acute kidney injury

1. ACUTE KIDNEY
INJURY

2. DR/ Walaa Farah
Neonatologist in
Elnasr nicu
Presented
by

3. DEFINITION
Acute kidney injury, previously called acute
renal failure, is characterized by a reversible
increase in the blood concentration of creatinine
and nitrogenous waste products and by the
inability of the kidney to appropriately 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.

4. 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

5. > 3 months

7. INCIDENCE
Incidence of AKI in hospitalized children appears to be
increasing in a pediatric tertiary care center, 227 children
received dialysis therapy during an 8-year interval, for an
overall incidence of 0.8 per 100,000 total population.
Very low birth weight (<1,500 g), a low Apgar score, a patent
ductus arteriosus, and maternal administration of
antibiotics and NSAIDS have been associated with the
development of AKI. In addition to environmental factors,
some children may have genetic risk factors for AKI.
 4-6 % case of AKI seen in general ward and up to 40% in
PICU .
 Affects children who have sepsis and multi-organ failure.
 Children undergoing major cardiac surgery and organ
transplantation are at considerable risk for developing
AKI.

8. 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

12. INTRINSIC RENAL
 Renal vessel obstruction:
- renal vein thrombosis , renal arterial obstruction, hemolytic uremic
syndrome , HSP , polyarteritis nodosa and other vasculitis
 Glomerular :
Acute glomerulonephritis (poststreptococcal ,other infections ),
rapidly progressive GN , lupus nephritis.
 Acute interstitial nephritis
 Acute tubular necrosis
Prolongation of pre-renal insult , intravascular hemolysis , sepsis ,
nephrotoxixc agents , multi-organ failure , rhabdomyolysis , snakebite
, other envenomations , falciparum malaria , leptospirosis
 Developmental:
Polycystic kidney or hypoplasia.

13. POST RENAL
• Posterior urethral valves.
• Ureteropelvic junction obstruction.
• Ureterovesicular junction obstruction.
• Ureterocele.
• Tumor.
• Urolithiasis.
• Hemorrhagic cystitis.
• Neurogenic bladder.
 A renal ultrasound should be performed promptly in a
child with AKI to evaluate for obstructive uropathy,
which can be treated by relieving the obstruction.

15. PRE RENAL
 Also called prerenal azotemia, is characterized
by diminished effective circulating arterial
volume, which leads to inadequate renal
perfusion and a decreased GFR.
 The kidneys are intrinsically normal, and
prerenal failure is reversible once the blood
volume and hemodynamic conditions are
restored to normal.
 Several urinary parameters, including Uosm,
urine sodium concentration, the fractional
excretion of sodium, and the renal failure index,
have all been proposed to help differentiate
prerenal failure from vasomotor nephropathy.

16. •During prerenal failure, the tubules are able to respond to
decreased renal perfusion by appropriately conserving sodium
and water such that the Uosm is greater than 400 to 500 mOsm/L,
the urine sodium is less than 10 to 20 mEq/L, and the fractional
excretion of sodium is less than 1%:
FENa+ (%) = [UNa+/SNa+] × [SCr/UCr] × 100
• Because the renal tubules in newborns and premature infants
are relatively immature compared with those in older infants and
children, the corresponding values suggestive of renal
hypoperfusion are Uosm greater than 350 mOsm/L, urine sodium
less than 20 to 30 mEq/L, and a fractional excretion of sodium of
less than 2.5%.
• When the renal tubules have sustained injury, as occurs in ATN,
they cannot conserve sodium and water appropriately, so the
Uosm is less than 350 mOsm/L, the urine sodium is greater than
30 to 40 mEq/L, and the fractional excretion of sodium is greater
than 2.0%. However, the use of these numbers to differentiate
prerenal failure from ATN requires that the patient have normal

17. Renin
Angiotensin II
Aldosterone
Renal Tubular Na
Reabsorption
Vasopressin
Renal Tubular H2O
Reabsorption
Urine Volume
Concentrated Urine
Urine Sodium
Decreased Renal Perfusion
Mechanisms of Sodium and Water
Conservation in Prerenal Azotemia

18. 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.

19. RENAL CAUSES
 It includes a variety of disorders
characterized by renal parenchymal damage,
including sustained hypoperfusion , ischemia
and nephrotoxins.

