Guidance Teacher Prepared by

Trainer Specialist of Int. Pediatrics 2nd Year Trainee

Ataturk National Children Hospital Ataturk National Children Hospital
 1. Review of the Renal System
2. Definition of the Acute Kidney Injury
2
3. RIFLE criteria for Renal injury
4. KDIGO staging of AKI
5. Etiology of Acute Kidney Injury
6. Major toxins causing AKI
7. Epidemiology
8. Pathophysiology
9. Clinical Manifestations and Diagnosis
10. Differential Diagnosis
11. Diagnostic Tests & Interpretation
12. Urinalysis in AKI
13. Renal Biopsy in AKI
14. Dialysis in AKI
15. Management of AKI
16. Common Complications of AKI
17. Management of Complications of AKI
18. Follow Up Recommendations & Prognosis
19. Acute Renal Failure in New Born

Prepared by Dr. Shams

 3 Review of the Renal System

Excretion is the process by

which unwanted substances and
metabolic derangements are
eliminated from the body.

Renal system includes:

1. A pair of kidneys
2. Ureters
3. Urinary bladder
4. Urethra

Prepared by Dr. Shams

 4 Review of the Renal System

FUNCTIONAL ANATOMY OF KIDNEY

 DIFFERENT LAYERS OF KIDNEY
1. Outer cortex, contains renal corpuscles & convoluted
tubules.
2. Inner medulla, divided into 8-18 Malpighian pyramids.
3. Renal sinus, consists of renal pelvis, 2-3 major calyces &
8 minor calyces, Branches of the nerves, arteries and veins.
 TUBULAR STRUCTURE OF THE KIDNEY
Kidneys is made of tubular structures called uriniferous
tubules, which includes:
1. Nephrons
2. Collecting ducts

Prepared by Dr. Shams

 5 Review of the Renal System

FUNCTIONS OF KIDNEY
1. ROLE IN HEMOSTASIS
its accomplished by the formation of urine.
 Excretion of waste products
Urea, Uric acid, Creatinine, Bilirubin, toxins, drugs, heavy
metals etc.
 Maintenance of water, electrolytes and Acid-Base balance

2. ENDOCRINE FUNCTION
Hormones secreted by kidney are:
 Erythropoietin
 Thrombopoietin
 Renin
 1.25 dihydroxycholecalciferol (calcitriol)
 Prostaglandins

Prepared by Dr. Shams

 6 Review of the Renal System

FUNCTIONS OF KIDNEY
3. HEMOPOIETIC FUNCTION
Erythropoietin or Hemopoietin & Thrombopoietin is a
glycoprotein produced by peritubular capillaries of kidney &
small amount by liver and brain.

4. REGULATION OF BLOOD PRESSURE

 By regulating the volume of extracellular fluid
 Through Renin-Angiotensin mechanism

5. REGULATION OF BLOOD CALCIUM LEVEL

 By activating of calcitriol into vitamin D. Vitamin D is
necessary for absorption of calcium from intestines.

Prepared by Dr. Shams

 7 Review of the Renal System
RENAL FUNCTION TESTS
 PROPERTIES OF URINE
Volume: 1000-1500ml/day
Reaction: slightly acidic with pH of 4.5-6
Specific gravity: 1.010 to 1.025
Osmolarity: 1200 mOsm/L
Color: Normally straw colored
Odor: Fresh urine has aromatic odor. If stored for some time,
the odor becomes stronger due to bacterial decomposition.
Solids excreted in urine (mMols/day)
Organic Substances Inorganic Substances
1. Urea – 400 1. Sodium – 200
2. Uric Acid – 4 2. Potassium – 50
3. Creatinine – 10 3. Calcium – 5
4. Ammonia – 40 4. Chloride – 200
5. Phosphate – 25
6. Sulphate – 50
Prepared by Dr. Shams
 8 RENAL FUNCTION TESTS
Renal function tests include BUN, Serum Creatinine, Serum Electrolytes, Serum Bicarbonate, GFR.
Blood Urea = BUN × 2.14
GFR may be estimated by Schwartz formula: Values of “k”
ℎ𝑒𝑖𝑔ℎ𝑡 (𝑐𝑚) Preterm Newborn = 0.27
GFR = k × 𝑚𝑔 “k” is a constant.
𝑠.𝑐𝑟𝑒𝑎𝑡𝑖𝑛𝑖𝑛𝑒 ( )
𝑑𝐿
Full Term Newborn = 0.37
Normal GFR >60ml/min (used to classify stages I-V CKD) Infant = 0.45
Serum Creatinine: infant: 0.2-0.4 mg/dL 1 – 12 years = 0.55
Girls up to 18 years = 0.55
1 – 2 years = 0.3 – 0.7 mg/dL
Boys 12-18 years = 0.7
Normal urea: 3 – 7 mmol/L
Normal Urine output: 1.5 – 2.0 L / day (1ml/kg/hr)
Oliguria = 100 – 500 ml/day ( 0.1 – 0.5 ml/hr)
Anuria = < 100 ml/day (< 0.1 ml/hr)
Absolute anuria = nil output
Serum Sodium = 135 – 145 mEq/L
Serum Potassium = 3.5 – 5.5 mEq/L
Serum Chlorine = 90 – 110 mEq/L
Serum Bicarbonate = 21 – 28 mEq/L

