acute kidney Injury in pediatric patient include - Introduction Defenition Risk Factors Classifications Etiology Clinical Findings Diagnosis Managmement

1. ACUTE KIDNEY INJERY AKI
Mohammed alqauyyed
Pediatric R4
PSMMC - KSA

2. OBJECTIVES
Introduction
Defenition
Risk Factors
Classifications
Etiology
Clinical Findings
Diagnosis
Managmement

3. INTRODUCTION TO AKI
 AKI is defined as the abrupt loss of kidney function that results in a
decline in GFR, retention of urea and other nitrogenous waste
products, and dysregulation of extracellular volume and electrolytes.
 The term AKI has largely replaced acute kidney failure (AKF).
 Wide range of clinical manifestations from a minimal elevation in
serum creatinine to anuric kidney failure, arises from multiple
causes, and occurs in a variety of clinical settings.

4. DEFENITION OF AKI
The most widely used laboratory finding to make the diagnosis of AKI
remains an elevated serum creatinine. But Cr often a delayed and
imprecise test .. Need time to be accumulated.
Serum creatinine levels can vary with several nonrenal factors,
including age, gender, muscle mass, presence of sepsis, and the
nutritional and hydration status of the child.
Also, decrease in urine output is an important criterion for the
diagnosis of AKI.

5. DEFENITION OF AKI
Standardized and validated definitions for pediatric AKI include
Pediatric Risk, Injury, Failure, Loss, End-Stage Renal Disease (pRIFLE).
Acute Kidney Injury Network (AKIN)
Kidney Disease Improving Global Outcomes (KDIGO) classifications.

6. DEFENITION OF
AKI
 pRIFLE
Consists of:
 Three graded levels of injury
based upon estimated GFR or
urine output
 And two outcome measures
(Loss of kidney function and
ESRD)

7. DEFENITION OF
AKI
 AKIN

8. DEFENITION OF
AKI
 KDIGO

9. DEFENITION OF
AKI
 KDIGO
●Increase in serum creatinine by ≥0.3 mg/dL from baseline (≥26.5 mcmol/L)
within 48 hours;
OR
●Increase in serum creatinine to ≥1.5 times baseline within the prior seven
days;
OR
●Urine volume ≤0.5 mL/kg/hour for six hours

10. RISK FACTOR OF AKI
 Critically ill patients.
sepsis, multi-organ failure, nephrotoxins, congenital heart disease, malignancies,
primary kidney disease, hypotension and shock, hypoxemia, and renal ischemia
 Neonate in NICU
VLBW < 1500g , CHD , sepsis , low gestational age , and perinatal asphyxia.

11. RISK FACTOR OF AKI
 Nephrotoxin use
Abx (aminoglycosides, vancomycin , tazocin ) and antiviral agents.
Radiocontrast agents, ACE inhibitors and (NSAIDs).
Diuretics
 Comorbid conditions
Transplantation , nephrotic syndrome , CHD or SCD

12. CLASSIFICATION OF AKI
•due to hypovolemia (bleeding or gastrointestinal, urinary or cutaneous losses), or reduction of effective
circulation (eg, heart failure, septic shock, and cirrhosis).
Prerenal disease
•structural damage to the renal parenchyma.
•The most common causes are prolonged hypoperfusion, sepsis, nephrotoxins, or severe glomerular
diseases.
Renal disease
•AKI is typically the result of congenital or acquired anatomic obstructions to the lower urinary tract.
Postrenal disease

16. ETIOLOGY OF
AKI
 Prerenal and renal couses.

17. ETIOLOGY OF AKI
 Postrenal couses:
 Postrenal AKI is due to bilateral urinary tract obstruction or obstruction of the
urinary tract of a solitary kidney.
 Causes include renal calculi, clots, neurogenic bladder.
 Children with chronic kidney disease from uncorrected congenital obstructive
uropathies remain at significant risk of AKI from ischemic, septic, and
nephrotoxic insults.

18. CLINICAL PRESENTATION
OF AKI

19. CLINICAL
FINDINGS IN
AKI
 History
The initial history is
directed towards
uncovering an obvious risk
factor or cause for AKI

20. CLINICAL
FINDINGS IN
AKI
 Physical examination
Should include measurement of
blood pressure, and assessment
for edema, recent weight gain,
and signs of systemic disease,
such as rash or joint disease.

21. EVALUATION AND
DIAGNOSIS OF AKI

22. DIAGNOSIS OF AKI
 Clinically based on the presence of characteristic signs and
symptoms, and laboratory findings indicative of an acute change in
kidney function.
• Signs and symptoms include edema, fluid overload, decreased or no urine
output, gross hematuria and/or hypertension.
• Laboratory findings include elevated or rising serum creatinine. An abnormal
urinalysis may also provide support for acute injury to the kidney.