20. 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.

21. PATHOLOGICALLY RADIOLOGICALLY

22. INVOLVEMENT OF RENAL MICROVASCULATURE
 Hemolytic uremic syndrome is a common cause in children
developing AKI .
 Following dysentery 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.
 Triad of renal impairment, thrombocytopenia and micro-
angiopathic hemolytic anemia.
 Need early and aggressive dialysis.
 Antibiotic should not be prescribed in cases of enteritis
especially with E.coli as it increase destruction of bacteria
and increase toxins production (controversial).
 Shiga toxin inhibitors are under trial.

26. ACUTE CORTICAL NECROSIS
• More common in young children, particularly in the neonate.
• Associated with hypoxic-ischemic insults resulting from
perinatal anoxia, placenta abruption, and twin-twin or twin-
maternal transfusions with resultant activation of the coagulation
cascade.
• Clinically, child shows gross or microscopic hematuria and
oliguria and may have hypertension.
•Laboratory features of an elevated BUN and creatinine,
thrombocytopenia may also be present as a result of the micro
vascular injury.
• Radiographic features include a normal renal ultrasound in
the early phase, and ultrasound in the later phases may show
that the kidney has undergone atrophy and substantially
decreased in size. A radionuclide renal scan will show decreased
to no perfusion with delayed or no function.

28. ACUTE INTERSTITIAL NEPHRITIS
 Allergic: antibiotics (β-lactams, sulfonamides, quinolones,
rifampin), nonsteroidal anti-inflammatory
drugs,diuretics,others
 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 .
 Radiographic studies demonstrate large echogenic kidneys.
 Kidney biopsy demonstrates interstitial infiltrate with many
eosinophils.
 Therapy for AIN includes withdrawal of the drug implicated
in causing AIN. In addition, corticosteroids may aid in the
resolution of the renal failure.

30. Etiology of AIN

32. 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.

34. LUPUS NEPHRITIS
Systemic lupus erythematosus is a systemic inflammatory
disease of uncertain etiology that involves many organs, including the
kidney. Children initially may present with renal disease without extra
renal signs of SLE, but they usually rapidly develop other symptoms
and fulfill the diagnostic criteria for SLE.
More common in young adolescent females (F/M, 8:1), but 20%
to 25% of cases occur in childhood and even, rarely, in infancy.
Asian, black, and Hispanic children are more affected than white
children.
Nephritis is more common in childhood lupus, affecting up to 80%
of patients at some point, usually within the first 6 months after
diagnosis. Children often present with fever, malaise, arthritis, and
anemia.Less than half of children have a classic malar rash, but more
than half have hematuria or proteinuria, and a few have edema, NS,
or hypertension. The extent of the renal involvement may not be
clinically apparent and usually requires referral to a pediatric

36. Laboratory evaluation of SLE may reveal anemia,
leucopenia, and thrombocytopenia, as well as severely
decreased concentrations of serum C3 and C4.
Antinuclear antibody and anti–double-stranded DNA
antibody titers are elevated at diagnosis in 95% of
patients with nephritis. Urine abnormalities include
microscopic and gross hematuria, proteinuria, and casts
(red cell, white cell, hyaline, and/or broad-waxy).
Proteinuria may be mild, moderate, or in the nephrotic
range. Heavy proteinuria is usually associated with more
severe disease. One-half of children with SLE nephritis
have elevated serum creatinine levels and decreased
creatinine clearance during the initial course of their
disease.
Lupus nephritis has been divided into 6 classes by
the appearance of the renal biopsy.

37. Treatment:
Predinsolone, azathroprine, cyclophosphamide and rituximab.
Prognosis:
No complete cure just remission with frequent relapses.

38. 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 .

39. 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.

40.  Allergic interstitial nephritis should be
suspected with fevers, rash, arthralgias, and
exposure to certain medications, including
NSAIDs and antibiotics.

41. POST RENAL
 History of interrupted urinary stream and
palpable bladder or kidney suggest
obstructive uropathy.
 Abdominal colic hematuria and dysuria
suggest urinary tract calculi.