Prepared by Dr. Shams

 Imaging of Urinary Tract
 Ultrasonography: It can help diagnose obstruction, malformation, cysts,
9
tumors, stones etc.
 Plain abdominal x-ray film: Helpful in detecting small renal & ureteric calculi
& spinal evaluation in neuropathic bladder.
 Micturating Cystourethrography: helps to diagnose severity of
vesicoureteral reflux and detection of abnormalities of bladder and urethra.
 DPTA (Diethylene Penta Acetic Acid) : it provides estimation of GFR.
With post-furosemide study, it helps in diagnosing obstruction.
 DMSA (Dimercaptosuccinic acid ) Renal Scan: it helps to detect renal scars
and ectopic kidney.
 MAG3 (Mercaptoacetyltriglycine) Renal Scan: it helps in detecting
obstructive uropathy.
 Intravenous Urography (IVU): Due to risk of contrast induced nephropathy,
IVU is now replaced.
 Computed Tomography (CT): Helpful in examining mass lesions of kidney,
bladder or retroperitoneum.
 Magnetic Resonance Imaging (MRI) : MR angiography in suspected renal
artery stenosis.
 Renal Biopsy: The most common indications include steroid resistant
nephrotic syndrome, lupus nephritis, suspected glomerular and interstitial
diseases.
Prepared by Dr. Shams
 10
Acute Renal Failure
Definition:
1. Acute impairment of renal function resulting in retention of nitrogenous
wastes and other metabolic derangements.
2. Abrupt loss of kidney function leading to a rapid decline in the GFR,
accumulation of waste products such as BUN and Creatinine and
dysregulation of extracellular volume and electrolyte hemostasis.
3. Oliguria and Anuria is a prominent feature of ARF.
4. Increase in serum creatinine by ≥ 0.3 mg/dL from baseline within 48 hr;
OR
Increase in serum creatinine to ≥ 1.5 times baseline within the prior 7 days;
OR
Reduction in urine output < 0.5 ml/Kg/hr for > 6 hours

Note: In AKI, the urine output is variable: anuria, oliguria and, in some cases,
polyuria can all be observed at presentation.

Prepared by Dr. Shams

11
RIFLE criteria for Renal Injury
Risk: Increased creatinine (Cr×1.5) or GFR decrease > 25% , Urine output <0.5 ml/Kg/hr > 6h
3 stages of Injury: Increased Cr х 2 or GFR decrease >50%, Urine output< 0.5ml/Kg/hr > 12 hours
Renal injury Failure: Increased creatinine (Cr × 3) or GFR decrease > 75% or Cr≥ 4mg/dL
(Acute rise of ≥ 0.5 mg/dL , Urine output <0.3 ml/Kg/hr for 24 hours or anuria for 12 hours)
2 stages of Loss: loss of renal function for > 4 weeks
outcome ESRD: loss of renal function for > 3 months

Note: Higher RIFLE stages correlate with higher

1-6 months mortality for hospitalized patients

Prepared by Dr. Shams

 12 KDIGO Staging of Acute Kidney Injury
Stage Serum Creatinine Urine Output
Increase in serum creatinine of ≥ 0.3mg/dL over 48 hours OR Less than 0.5 mL/Kg/hr for 6-12hours
1
≥1.5 – 1.9 times base line in last 7 days
2 Increase in serum creatinine 2 – 2.9 times base line Less than 0.5 mL/Kg/hr for ≥ 12 hours
Increaser in serum creatinine 3 times base line OR Less than 0.3 mL/Kg/hr for ≥ 24 hours
serum creatinine ≥ 4.0 mg/dL OR OR
3
Initiation of renal replacement therapy OR anuria for ≥12 hours
eGFR < 35mL/min per 1.73 m² (<18yrs)

