1. PEDIATRIC ACUTE KIDNEY INJURY
Sunee Panombualert, M.D.
Department of Peditric, Faculty of Medicine,
Khon Kaen University, Thailand

2. Outline Diagnosis and definitions of AKI Evaluation of causes of AKI
Management of AKI
Fluid resuscitate
Blood pressure management
Diuretics
Nutrition
Renal replacement therapy

3. Acute kidney injury (AKI)
Previously called acute renal failure
Rapid (over hours to days) and usually reversible decline in GFR
Acute, impairment of kidney function, manifest by changes in urine output and blood chemistries, portend serious clinical consequences

4. AKI definitions AKI is defined as any of the following:
Increase in SCr by > 0.3 mg/dl within 48 hours or
Increase in SCr to > 1.5 times baseline, which is known or presumed to have occurred within the prior 7 days
Urine volume < 0.5 ml/kg/h for 6 hours.

5. Staging of AKI

6. Normal serum Creatinine (Cr)
Age
Normal Cr (mg/dl)
Newborn
Infant
0.2 – 0.4
Child
0.3 – 0.7
adolescent
0.5 – 1.0
The Harriet lane handbook 19th edition

7. ESTIMATED CREATININE CLEARANCE
eGFR / eCrCl = x Ht (cm)
Cr (mg/dl)
(ml/min/1.73m2)
Pediatrics 1976;58:
J Am Soc Nephrol 2009;20:

8. Evaluation of Kidney Function in the Acute Care Setting
Case: You are asked to see a 5-year-old boy with PUV and known chronic kidney disease (CKD; baseline Scr 2.0 mg/dL) who is admitted with urosepsis. Admission Scr concentration was 2.3 mg/dL and increased to 2.6 mg/dL the following day.
Question 1: Which statement regarding his kidney function is correct?
Using the MDRD (Modification of Diet in Renal Disease) Study equation, his estimated GFR (eGFR) is 34 mL/min/ 1.73 m2
Use of the CKD-EPI (CKD Epidemiology Collaboration) equation is more appropriate for this patient, and his eGFR is 32 mL/min/1.73 m2
Using the Cockcroft-Gault formula, his creatinine clearance is 20 to 32 mL/min
His eGFR cannot be calculated because his Scr concentration is not stable

9. Evaluation of causes of AKI
1. Decreased kidney perfusion
(pre-renal states)
2. Intra-renal causes
3. Post-renal causes
(obstructive uropathy) 1 2 3
Lancet :418.

10. Prerenal Intrinsic Post renal
Decreased true intravascular volume: hemorrhage, volume depletion
Decreased effective intravascular volume: CHF,NS
Arterial occlusion, RAS
Drugs : ACEI, NSAIDS
Intrinsic
AGN : SLE, APSGN, HSP, MPGN, IgAN
ATN : ischemic/ nephrotoxic
Acute TIN : drug
Vascular : vasculitis, HUS
Post renal
Obstruction
Congenital malformation : PUV
Neurogenic bladder
Compression
Lancet :418.

11. Decreased kidney perfusion (pre-renal states)
Hypovolemia : Increased losses (hemorrhage, burns, massive vomiting or diarrhea), poor oral intake
Reduced cardiac output : Heart failure, cardiac tamponade, massive pulmonary embolism
Renal vasomodulation/shunting : Medications (NSAID, ACEi/ARB, cyclosporine, iodinated contrast), hypercalcemia, hepatorenal syndrome, abdominal compartment syndrome
Systemic vasodilation : Sepsis, SIRS, hepatorenal syndrome

12. Prerenal Intrinsic Post renal
Decreased true intravascular volume: hemorrhage, volume depletion
Decreased effective intravascular volume: CHF
Arterial occlusion, RAS
Drugs : ACEI, NSAIDS
Intrinsic
1.AGN
2.ATN
3.Acute TIN
4.Vascular
Post renal
Obstruction
Congenital malformation : PUV
Neurogenic bladder
Compression
Lancet :418.

13. Intra-renal causes Glomerular:
Rapidly progressive (crescentic) GN: anti–glomerular basement membrane
immune complex diseases: IgA nephropathy, postinfectious, lupus, mixed cryoglobuminemia with MPGN
pauciimmuneglomerulonephritis:ANCA-associatedvasculitides:GPA,MPA,EGPA(Churg-Strauss)
ANCA-negative
nephrotic-range proteinuria with associated AKI: HIV-associated nephropathy (secondary FSGS)
Other causes of nephrotic-range proteinuria that commonly associate with AKI:minimalchangediseasewithATN/AIN
Membranous nephropathy+crescenticGNorrenal vein thrombosis; myeloma +multiple different pathologies, but in particular light chain cast nephropathy

14. Acute glomerulonephritis:
APSGN
Lupus nephritis
HSP
Ig A nephropathy

15. Tubulo-interstitium
AIN: medications, infection, lymphoproliferative disease
Pigment nephropathy: rhabdomyolysis (myoglobin), massive hemolysis (hemoglobin)
Crystal nephropathy: uric acid (tumor lysis), acyclovir, sulfonamides, protease inhibitors (indinavir, azatanavir), methotrexate, ethylene glycol, acute phosphate nephropathy, oxalate nephropathy, myeloma-associated AKI (cast nephropathy)
ATN: ischemia (shock, sepsis), inflammatory (sepsis, burns), medications
Osmotic nephrosis in setting of sucrose, mannitol and hydroxyethyl starch use

