2. Acute Kidney Injury (AKI): Definition
Formerly referred to as acute renal failure (ARF).
Defined as an “sudden deterioration in kidney function
results in the inability to maintain fluid and electrolyte
homeostasis”
3. Kidney function is dependent on
Adequacy of blood supply to the kidney
– Prerenal
Integrity of renal parenchyma
– Renal
Patency of urinary tract
– Post renal
5. The incidence of AKI varies in different regions of
the world.
Estimates range from 20 cases per year per
1,00,000 population in neonates to as low as 2
cases per year per 1,00,000 population in older
children
The co-existence of AKI with critical illness occurs
at a rate of 10% and has 50% mortality in children
requiring dialysis.
8. Pre Renal AKI
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.
11. 1. OBSTRUCTION OF RENAL ARTERIES AND
VEINS
Bilateral renal arterial thrombosis may occur after
umbilical artery catheterisation in neonates
Renal vein thrombosis may be a complication of IDM
especially following dehydration.
In older children, renal vein thrombosis may occur
with nephrotic syndrome with anasarca and
dehydration.
Gross haematuria, enlargement of kidneys and
azotemia are typical manifestation.
12. 2. INVOLVEMENT OF RENAL
MICROVASCULATURE
HUS is a common cause of AKI in chidren.
Causes thrombotic microangiopathy
2 types- D+HUS and D-HUS
Common causes of D+HUS – EHEC(in developed countries),
Shigella dysentriae type I (in India)
Following dysentery shigella-toxin enters the circulation and leads
to endothelial injury in microvasculature .
Localized coagulation and deposition of platelet thrombi and fibrin
occurs in glomeruli causing decrease in GFR.
14. 4. ACUTE INTERSTITIAL NEPHRITIS
Usually occurs due to hypersensitivity reaction to some
drugs (ampicillin, cephalosporins, sulfonamides,
quinolones, NSAID’s, phenytoin etc)
The patient may have fever , arthralgia , rash and
eosinophilia : urine often shows eosinophils
Renal biopsy should be done if it is strongly suspected.
15. 5. Acute Tubular Necrosis
Characterized by renal tubular injury, may occur due to
ischaemia/hypoperfusion or due to injury froms drugs or
toxins.
Ischaemic ATN is a continnum of physiologic responses
that is observed in prerenal azotemia.
If the hypoperfusion is severe and prolonged, ATN can progress to
renal infarction and irreversible renal damage
16. The course is subdivided into 4 phases :
Initiation
Extension
Maintainance
Recovery
17. (C) 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.
18. Causes of post renal AKI
Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Ureterocele
Tumor
Urolithiasis
Hemorrhagic cystitis
Neurogenic bladder
20. Clinical features range from asymptomatic with
mild to moderate elevation in S.creatinine to
anuric renal failure
Decrease or no urine output
Fluid overload
Hypertension
Uraemia, dyselectrolytemia
21. HISTORY
H/o blood loss, diarrhea, vomitting – prerenal aki.
Past h/o pharyngitis with gross hematuria, edema,
hypertension – acute PSGN.
Dysentery, petechiae, pallor- HUS.
Sudden passage of dark red urine, pallor and jaundice
with h/o drug exposure – acute intravascular hemolysis
(G6PD def.).
Rash with arthritis – SLE or HSP.
22. H/o prolonged hypotension or exposure to nephrotoxic
drugs – ATN.
H/o poor urinary stream with palpable UB or kidney –
obstructive uropathy.
Abdominal colic, haematuria, dysuria – urinary tract
stones.
23. PHYSICAL EXAMINATION
Obtaining a thorough physical examination is extremely
important . Clues may be found in any of the following –
Skin
Eyes
Ears
Respiratory system
Cardiovascular system
Abdomen
32. Urinanalysis
Pre-Renal Renal
Urinary sodium (mEq/l) < 20 > 40
Urinary osmolality (mOsm/kg) > 500 < 350
Blood urea to creatinine ratio >20:1 < 20:1
Fractional excretion of sodium < 1 > 1
Specific gravity >1.020 <1.010
33. Imaging
Ultrasound of KUB - evaluates renal size, able to detect
masses, obstruction, stones.
X-ray Abdomen
Renal Scintigraphy
DTPA : the differential functions of each kidney can be
derived.
DMSA : gives excellent images of cortex and useful to define
areas of inflammation
34. RENAL BIOPSY
Indicated in
Patient in whom the etiology is not identified.
Unremitting AKI lasting longer then 2-3 wks or
in assessing the extent of renal damage and
outcome.
Suspected drug induced AKI in a patient
receiving therapy with a potentially nephrotoxic
drugs.
