Reference : Nelson Textbook of Pediatrics and Netter Pediatrics. Here, we go with Definition, Etiology, Presentation, Cause, Diagnose and Evaluation and Treatment Plan with 4 cases and Quiz with answer

1. Acute Kidney Injury
Or
Acute Renal Failure
November 17, 2021

2. AKI/ARF
AKI referred to abrupt
reduction in kidney
function by falling GFR
and increasing waste
products in the body
Etiology &
Pathogenesis
Pre-Renal
IntraRenal
Post-Renal
Physical
Exam
Underlie AKI suggest
underlying diagnosis.
Clinical Presentation
[Cr], U/A, Urine Na excretion,
Fractional Excretion of Na,
Urine Osm, Urine Volume, CBC
Renal Scan, Renal Biopsy,
Management
Maintenance of electrolyte and fluid balance
Adequate nutritional support
Avoidance of life-threatening complications
Treatment of the underlying cause
…………………………………………………………………………….
Hyperkalemia , Metabolic Acidosis, HTN,
Hyperphosphatemia and Hypocalcemia,
Nutrition , Renal Replacement Therapy
Diagnose &
Evaluation

3. AKI/ARF
● Abrupt reduction in kidney function
measured by a rapid decline in
glomerular filtration rate (GFR).
● Acute decline in kidney function is
secondary to an injury
● AKI is characterized by a disturbance
of renal physiologic functions as,
* Impairment of nitrogenous waste
product excretion
* Inability to regulate water,
electrolyte, and acid–base
homeostasis

4. Etiology and
Pathogenesis
● Each and every Structure or
Function has interfere with
Renal vasculature
Glomeruli
Renal tubules
Interstitium
Urinary tract.

5. Classification
over cause
● PreRenal
● IntraRenal
● PostRenal

6. Images Courtesy: Nelson Textbook of Pediatrics
PreRenal Causes of AKI
Dehydration
Gastroenteritis
Hemorrhage
Burn
Sepsis
Capillary Leak
Hypoalbuminemia
Cirrhosis
Abdominal Compartment Syndrome
Cardiac Failure
Anaphylaxis

7. PreRenal
● Volume depletion caused by
bleeding, gastrointestinal (vomiting,
diarrhea), urinary (diuretics,
diabetes insipidus), cutaneous
losses (burns)
● Decreased effective blood
volume (heart failure, cardiac
tamponade, hepatorenal
syndrome, shock, sepsis)
● Drugs: NSAIDs and ACEIs

8. Images Courtesy: Nelson Textbook of Pediatrics
IntraRenal Causes of AKI / INTRINSIC RENAL
Glomerulonephritis Acute interstitial nephritis Tumor infiltration
Postinfectious/poststreptococcal Toxin and drugs
Lupus erythematosus Tumor lysis syndrome
Henoch-Schönlein purpura Vasculitis
Membranoproliferative
Anti-glomerular basement
Hemolytic-uremic syndrome
Acute tubular necrosis Cortical necrosis
Renal vein thrombosis Rhabdomyolysis

9. Renal
AKI Renal disorder that involve the
Renal vascular, Glomerular or Tubular-
Interstitial pathology.
● ATN (All cases can progress to)
● Rhabdomyolysis
● Contrast Dye
● Aminoglycosides , Amphotericin B
● Uric Acid Nephropathy and Tumor
Lysin Syndrome

10. Renal AKI and
Association
● Penicillin Analogue like Methicillin
● Glomerulonephritis
● PPI, NSAIDs, Sulfonamides and
Rifampicin
● SLE, Vasculitis, Goodpasture,
RPGN
● HUS

11. Images Courtesy: Nelson Textbook of Pediatrics
PostRenal Causes of AKI
Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesical junction obstruction
Ureterocele
Tumors
Urolithiasis
Urethral strictures
Hemorrhagic cystitis
Neurogenic bladder
Anticholinergic drugs

12. PostRenal
AKI is caused by bilateral urinary tract
obstruction unless there is a solitary kidney or
caused by urethral obstruction.
Congenital disorders causing obstruction and
AKI are
Posterior urethral valves (PUVs)
Bilateral ureteropelvic junction obstruction
Bilateral ureteroceles.
Acquired causes of obstruction & AKI
Kidney stones
Tumors