16. Acute tubular necrosis: Ischemic ATN Nephrotoxic ATN
Tubule
Acute tubular necrosis:
Ischemic ATN
Nephrotoxic ATN

17. Intrinsic renal disease
Acute tubular necrosis
Ischemic ATN : shock, post cardiac arrest, severe hypoxia, prolong dehydration
Nephrotoxic ATN:
Exogenous : antibiotic,
radio contrast agents, cisplatin,heavy metals
Endogenous :
Intratubular pigment: hemoglobin,myoglobin
Intratubular crystals: uric acid, oxalate
Lancet :418.

18. Medications Commonly Associated With ATN
Aminoglycosides (tobramycin, gentamycin)
NSAIDs (ibuprofen, naproxen, celecoxib)
ACEI (captopril, lisinopril, benazepril, ramipril)
ARB (losartan, valsartan, candesartan, irbesartan)
Amphotericin
Cisplatin
Foscarnet
Iodinated contrast
Pentamidine
Tenofovir
Zolendronic acid

19. Acute interstitial nephritis: Drug- associated Infection

20. Vascular
Vascular:
Vasculitis
HUS

21. Intra-renal causes
Vascular: Renal artery stenosis, arterial/venous cross-clamping
Microvascular: Thrombotic microangiopathies (TTP, HUS, aHUS, DIC, APS, malignant hypertension, scleroderma renal crisis, preeclampsia/HELLP syndrome, drug-induced), cholesterol emboli

22. Prerenal Intrinsic Post renal
Decreased true intravascular volume: hemorrhage, volume depletion
Decreased effective intravascular volume: CHF
Arterial occlusion, RAS
Drugs : ACEI, NSAIDS
Intrinsic
AGN : SLE, APSGN, HSP, MPGN, IgAN
ATN : ischemic/ nephrotoxic
Acute TIN : drug
Vascular : vasculitis, HUS
Post renal
Obstruction
Congenital malformation : PUV
Neurogenic bladder
Compression
Lancet :418.

23. Post-renal causes Bladder outlet: Posterior urethral valve
Ureteral: Bilateral obstruction (or unilateral with one kidney): stones, malignancy, retroperitoneal fibrosis
Renal pelvis: Papillary necrosis (NSAIDs), stones

24. Post- renal injury Stone Posterior urethral valve Tumor
Lancet :418.

25. Acute kidney injury AGN ATN AIN
Pre-renal
Intrinsic
Post renal
AGN
ATN
AIN
Vascular
Ischemic ATN
Nephrotoxic ATN

26. Approach AKI Prerenal AKI Intrinsic AKI Postrenal AKI History
GI loss or bleed
Underlying disease : congenital heart disease, nephrotic syndrome
Prolong shock, drug, rhabdomyolysis, TLS : ATN
Hematuria, edema : AGN
Drug : AIN, ATN
Hx of UTI
Abnormal voiding pattern
Physical examination
Sign of dehydration
Volume overload esp ATN/AGN : edema, rales, cardiac gallop
Abdominal mass

27. FE Urea(%)=U urea/S urea *100
Further Investigation
AGN : C3 C4, ANA, Anti dsDNA
KUB ultrasonography
Initial Investigation
Blood : BUN/Cr, electrolyte, Ca, PO4, CBC
Urine : UA, urea, urine Na
FE Na(%) = U Na/S Na * 100
U Cr/ S Cr
FE Urea(%)=U urea/S urea *100

28. Laboratory assessment in AKI
Blood : BUN/Cr, electrolyte, Ca, PO4, uric, CBC
Urine : UA, urea, Na, Cr
FE Na(%) = U Na / S Na * 100
U Cr/ S Cr
FE Urea(%)= U urea / S urea *100
Pre-renal: < 1%
ATN: > 2%
Pre-renal: < 35%
ATN: > 50%

29. Granular cast, cellular casts Pediatric nephrology, 5th edition
Prerenal cause
ATN
Postrenal cause
Urinalysis
Hyaline cast
Granular cast, cellular casts
Hyaline casts
Urine sp gr
> 1.020
~ 1.010
< 1.010
Urine osm (mmol/kg)
> 350
~ 300
Urine Na (mmol/L)
< 20
> 30
> 40
FE Na (%)
< 1
> 2
> 3
FE urea (%)
< 35
> 50 -
BUN/Cr ratio
> 20 : 1
10 – 20 : 1
Urine/plasma Cr
Ultrasound
normal
normal or increased echogenicity with loss of corticomedullary differentiation
dilated pelvis, ureter and/or bladder depending on level of obstruction
Pediatric nephrology, 5th edition

