Acute kidney injury (AKI), formerly known as acute renal failure, is defined as a sudden deterioration of kidney function resulting in the inability to maintain fluid and electrolyte homeostasis. It can be caused by prerenal issues affecting blood flow to the kidneys, intrinsic renal parenchymal damage, or postrenal urinary tract obstruction. The incidence of AKI varies globally and it commonly occurs in critically ill children with coexisting conditions. Etiologies include pre-renal causes like decreased intravascular volume, intrinsic renal diseases affecting glomeruli or tubules, and post-renal obstruction. Diagnosis involves lab tests of kidney and liver function as well as imaging studies. Treatment focuses on fluid management, electrolyte

1. ACUTE KIDNEY
INJURY IN CHILDREN
Dr. Raghav Kakar
M.D. Paediatrics

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

4. Epidemiology

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.

6. ETIOLOGY

7.  Pre renal
 Intrinsic or renal
 Post renal

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.

9. Causes of PreRenal Azotemia
 Decreased true intravascular volume
 Acute gastroenteritis, Burns, Hemorrhage, Sepsis
 Decreased effective intravascular volume
 Burns, Nephrotic syndrome, Massive ascites, Anaphylaxis, Cardiac
failure, Shock
 Medications
 NSAIDs ,ACE inhibitors, ARBs

10. Renal (Intrinsic)
CAUSES –
1. Obstruction of renal artery or veins –
Renal vein thrombosis, Renal arterial obstruction,
2. Involvement of renal microvasculature –
HUS, HSP, Poly-arteritis, Collagen vascular disease
3. Glomerular causes-
PSGN, Crescentic GN
4. Interstitial causes-
Acute tubulointerstitial nephritis
5. Tubular causes (ATN)
Prolongation of pre-renal insult, intravascular hemolysis, sepsis,
nephrotoxic agents, multiorgan failure, rhabdomyolysis, snakebite,
falciparum malaria.

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.

13. 3. Glomerular disease
 PSGN,
 Post infectious GN,
 Cresentic GN,
 IgA nephropathy .

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

19. CLINICAL EVALUATION

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

24. Skin :-
 Palpable purpura - Systemic vasculitis
 Maculopapular rash - Allergic interstitial nephritis
Eye :-
 Uveitis – interstitial nephritis and necrotizing
vasculitis.
Ear :-
 Hearing loss - Alport disease and aminoglycoside
toxicity
 Mucosal or cartilaginous ulcerations – Wegener’s
granulomatosis

25. Respiratory system :-
 rapid and deep breathing – met. Acidosis
 basal crepts - volume overload
Cardiovascular examination :
 Pericardial friction rub - Uremic pericarditis
 Increased JVP, Gallop rhythm, pitting edema – CHF
due to volume overload.

26. Abdomen :
 Renal angle tenderness – nephrolithiasis, renal artery or
vein
thrombosis.
 Distended bladder – urinary obstruction.
 F/s/o chronic liver disease with ascites with prerenal AKI
– hepatorenal syndrome

27. Classification System

28. pRIFLE and AKIN grading

29. KDIGO Staging

30. DIAGNOSIS

31. LAB INVESIGATIONS
 Urine R/M
 CBC
 24 hour urinary protein
 Blood urea and S.
creatinine level
 Serum electrolytes
 Urine
 ASO titer
 C3 level
 Serum calcium
 Serum phosphate
 Serum uric acid
 ANA
 ABG

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.

35. Biomarkers

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

39. Promising AKI Biomarkers
 Neutrophil gelatinase-associated lipocalin (NGAL)
 Interleukin 18 (IL-18)
 Kidney injury molecule 1 (KIM-1)
 Atrial Natriuretric Peptide
 Cystatin-C

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.

42. Management

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.

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.

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

60. Thank you