13. Clinical
Presentation
● Careful Hx
● Physical Exam
Can help us in underlying diagnose.

14. Clinical Presentation in AKI with underlying Cause
PreRenal
A history of vomiting, diarrhea, hemorrhage, sepsis, or decreased oral
intake resulting in hypovolemia associated with decreased urine output
suggests AKI caused by prerenal disease or ATN.
Physical examination findings that include tachycardia, dry mucous
membranes, sunken eyes, orthostatic blood pressure changes, and
decreased skin turgor suggest hypovolemia, resulting in AKI caused by
prerenal disease or ATN.
PreRenal Nephrotic syndrome, heart failure, and liver failure causing prerenal AKI
caused by a decrease in effective intravascular volume present with edema
Renal
History of use of medications that are known to cause a hypersensitivity
reaction, together with a rash, fever, and arthralgias, suggests AKI caused
by acute interstitial nephritis

15. Clinical Presentation in AKI
Renal
Clinical presentation that includes hypertension, edema, and gross
hematuria is likely caused by AKI attributable to a glomerulonephritis.
Renal
A history of pharyngitis or impetigo a few weeks before the onset of gross
hematuria suggests postinfectious glomerulonephritis.
Renal
History of bloody diarrhea and pallor and petechiae on physical
examination are associated with HUS
Renal
Hemoptysis in the presence of renal impairment suggests a diagnosis of
pulmonary–renal syndrome, such as Goodpasture’s syndrome.

16. Clinical Presentation in AKI
Renal
Skin findings, such as purpura, malar rash, or petechiae or joint pain favor
a diagnosis of vasculitis, such as systemic lupus erythematosus or
Henoch-Schönlein purpura.
PostRenal
Anuria or oliguria in a newborn suggests a congenital malformation (i.e.,
PUVs) or bilateral renal vein thrombosis.

17. Approach
Consideration
Evaluation and
Diagnosis
● Serum Cr Concentration
● Urinalysis
● Urine Na Excretion
● Fractional Excretion of Na
● Urine Osmolality
● Urine Volume
● CBC, Serological and
Biochemical markers
● Renal Imaging and Biopsy

18. Serum Cr
Concentration
● AKI is diagnosed by Increase in Serum Cr
● Decrease in GFR
Serum Creatinine is insensitive and delay
measured for Kidney Functions.
Biomarkers for Early Stages:
1- Serum Neutrophil
2- Gelatinase-associated lipocalin (NGAL)
3- Cystin C
4- Urinary NGAL
5- Interleukin-18
6- Kidney injury molecule-1 (KIM-1)

19. Images Courtesy: Nelson Textbook of Pediatrics
Staging of Acute Kidney Disease
Stage Serum Creatinine Urine Output
1
1.5-1.9 times baseline OR
>0.3 mg/dL increase
<0.5 mL/kg/hr for 6-12 hrs
2 2.0-2.9 times baseline <0.5 mL/kg/hr for >12 hrs
3
3.0 times baseline OR
>4.0 mg/dL increase OR
eGFR<35 mL/min per 1.73 m2 (<18 years)
<0.3 mL/kg/hr for >24 hrs
Anuria for >12 hours

20. Images Courtesy: Google Images (p-RIFLE)
Creatinine Clearance and Kidney Disease]
Stage Estimated Creatinine Clearance Urine Output
Risk eCrCl decreased by 25% <0.5 mL/kg/hr for 8 hrs
Injury eCrCl decreased by 50% <0.5 mL/kg/hr for >16 hrs
Failure
eCrCl decreased by 75% OR
eCrCl<35 ml/min/1.73m2
<0.3 mL/kg/hr for >24 hrs
Anuria for >12 hours
Loss Persistent Failure >4 weeks ?
End
Stage
End Stage Renal Disease -
Persistent Failure >3 Months
?