23. DIAGNOSIS OF AKI
 Laboratory test:
Seriolgy labs
Urinalysis
Fractional excretion of sodium
Renal U/S

24. DIAGNOSIS OF AKI
 Serology and Urine labs :
CBC
BUN and S. creatinine level
Serum electrolytes
24hour urinary protein
ASO titer
C3 level
Serum calcium
Serum phosphate
Serum uric acid
ANA , dsDNA
ABG

25. DIAGNOSIS OF AKI
CBC
 Microangiopathic hemolytic anemia associated with thrombocytopenia in
the setting of AKI is diagnostic for HUS.
 Severe hemolysis, whether drug-induced or secondary to
hemoglobinopathies, may also result in ATN due to massive
hemoglobinuria.
 Eosinophilia and/or urine eosinophiluria may be present in some cases of
interstitial nephritis.

26. DIAGNOSIS OF AKI
 Complement studies – including C3, C4, (Hypocomplementemia) is seen in
patients with (PSGN), shunt nephritis, and nephritis associated with
subacute bacterial endocarditis.
 ASO titer – The presence of antistreptococcal antibodies is a diagnostic
criterion for PSGN.
 ANA , dsDNA – SLE and vasculitis
 antiglomerular basement membrane (GBM) – Goodpasture syndrome

27. DIAGNOSIS OF AKI
 Elevated serum levels of aminoglycosides – are associated with ATN.
 Uric acid – may occur in children with tumor lysis syndrome secondary to
chemotherapy treatment of childhood leukemia or lymphoma.

28. DIAGNOSIS
OF AKI
 Urinalysis
Muddy brown granular
casts and epithelial cell
casts are highly suggestive
of intrinsic AKI or (ATN)

29. DIAGNOSIS
OF AKI
 Urinalysis
The finding of red cell
casts is diagnostic of
glomerulonephritis.
The concurrent finding of
dysmorphic red cells and
heavy proteinuria indicates
an active "nephritic"
urinary sediment, which is
also commonly associated
with glomerulonephritis.

30. DIAGNOSIS
OF AKI
 Urinalysis
The finding of red cell
casts is diagnostic of
glomerulonephritis.
The concurrent finding of
dysmorphic red cells and
heavy proteinuria indicates
an active "nephritic"
urinary sediment, which is
also commonly associated
with glomerulonephritis.

31. DIAGNOSIS OF AKI
 Urinalysis
Pyuria with white cell, granular, or waxy casts are suggestive of tubular or interstitial
disease, or UTI
White cells and white cell casts may also be seen in acute glomerulonephritis.
A positive response for heme on a urine dipstick in the absence of red blood cells in
the sediment is seen in patients with hemolysis or rhabdomyolysis.
The urinalysis in children with prerenal AKI is typically normal.

32. DIAGNOSIS
OF AKI
Prerenal VS
Renal
In urinalysis

33. DIAGNOSIS OF AKI
 Renal U/S
 Biomarkers of AKI
Neutrophil gelatinase-associated lipocalin (NGAL)
Interleukin 18 (IL-18)
Kidney injury molecule 1 (KIM-1)
Atrial Natriuretric Peptide
Cystatin-C
 Renal biopsy

34. CKD VS
AKI

35. MANAGEMENT OF AKI

36. MANAGEMENT OF AKI
Maintenance of volume homeostasis and correction of biochemical
abnormalities remain the primary goals of treatment and may include
the following measures:
 Treat underling disease.
 Correction of fluid overload with furosemide
 Correction of severe acidosis with bicarbonate administration.
 Correction of hyperkalemia , hyponatremia, and hyperphosphatemia.
 Correction of hematologic abnormalities.
 Dietary modification
 If all failed to consider the Dialysis.

37. MANAGEMENT OF AKI
 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

38. MANAGEMENT OF AKI
 Hyperkalemia (>7.0 mEq/L):
ECG findings + acute management.
If medically failed to consider dialysis.
 Hyponatremia
Most commonly dilutional
Management: - Fluid restriction.
- 3% Hypertonic saline to symptomatic patients or Na < 120 mEq/L

39. MANAGEMENT OF AKI
 Hypocalcemia
Primarily treated by lowering the serum phosphate levels.
Phosphate binders can be administered.

40. MANAGEMENT OF AKI
 Nutrition
Sodium, potassium and phosphorous should be restricted.
Protein intake should also be moderately decreased.
Adequate calories are needed to promote recovery.
Patients with inappropriate nutrition have poorer prognosis.

41. MANAGEMENT OF AKI
 Indications for Dialysis in AKI
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.

42. RESOURCES