30. Granular cast, cellular casts Pediatric nephrology, 5th edition
Prerenal cause
ATN
Postrenal cause
Urinalysis
Hyaline cast
Granular cast, cellular casts
Hyaline casts
Urine sp gr
> 1.020
~ 1.010
< 1.010
Urine osm (mmol/kg)
> 350
~ 300
Urine Na (mmol/L)
< 20
> 30
> 40
FE Na (%)
< 1
> 2
> 3
FE urea (%)
< 35
> 50 -
BUN/Cr ratio
> 20 : 1
10 – 20 : 1
Urine/plasma Cr
Ultrasound
normal
normal or increased echogenicity with loss of corticomedullary differentiation
dilated pelvis, ureter and/or bladder depending on level of obstruction
Pediatric nephrology, 5th edition

31. Granular cast, cellular casts Pediatric nephrology, 5th editionC
Prerenal cause
ATN
Postrenal cause
Urinalysis
Hyaline cast
Granular cast, cellular casts
Hyaline casts
Urine sp gr
> 1.020
~ 1.010
< 1.010
Urine osm (mmol/kg)
> 350
~ 300
Urine Na (mmol/L)
< 20
> 30
> 40
FE Na (%)
< 1
> 2
> 3
FE urea (%)
< 35
> 50 -
BUN/Cr ratio
> 20 : 1
10 – 20 : 1
Urine/plasma Cr
Ultrasound
normal
normal or increased echogenicity with loss of corticomedullary differentiation
dilated pelvis, ureter and/or bladder depending on level of obstruction
Pediatric nephrology, 5th editionC

33. Abnormal glomerular function
Glomerulonephritis
Abnormal glomerular function
Decrease GFR

35. Eosinophiluria

36. Management of AKI Fluid Dialysis Drugs Treatment causes Nutritions
Electrolytes
disturbance
Nutritions
Dialysis
Drugs
Hypertension

37. Management : Fluid Pre-renal:
Fluid loss : fluid rehydration, blood transfusion
Heart failure : fluid restriction, inotropic drug, diuretics
Intrinsic renal cause:
AGN: fluid & salt restriction, diuretic(furosemide)
ATN: Depends on phase of ATN

38. Pediatric nephrology, 6th edition
Clinical course : ATN
3 Phases of ATN
Oliguric phase : 1-2 weeks
Diuretic phase : replace urine ml/ml
Recovery phase
Pediatric nephrology, 6th edition

39. Acute tubular necrosis

40. Fluid management : oliguria
Restrict fluid = ISL+ urine output + ongoing loss
Diuretic change oliguric to non-oliguric phase
GI loss
CSF
Third space loss
Insensible water loss =
ml/m2/day
30-40 ml/kg in neonate
Pediatric nephrology, 6th edition

41. Management : post-renal AKI
Correct obstruction
After release obstruction
Post-obstructive diuresis
Close observe vital signs, urine output
Replace fluid & electrolyte

42. Electrolyte and acid-base balance
Hyponatremia: fluid restriction, symptomatic  3% NaCl
Hyperkalemia: Kayexalate or Kalimate, bicarbonate, insulin+glucose, beta2-agonist
Hyperphosphatemia: PO4-binder(CaCO3),restrict PO4, avoid aluminum containing compounds
Hypocalcemia : calcium supplement
Metabolic acidosis:7.5%NaHCO3,sodamint
Pediatric nephrology, 6th edition

43. Management hyperkalemia
Monitor ECG : if change10%calcium gluconate
Decrease K intake/ remove cause : low K diet, off aldactone, ACEI
Shift of K from extracellular to intracellular compartment : NaHCO3, insulin, salbutamol
Remove K from body
Ca+/Na+ polystyrene sulfonate
Furosemide diuretic
Dialysis

44. Drugs
Dose
10%Ca gluconate
(onset 1-2 min)
1 ml/kg (Max 10 ml/dose) dilute with sterile water 1 ml/kg IV in 15 min, repeat 2nd dose in 3-5 min
Glucose + insulin
(onset 5-10 min)
Dextrose gm/kg + insulin 0.2 unit/1 gm dextrose IV drip in min
Salbutamol
(onset 30 min)
2.5-5 mg nebulizer q 2-4 hr
7.5%NaHCO3
(onset min)
1 mmol/kg dilute with sterile water 1 ml/kg IV in min

45. Drugs
Dose
Kalimate
(Ca polystyrene sulfonate)
1 gm/kg + water 1-2 ml/kg oral or per rectal q 4-6 hr
(Max. 15 gm/dose)
Kayexalate
(Na polystyrene sulfonate)
1 gm/kg + 5%DW or 10%DW or sorbitol 2-4 ml/kg oral or per rectal q 4-6 hr

46. Dialysis indications Fluid overload Symptoms of uremia
Severe hyperkalemia
Severe metabolic acidosis
Severe hyperphosphatemia (especially if accompanied by hypocalcemia)
Prevention or treatment of tumor lysis syndrome and removal of toxins (ingestions or inborn errors of metabolism)

47. Mode of dialysis Hemodialysis Peritoneal dialysis
CRRT (Continuous Renal Replacement Therapy)

48. Hemodialysis

49. Peritoneal dialysis

50. CRRT

51. “ຂອບໃຈຫຼາຍໆທ່ານ”