21. Urinalysis
● Non-Invasive Test in Diagnose
● Microscopic more important
A normal, Near-normal U/A by few cells with
little or no casts or Proteinuria
-PreRanal or Urinary Tract Obstruction

22. U/A presentation of AKI underlying diseases
ATN
Muddy brown granular casts and epithelial cell casts are highly suggestive of
ATN
Glomerulonep
hritis
The finding of red blood cell (RBC) casts is diagnostic of glomerulonephritis,
and heavy proteinuria is indicative of glomerular disease, both suggesting AKI
caused by glomerulonephritis. Hematuria can be seen in glomerulonephritis
and renal vein thrombosis and with renal calculi.
Tubular or
Interstitial
disease.
The presence of many white blood cells (pyuria) suggests urinary tract
infection, and white blood cells with granular or waxy casts and mild to
moderate proteinuria suggest tubular or interstitial disease.
Interstitial
Nephritis by
HS-Reaction
Eosinophils in the urine suggest interstitial nephritis caused by a
hypersensitivity reaction.

23. Urine Na Excretion
● This tool is not diagnostic but can
help in distinguished between
ATN vs PreRenal
ATN = Urine Na >30-40 mEq/L
PreRanal = Urine Na <10-20 mEq/L

24. Fractional Excretion of
Na
Excretion of A = UV/P (Urine A/Plasma A) X V
FENa = FENa = [(UNa × PCr)/(PNa × UCr)] × 100
<1 PreRenal Disease
(Reabsorption of all filtered Na represent an
appropriate response to decreased renal perfusion.
1-2 either disorder
>2 ATN
because of the decreased ability to reabsorb sodium

25. Urine Osmolality
● Loss of concentrating ability is an
early and almost universal finding
in ATN with the urine osmolality
usually being below 350
mOsmol/kg.
● In contrast, a urine osmolality
above 500 mOsmol/kg is highly
suggestive of prerenal disease.

26. Urine Volume
Urine Output is typically, but not always
Low (Oliguria) in prerenal AKI because of
combination of Na and H2O avidity.
AKI can present with decreased (oliguria), absent
(anuria), normal, or increased (nonoliguric) urine
output.
Oliguria is defined as urine output less than 500
mL/24 h in older children, less than 0.5 mL/kg/h in
younger children, and less than 1 mL kg/h in infants

27. Clinical Presentation in AKI
Oliguric or anuria
Oliguric or anuria is likely to occur in AKI because of hypoxic or ischemic
insults, HUS, glomerulonephritis or urinary tract obstruction.
Nonoliguric
Nonoliguric AKI is associated with acute interstitial nephritis and
nephrotoxic renal insults.

28. CBC
● Microangiopathic hemolytic anemia
associated with thrombocytopenia in the
setting of AKI confirms the diagnosis of HUS.
● Severe hemolysis, whether drug induced or
secondary to hemoglobinopathies, may also
result in ATN caused by massive
hemoglobinuria.
● Eosinophilia is associated with interstitial
nephritis caused by a hypersensitivity reaction.

29. Serology and
Biochemical Marker
● ANCA
● ANA
● GBM
● RPGN
Hyperkalemia, Hyperphosphatemia occur in AKI
because of their decreased renal excretion.
Hypocalcemia in AKI can result secondary to
hyperphosphatemia and decreased calcium
absorption in the gastrointestinal tract because of
inadequate renal production of 1,25-vitamin D.
Acidosis seen in AKI results from decreased urinary
excretion of hydrogen ions.

30. Renal Imaging
● Renal ultrasonography should be performed in
all children with AKI. It can document the
presence of one two kidneys, determine renal
size (often enlarged in those with AKI) assess
the renal parenchyma, and diagnose urinary
tract obstruction or occlusion of the major
renal vessels.

31. Renal Biopsy
● A renal biopsy is done if diagnosis cannot be
established by other noninvasive tests or if the
initial presentation is suggestive of RPGN.

32. Table
PreRenal Renal PostRenal
Hypovolemia ATN AIN GN Obstruction
Sediment
Bland, May
have Hyaline
Casts
Broad
Brownish,
Granular
Cast
WBCs,
Eosinophils,
Cellular Cast
RBCs, RBCs
Casts
Bland or
Bloody
Protein None or Low None or Low
Minimal but
NSAIDs +
INCREASED,
>100 mg/dL
Low
Urine Sodium
U.Na
<20 >40 >30 <20
<20 (Acute)
>40 (Few)
Urine
Osmolality
>400 <350 <350 >400 <350
Fractional
Excretion of Na
<1 >2 Varies <1
<1 (Acute)
>1 (Few Days)

