMENT OF RENAL MICROVASCULATURE  Hemolytic uremic sundrome is a common cause in children developing AKI .  Following dysentry shigela-toxin enters the circulation and lead to endothelial injury in microvasculature .  Localized coagulation and deposition of platelet thrombi and fibrin in glomeruli causing decrease in GFR.
  • 20. ACUTE INTERSTITIAL NEPHRITIS  Allergic: antibiotics (β-lactams, sulfonamides, quinolones, rifampin), nonsteroidal anti-inflammatory drugs, diuretics, other drugs  Infection: pyelonephritis (if bilateral)  Infiltration: lymphoma, leukemia, sarcoidosis  Inflammatory, nonvascular: Sjögren’s syndrome, tubulointerstitial nephritis with uveitis  The patient may have fever , arthralgia , rash and eosinophilia : urine often shows eosinophils .
  • 22. ACUTE TUBULAR NECROSIS  Occurs most often in critically ill infants and children who have been exposed to nephrotoxic and/or perfusion insults.  Common causes of ATN include renal hypoperfusion following volume contraction , severe renal vasoconstriction , nephrotoxic agents , sepsis , shock and hypotension.  The mechanisms of injury in ATN can include alterations in intrarenal hemodynamics, tubular obstruction, and passive backleak of the glomerular filtrate across injured tubular cells into the peritubular capillaries.
  • 23.
  • 24. CLINICAL PRESENTATION Pre renal There may be history of volume loss from vomiting, diarrhea, or blood loss and may present with dehydration , hypotension , tachycardia , pallor , and decreased urine output .
  • 25. RENAL  Hematuria, edema, and hypertension indicates a glomerular etiology for AKI.  Dysentry, patechie and pallor- HUS  Sudden passage of dark red urine, pallor and jaundice- acute intravascular hemolysis  Presence of rash, arthritis might suggest SLE or HSP.  History of prolong hypotension or with exposure to nephrotoxic medication most likely have ATN.
  • 26.  Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and antibiotics.
  • 27. POST RENAL  History of interrupted urinary stream and palpable bladder or kidney suggest obstructive uropathy.  Abdominal colic hematuria and dysuria suggest urinary tract calculi.
  • 28. DIAGNOSIS Physical examination Obtaining a thorough physical examination is extremely important when collecting evidence about the etiology of AKI. Clues may be found in any of the following  Skin  Eyes  Ears  Cardiovascular system  Abdomen  Pulmonary system
  • 29. Skin :- Palpable purpura - Systemic vasculitis Maculopapular rash - Allergic interstitial nephritis Eye :- Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis. Ocular palsy may indicate ethylene glycol poisoning or necrotizing vasculitis Ear :- Hearing loss - Alport disease and aminoglycoside toxicity Mucosal or cartilaginous ulcerations - Wegener granulomatosis Pulmonary system :- Respiratory rate , pattern On Auscultation of lungs basal crepts
  • 30. CARDIOVASCULAR EXAMINATION  Pulse rate and blood pressure recordings  Close inspection of the jugulovenous pulse  Careful examination of the heart and lungs  Assessment for peripheral edema Cardiovascular examination may reveal the following:  Murmurs - Endocarditis  Pericardial friction rub - Uremic pericarditis  Increased jugulovenous distention, rales, S3 - Heart failure
  • 31. Abdomen  Abdominal or costovertebral angle tenderness - Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis  distended bladder – Urinary obstruction  The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return and result in AKI.
  • 32. CONT…….  Urine R/E  CBC with PBF  24 hour urinary protien  Blood urea and S. creatinine level  Serum electrolyte  ASO titer  C3 level  Serum calcium  Serum phosphate  Serum uric acid  ANA  ABG
  • 33. IMAGING  Ultrasound of KUB - evaluates renal size, able to detect masses, obstruction, stones  Chest x-ray  DTPA  DMSA
  • 34. RENAL BIOPSY Indicated in  Patient in whom the etiology is not identified.  Unremitting AKI lasting longer then 2-3 wks or in accessing the extent of renal damage and out come.  Suspected drug induced AKI in a patient receiving therapy with a potentially nephrotoxic drugs.