42. 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

43. 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

44. 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, rakles, S3 -
Heart failure

45. Abdomen
 Abdominal or costo vertebral 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.

46. INVESTIGATIONS
 Urine R/E: hematuria, proteinuria and casts.
 CBC with PBF:
*Anemia dilutional, microangiopathic hemolytic
anemia(MAHA) or blood loss.
*Leucopenia SLE * Leucocytosis sepsis
*Thrombocytopenia MAHA
 24 hour urinary protien
 Blood urea and S. creatinine level : elevated
 Serum electrolyte : hyperkalemia, hyponatremia,
hypocalemia and hyperphosphatemia.
 ASO titer : PSGN
 C3 level
 Anti ds-DNA: SLE.
 ABG : Metabolic acidosis with wide anion gap.

48. 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

49. IMAGING
 Ultrasound of KUB - evaluates renal size,
able to detect masses, obstruction, stones
 Chest x-ray: cardiomegaly or pulmonary
edema.
 DTPA
 DMSA

50. 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.

51. ALGORISM FOR DIAGNOSIS OF AKI

52. 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

53. LIFE THREATENING COMPLICATIONS
 Hyperkalemia
 Fluid overload with heart failure
 Severe hypertension with encephalopathy
 Profound acidosis
 Severe anemia

54. MANAGEMENT OF COMPLICATION
Hyperkalemia :
K restriction
 Calcium gluconate 0.5-1 ml/kg over 5 to 10
minute to stabilize cardiac muscle.
 Salbutamol nebulization: increase K cellular
uptake.
 Sodium bicarbonate 1-2 ml/kg .
 Kayexelate ( Na polystyrene resin) oral or enema
1mg/kg can be repeated every 2 hrs, exchange of
Na and K in the GIT.
 Glucose 0.5-1 gm/kg with insulin 1 iu/4 gm

55.  Acidosis
Sodium bicarbonate (if PH<7.15 and Hco3<8)
0.3*BW*(12- actual)
 Hypocalcemia:
Due to hyperphosphatemia which can be lowered
by Al(OH)3 or CaCo3.
IV Ca gluconate only if tetany occur as it will
increase phosphate.
 Hyponatremia:
Fluid restriction, if Na < 120 give hypertonic saline
3%
(125-actual)*0.6*BW.
 Anemia

56. Fluid overload :
 fluid restriction (insensible loss + POD)
Pulmonary Oedema:
 Oxygen
 Dopamine (5-10) mcg /kg /min infusion
 Frusemide (2-4)mg /kg
GIT bleeding:
 Due to platelets dysfunction, stress ulcer or
heparin used in haemodialysis.
 Treated with antacids , ranitidine or omperazole.
Convulsion:
 due to hypocalcemia , hyponatremia,
hyepertensive encephalpathy, uremia or cerebral
hge.

57.  Hypertension :
MILD: salt restriction, frusemide, B blocker
and hydralazine.
Severe: (Heart failure or hypertensive
encephalopathy)
Nitroprusside 1-8 mcg/kg/min
Frusemide 2-4 mg/kg
Nifedipine 0.3-0.5 mg/kg

58. 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

59. DIALYSIS
 Uremia: altered sensorium abnormal behavior
seizure.
 BUN>100mg/dl.
 Hyperkalemia: k+ > 6.5 meq/l, k+ 5.5-6.5 meq/l
with ECG changes
 Hyponatremia: Na+ < 120 meq/l if symptomatic
and not respond to treatment.
 Fluid overload: resistant to diuretics, CCF,HTN
 Metabolic acidosis: PH< 7.2 despite sodium
bicarbonate therapy.
 Ca/P imbalance with tetany.
 Inability to provide nutritional intake due to severe
fluid restriction.

60. Forms of dialysis:
•Intermittent hemodialysis.
• Peritoneal dialysis.
• Continous renal replacement therapy:
Used in sepsis, unstable hemodynamic state
and multi-organ failure.

61. 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, steroids and immunosuppressive
medication.

62.  HUS: supportive care, early dialysis, plasma exchange
 Vasculitis: immunosuppressive medication, plasma
exchange
 Interstitial 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 catheterization or
nephrostomy, surgical treatment of obstruction.

63. OUTCOME
 Mortality rates from 30-50% have been reported
from developing countries. But the results have
markedly improved at tertiary centers with proper
expertise and modern facilities.
 Outcome depend upon underlying cause.
 Prognosis is favorable in ATN from volume
depletion, intravascular hemolysis, acute intestinal
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 .

64. 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.