33. Table PreRenal Renal PostRenal
U/A Normal Casts, WBCs, RBCs, Pr Varies
Urine Sodium
U.Na
<15 meq/L
(10)
>40 meq/L
(20)
>40 meq/L
(20)
Urine
Osmolality
>400
(500)
<300 <350
Fractional
Excretion of Na
<1 >2 >2
(N)

34. Complications ● Common Complications of AKI

35. Metabolic Cardiopulmonary Gastrointestinal Neurologic Hematology Infectious Others
Hyperkalemia P. Edema Nausea
Neuromuscular
Irritability
Anemia Pneumonia Hiccups
M. Acidosis Arrhythmias Vomiting Asterixis Bleeding Septicemia PTH High
Na+ Low Pericarditis Malnutrition Seizures UTI
Low Total
Thyroxine
Ca+2 Low P Effusion Hemorrhage
Mental
Status
change
Ph+ More HTN
Mg2+ More MI
Complication of AKI
Uricemia +
Pulmonary
Embolism

36. Prevention and
Management
● Taking weight of the patient
● Stop using K (If Using)
- EKG
● Treat Metabolic Acidosis with
Bicarbonate 0.5-1 meq/kg
● Limited the use of Phosphate
● IV Ca2+ if Hypocalcemia if
severe and Oral if controlled or
Calcitriol

37. Intervention and it’s Rationale
Hydration
Saline Bolus or Mannitol - Restore effective circulating volume, provide better renal
perfusion, may convert oliguric ARF to non-Oliguric ARF (better prognosis)
Diuretics
No lasting effects on GFR or GFR preservation - May assist in promoting non-oliguric
AKI
Electrolyte Therapy
Avoid Hyperkalemia (Remove K from intake, diuretics, Kayexalate, (Sodium
Polystyrene sulfonate).
Sympathomimetic Aerosols
IV NaHCO2 / Calcium / Glucose-Insulin
Dialysis
No absolute Cr/BUN indication (BUN<100 ruke?).
Use to avoid complication, provide better Nutrition (improve outcome),
Earlier may improve outcome

38. General
● Clos monitor level of
Nephrotoxic Drugs
● Adequate fluid repletion with
hypovolemia patients,
hydration and Alkalization.
● Hx of fluid loss vomiting
diarrhea- PE Hypotension and
Tachycardia or Oliguric
(Immediately) IV fluid therapy
to restore Renal function.

39. Hyperkalemia
● Life threatening complication- May
result in Fatal Cardiac Arrhythmia.
● Treated with shift of K from
intravascular to the intracellular
space using IV glucose and Insulin,
Beta agonist, Bicarbonate and by
using enteric exchange resins such
as polystyrene sulfonate.
● IV infusion of Ca2+ also stabilize
the cells of membrane to avoid
Cardiac Arrhythmias.
● Dialysis may require to remove K+

40. Hyperkalemia
● Cardiac symptom if K+>6 stop
taking K.
● Monitor EKG Peaked T wave, wide
QRS interval and ST Depression.
● Sodium polystyrene sulfonate resin
(Kayexalate), 1 g/kg lower K by 1
mEq/L (Repeated each 2 Hours)
● K+>7 mEq/L
- Calcium Gluconate 10% solution,
100 mg/kg/dose (Max 3000 mg/D)
- Sodium Bicarbonate 1-2 mEq/kg
IV (5-10 min)
- Regular Insulin 0.1 unit with
Glucose 50% , 1 mL/kg, over 1 hr

41. Metabolic Acidosis
Acid (H+) by diet and immediately
metabolised and excreted by
kidney but AKI ???? Decreased
excretion - Metabolic Acidosis
Because of retention of H+,
Phosphate and sulfate.
Treated with IV or Oral Sodium
Bicarbonate or Oral Sodium Citrate
solution.
Not always requires treatment

42. Metabolic Acidosis
Indication for Treatment:
- Arterial pH<7.15
- Bicarbs <8 mEq/L
- Significant Hyperkalemia
Goal:
pH 7.20
Serum Bicarb 12 mEq/L
Tx:
Oral Sodium Bicarbonate after
normalized Serum calcium and
phosphorus level.