  • 35. INDICES FOR DIFFERENTIATING PRE-RENAL FROM RENAL AKI PRE-RENAL INTRINSIC URINARY SODIUM (mEq/l) < 20 > 40 Urinary osmolality (mOsm/kg) > 500 < 300 Blood urea to creatinine ratio >20:1 < 20:1 Urine to plasma osmolality ratio >1.5 < 0.8 – 1.2 Fractional excretion of sodium < 1 > 1
  • 36. MANAGEMENT The basic principles of management include  Treatment of life-threatening complications  Maintenance of fluid and electrolyte balance  Nutritional support.  Specific management of underlying disorder
  • 37. LIFE THREATENING COMPLICATIONS  Hyperkalemia  Fluid overload with heart failure  Severe hypertension with encephalopathy  Profound acidosis  Severe anemia
  • 38. MANAGEMENT OF COMPLICATION Hperkalemia :  Calcium gluconate 0.5-1 ml/kg over 5 to 10 minute  Salbutamol nebulization  Glucose 0.5-1 gm/kg with 0.1-0.2 unit/kg insulin  Sodium bicarbonate 1-2 ml/kg
  • 39. Fluid overload :  fluid restriction (insensible loss + POD) Pulmonary Edema  Oxygen  Dopamine (5-10) mcg /kg /min infusion  Frusemide (2-4)mg /kg
  • 40.  Hypertension  Nitroprusside 1-8 mcg/kg/min  Frusemide 2-4 mg/kg  Nifedipine 0.3-0.5 mg/kg
  • 41.  Acidosis Sodium bicarbonate Anemia Pack red cell 3-5 ml/kg
  • 42. SUPPORTIVE CARE  Fluids: amount given equals insensible loss plus urine volume  Nutrition: protein intake of 1 gm/kg  Prevent infection and treat with appropriate antibiotics.  Avoid nephrotoxic drugs  Measure Weight daily, Prevent weight gain  Monitor urine output
  • 43. DIALYSIS Indication:  Uremia: altered sensorium abnormal behavior seizure  Hyperkalemia: k+ > 6.5 meq/l, k+ 5.5-6.5 meq/l with ECG changes  Hyponatremia: Na+ < 120 meq/l if symptomtic  Fluid overload: resistant to diuretics, CCF,HTN  Metabolic acidosis: PH< 7.2 despite sodium bicarbonate therapy.
  • 44. MANAGEMENT OF COMMON CONDITION CAUSING AKI  Prerenal AKI: administer crystalloids, stop diuretics, NSAIDs, ACE inhibitors.  ATN: supportive care, discontinue drugs or toxin, treat cause of circulatory failure.  Glomerulonephritis: supportive care If post-infectious, antibiotic for endocarditis, shunt infection, immunosuppressive medication.
  • 45.  HUS: supportive care, plasma infusion, plasma exchange  Vasculitis: immunosuppressive medication, plasma exchange  Interstital nephritis: discontinue offending drugs, consider steroid therapy.  Renal artery , vein occlusion: anticoagulation, thrombolysis or surgery.  Intrarenal obstruction: discontinue offending drugs, alkaline diuresis for rhabdomyolysis , haemoglobinuria or urate crystal.  Urinary tract obstruction: bladder cathaterization or nephrostomy, surgical treatment of obstruction.
  • 46. OUTCOME  Mortality rates from 30-50% have been reported from developing countries. But the results have markedly improved at tertiary centers with proper experties and modern facilities.  Outcome depend upon underlying cause.  Prognosis is favourable in ATN from volume depletion, intravascular hemolysis, acute interstial nephritis and drugs or toxin related AKI especially when complicating factor are absent .  In cresentic GN, atypical HUS, and AKI associated with sepsis, multi organ failure the prognosis is less satisfactory .
  • 47. PREVENTION OF AKI  Important measures includes prompt rehydration therapy in acute diarrhea, avoidance or judicious use of nephrotoxic drugs.  Maintenance of proper hydration for patients undergoing diagnostic procedures with radio contrast media.  Force diuresis along with the use of allopurinol is effective preventing AKI in patient with TLS.