36. Role of Biomarkers in AKI
Early prediction and diagnosis of AKI
Identify the primary location of injury
Pinpoint the duration and severity
Identify the etiology of AKI
Monitor response to intervention and treatment
37. Serum Creatinine
Serum creatinine alone is a poor indicator of renal
function
It varies widely with age, gender, diet, muscle mass,
medications, and hydration status
Up to 50% of kidney function may be lost before serum
creatinine even begins to rise
40. Renal Angina Index
The renal angina index is a predictive tool, performed on
admission to the pediatric intensive care unit, and used
to assess the risk for subsequent severe AKI (≥ doubling
of serum creatinine) 72 h later (Day-3 AKI).
The angina index is a composite of risk strata and
clinical signs of injury.
It consists of 3 risk factors and 2 markers of renal injury,
which are assigned points. Score more than 8 predicts
severe AKI.
43. Management Goals
A. Maintenance of electrolyte and fluid balance.
B. Avoidance of life-threatening complications.
C. Adequate nutritional support.
D. Treatment of the underlying cause.
44. Management: FLUIDS
If no evidence of volume overload or cardiac failure :
Fluid challenge of IV NS , 20 mL/kg over 30 min
No void within 2-4 hr points to intrinsic or postrenal ARF
Vigorous fluid resuscitation may be needed in sepsis
Diuretics if no void with adequate circulation.
In absence of urine output, strict fluid restriction.
Renal dose of dopamine (2-3 μg / kg / min)
45. Hyperkalemia
1. Severe hyperkalemia (>7.0 mEq/L):
Electrocardiographic changes or peripheral muscle
weakness
Can be life-threatening and requires immediate
attention.
2. Acute management includes administration of:
IV calcium to stabilize the cardiac membrane; and/or
glucose/insulin infusion,
Sodium bicarbonate or Glucose-Insulin infusion
(promotes extracellular K shift into the cells)
Kayexalate (an anion exchange resin): removes excess
K from the body.
46. Acidosis
1. In children with AKI:
impaired acid excretion
increased acid production (shock and sepsis)
2. Sodium bicarbonate should only be administered with
life threatening acidosis or hyperkalemia.
3. HCO3 > 12 mEq/L and/or arterial pH greater than 7.2
do not require immediate intervention.
47. Hypertension
Most often a result of hyper-reninemia or from
expansion of fluid volume.
Most commonly seen with AGN and HUS
Management :
Salt and water restriction.
Diuretic adminiistration
Anti-Hypertensives
48. Hyponatremia
Most commonly dilutional
Management:
Fluid restriction
3% Hypertonic saline to symptomatic patients or sodium
less than 120 mEq/L
mEq sodium required = 0.6 X weight(kg) X ( 125-serum
sodium in
mEq/L )
49. Hypocalcemia
Primarily treated by lowering the serum phosphate
levels.
Phosphate binders can be administered.
IV calcium should be avoided
Aluminium-based binders should also be avoided.
50. Nutrition
Sodium, potassium and phosphorous should be
restricted.
Protein intake should also be moderately decreased.
Adequate calories are needed to promote recovery
Renal replacement therapy if sufficient calories cannot
be achieved (patient with oliguria or anuria)
Patients with inappropriate nutrition have poorer
prognosis.
51. Indications for dialysis in ARF
Severe fluid overload unresponsive to management
Persistent hyperkalemia
Severe met.acidosis unresponsive to management.
Neurologic symptoms (altered mental status, seizures)
BUN >100-150 mg/dL (or lower if rapidly rising)
Ca:PO4 imbalance, with hypocalcemic tetany.
Nutritional support in a child with oliguria or anuria.
52. 3 types of dialysis-
a. intermittent haemodialysis (IHD)
b. peritoneal dialysis(PD)
c. CRRT.
a. Intermittent Haemodialysis:
Preffered in patients with relatively stable
hemodynamic state.
Highly efficient, 1 session completes in 3-4 hrs
Can be done 3-7 times/week
Complication : hypotension, bleeding, thrombosis.
53.
54. b. Peritoneal Dialysis:
Most commonly used in infants & neonates.
For 1 session→1 cycle of 45-60 min needs to be
repeated for 2-4 times/day.
The infused volume of the diasylate is 800-
1100ml/m2
No need for anticoagulation , so ↓sed risk of
bleeding , may cause abdominal pain & peritonitis
55. c. CRRT:
Continuous renal replacement therapy (CRRT) is
associated with reduced mortality.
CRRT usually involves the removal and return of
blood through a single cannula placed in a large vein
(venovenous therapy); arteriovenous therapies are
seldom used.
CRRT causes less haemodynamic instability, because
fluid removal is slower and there is time for fluid to re-
equilibrate between body compartments.
56. Indications - hemodynamic instability, sepsis,
extensive trauma, MODS.
Continuous removal of solutes ,fluid & electrolytes
3 types:
CVVH - based on convection
CVVHD - based on diffusion
CVVHDF - based on convection and
diffusion.
57.
58. Outcomes
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 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 .
59. Take Home Message
AKI is a common and serious problem
All AKI are Not equal
The diagnosis of AKI is often delayed.
Earlier recognition and treatment of AKI sequelae may
improve outcome
Novel biomarkers are providing tools for the early
prediction of AKI and outcomes, and for testing
therapies