43. Hyponatremia
By Fluid restriction rather than NaCl.
Hypertonic 3% must be limited for
symptomatic Hyponatremia (Seizure or
lethargy) or Na<120 mEq/L
mEq Sodium required =
0.6 X weight in Kg X (125-Serum Na)

44. Hyperphosphatemia
Normally, Kidney excrete large ingested
Phosphorus- Hyperphosphatemia is
common in AKI.
Treated with Restriction in dietary
Phosphorus and use Oral calcium
carbonate or calcium acetate (Other ca
compound).
Aluminium-Compound can be used.
(Indiaction)- Toxicity - Avoided now-a-day

45. Hypocalcemia
Hypocalcemia in AKI result from
Hyperphosphatemia and decrease
production of 1,25-Vitamin D. Calcium can
be treated by lowering phosphatemia.
In Acidosis setting, less Ca bounds
Albumin, more is free in ionized form.
BUT with Bicarbonate use (Acidosis-
HyperKalemia), More calcium bind to
Albumin, less free ionized calcium.
Symptomatic Hypocalcemia with Tetany.
If Hypocalcemia is severe or Using
Bicarbonate use IV Ca2+ Gluconate or
CaCl. (IV only in Seizures)
Hypocalcemia treated with Oral Calcium
Carbonate or Calcium Acetate (other salt).

46. Hyperphosphatemia
&
Hypocalcemia
Treatment of hypocalcemia in the setting
of severe hyperphosphatemia can result in
metastatic calcifications because of a high
Calcium × Phosphorus product.

47. Hypertension HTN
● HTN in AKI in Overload setting or
Alterations in vascular tone (Renin
mediated).
Loop Diuretics, fluid removal by Dialysis
or hemofiltration may required.
● Severe HTN, IV infusion therapy with
CaCB or Diltazem or Clonidine in less
severe and Acute.
● After Control, Oral Long Acting agent
can initiated.
ACEIs or ARBs should be used with
caution in AKI because they reduce
intraglomerular filtration pressure and
retain K+.

48. Hypertension HTN
● Isradipine 0.05-0.15 mg/kg/dose,
Maximum dose of 5 mg qid
● Amlodipine 0.1-0.6 mg/kg/24h
● Labetalol 4-40 mg/kg/24h
In severe case, Urgency-Emergency
Nicardipine 0.5-5.0 microgram/kg/min
Sodium Nitroprusside 0.5-10.0 microg/kg/min
Labetalol 0.25-3.0 ug/kg/hour
Esmolol 150-300 ug/kg/min

49. Neurological
Symptoms:
Headache, Seizures, Lethargy ,Confusion
(Encephalopathy)
Factors for Etiology:
HTN, Hyponatremia, Hypocalcemia, Cerebral
hemorrhage, Cerebral vasculitis, Uremic
State.
Tx:
Benzodiazepines

50. Anemia
● Anemia in AKI is generally mild
Hb = 9-10 g/dL
Primarily result from Volume
expansion. (Hemodilution)
● Child with HUS, SLE, Active Bleeding
or prolonged AKI can required Red
Blood cell in Hb is less than 7 g/dLQ
● If hypervolemic- Blood increase
Volume, to HTN, Heart Failure, and
Pulmonary edema.
Solution:
Slow 4-6 hours Transfusion with 10
mL/kg Packed Red blood cells.

51. Nutrition
● Severe Anorexia and Malnutrition
in AKI
● Restricted diet with Na,K,Ph
● Protein intake moderately
restricted
● Maximize the calories intake to
minimize accumulation of
Nitrogenous wastes.
● In Critically ill essential Amino
Acids should be considered.

52. Renal Replacement
Therapy
AKI patients are predisposed to GI bleeding
because of uremic platelet dysfunction,
increased stress, and heparin exposure if
treated with hemodialysis or continuous renal
replacement therapy. Oral or intravenous H2
blockers such as ranitidine are commonly
administered to prevent this complication.

53. Renal Replacement
Therapy Indications
Signs and symptoms of uremia
• Pericarditis
• Neuropathy
• Change in mental status
Azotemia
• BUN >80-100 mg/dL
• Rapid rate of increase of BUN
Severe fluid overload state
• Hypertension
• Pulmonary edema
• Heart failure
Severe electrolyte abnormalities (that are
refractory to supportive medical therapy)
• Hyperkalemia
• Hypernatremia
• Hyponatremia
• Acidosis
Need intensive nutritional support child with
• Oliguria
• Anuria

54. Cases

55. A 16 yo girl has recent
Vomiting and poor
energy. She has Oliguria
and difficulty voiding
over the last 2 days. Her
past Medical Hx is
negative.
Serum Cr = 5.8
BP = 122/74
Na = 133
K = 5.2
HCO3 = 19
Cl = 109
BUN = 59
U/A S.G 1.005
pH 6.5
Blood 1+
Protein 1+
LE 2+
Case-1

56. Because S G is 1.005, it can not
be because of Dehydration.
Kidney must be concentrating
urine if body is dehydrated
1- Prerenal Process such as Dehydration
2- Prerenal Process related to Renal Artery
Insufficiency
3- Postrenal Process
4- Renal Process such as Acute GN
5- Renal Process as acute Tubulointerstitial
Nephritis

57. A 9 year girl present
with 3 day history of
Diarrhea with blood and
poor oral intake. Past
medical Hx is negative.
No recent travel or
exposure. She had no
fever or rash.
Serum Cr = 1.4
Na = 133
K = 3.9
HCO3 = 17
Cl = 100
BUN = 27
U/A S.G 1.025
pH 5.5
Protein 1+
Hb 12
WBC 15.7
Platelets 185,000
Case-2

58. Platelets are normal.
1- Acute Dehydration
2- SLE
3- Hemolytic Uremic Syndrome
4- Acute GN
5- Acute Tubulointerstitial Nephritis

59. A 9 year girl present
with 3 day history of
Diarrhea with blood and
poor oral intake. Past
medical Hx is negative.
No recent travel or
exposure. She had no
fever or rash.
Serum Cr = 1.4
Na = 133
K = 3.9
HCO3 = 17
Cl = 100
BUN = 27
U/A S.G 1.025
pH 5.5
Protein 1+
Hb 12
WBC 15.7
Platelets 65,000
Case-3

60. Platelets are decreased.
1- Acute Dehydration
2- SLE
3- Hemolytic Uremic Syndrome
4- Acute GN
5- Acute Tubulointerstitial Nephritis

61. A 16 yo girl has recent
Vomiting and poor
energy. No fever or
rash. Past Medical is
positive for UTIs as a
younger child and
recurrent sinusitis over
the last 2 years.
Serum Cr = 1.9
Na = 133
K = 5.1
HCO3 = 16
Cl = 100
BUN = 18
U/A S.G 1.020
pH 6.5
Blood 1+
Protein 1+
LE 2+
PMNs but no Eosinophilis were noted on
urine micro
Case-4

62. Recurrent sinusitis and Past Hx of UTI
and PMNs.
1- Chronic Dehydration
2- SLE
3- Granulomatosis with polyangiitis
(Wegener’s)
4- MPGN
5- Acute Tubulointerstitial Nephritis

63. Indication of Dialysis
Indications for dialysis in AKi
1 symptoms and signs of uremia like uremic
pericarditis and uremic encephalopathy
2 hyperkalemia and severe acidosis not
responding to medical tx
3 intractable intravascular fluid overload that
unresponsive to diuretics
4 prophylactic dialysis if urea greater than
100-150 mg/dl and Cr greater than 8-10 mg/dl

64. Indication of Dialysis
-Anuria / oliguria
-Volume overload with evidence of hypertension
and/or pulmonary edema refractory to diuretic
therapy
-Persistent hyperkalemia
-Severe metabolic acidosis unresponsive to
medical management
-Uremia (encephalopathy, pericarditis,
neuropathy)
Calcium: phosphorus imbalance, with
hypocalcemic tetany that cannot be controlled by
other measures
Also - adequate nutritional intake plus need for
severe fluid restriction.
Dialysis support may be necessary for days or for
up to 12 wk. Many patients with AKI require
dialysis support for 1-3 wk.

65. Prognosis
● Depend on underlying disease
● AKI by Postinfectious GN has very
low mortality rate (<1%); with organ
involvement mortality is >50%.
● Prognosis also depend on recovery
of disease.

66. References:
Nelson Textbook of Pediatrics
Netter’s Pediatrics Textbook
Medstudy Video Series for USMLE 2015