Note: Only one criterion (creatinine or urine output)

should be fulfilled to qualify a stage.
KDIGO: Kidney Disease Improving Global Outcomes

Prepared by Dr. Shams

13
ARF is classified as Pre-renal, Intrinsic renal and Post-renal
IMPORTANT CAUSES OF ACUTE RENAL FAILURE
Pre-renal failure Intrinsic renal failure Post-renal failure
1. Glomerulonephritis
1. Dehydration  Post infectious/Post-streptococcal 1. Posterior urethral valve
2. Hemorrhage  Lupus erythematosus 2. Urethral strictures
3. Gastroenteritis  HSP 3. Bilateral ureteropelvic
4. Burns  Membranoproliferative junction obstruction
5. Sepsis  Anti-glomerular basement membrane 4. Ureterovesicular junction
6. Capillary leak 2. Acute Tubular Necrosis obstruction
7. Hypoalbuminemia 3. Prolonged pre-renal insult 5. Ureterocele
8. Abdominal compartment 4. Cortical Necrosis 6. Neurogenic bladder
syndrome 5. Renal vein thrombosis 7. Tumors
9. Cardiac Failure 6. Rhabdomyolysis 8. Urolithiasis
10. Anaphylaxis 7. Acute interstitial nephritis 9. Hemorrhagic cystitis
11. Drugs (ACE inhibitors, Diuretics) 8. Vasculitis 10. Anticholinergic drugs
12. Perinatal Asphyxia 9. Intravascular hemolysis
10. Hemolytic Uremic Syndrome
11. Bilateral renal vessel occlusion

Prepared by Dr. Shams

 Major Endogenous and Exogenous Toxins Causing AKI
14
ENDOGENOUS TOXINS EXOGENOUS TOXINS
MYOGLOBULINURIA ANTIBIOTICS
o Muscle breakdown : trauma, electric shock, hypo/hyperthermia, o Aminoglycosides
seizures, exercise, burns o Amphotericin B
o Metabolic: hypokalemia, hypophosphatemia o Antiviral agents: acyclovir, cidofovir etc.
o Infections: tetanus, influenza o Pentamidine
o Toxins: isopropyl alcohol, ethanol, snake & insect bite, cocaine, heroin o Vancomycin
o Drugs: statins, amphetamines, fibrates CALCINEURIN INHIBITORS
o Autoimmune and inherited diseases o Cyclosporine
o Tacrolimus
POISONS
o Snake venom
o Paraquat
HEMOGLOBINURIA MISCELLANEOUS
o Mechanical: prosthetic valves, microangiopathic hemolytic anemia o Radiocontrast media
o Drugs: hydralazine, methyldopa o IVIG
o Chemicals: benzene, arsine, glycerol, phenol o NSAIDS
o Immunologic: transfusion reaction o Chemotherapy
o Genetic: G6PD deficiency
Prepared by Dr. Shams
 15

EPIDEMIOLOGY
The epidemiology of AKI has changed over the
recent years from primary kidney disease to a
syndrome secondary to other systemic illness.
AKI may be seen in up to 10% of all hospitalized
children. The incidence is higher in intensive care unit
(ICU) admissions and with increasing multiorgan
disease severity.
AKI is seen in 27% of children admitted to an ICU.

Prepared by Dr. Shams

 PATHOPHYSIOLOGY

Acute Kidney Injury is classified as under:

1. Prerenal AKI
2. Intrinsic renal AKI
3. Post renal AKI
4. Iatrogenic AKI

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17
 Pre-Renal AKI also called Prerenal Azotemia or
Functional AKI, is characterized by systemic
hypovolemia that leads to inadequate renal perfusion
and decrease in GFR hence renal tubular injury occurs
due to which glomerular filtrate diffuse back into the
circulation across the damaged tubules.
 If the renal hypo-perfusion is reversed promptly, renal
function returns to normal but if sustained,
intrinsic renal parenchyma damage can develop.
 Tubular obstruction due from impaction of the casts
and cellular debris results in oliguria.
 The oliguric phase lasts about 3 – 10 days, during which
Note: The differentiation between “Prerenal” and
biochemical and clinical abnormalities gradually worsen,
“intrinsic” causes can be difficult because renal
more rapidly if infection, trauma or bleeding are
hypoperfusion may coexist with any stage of AKI. For
associated.
that reason “functional” has replaced Prerenal and
 A diuretic phase usually lasts for a week during which
“structural” has replaced intrinsic in the terminology.
large amount of fluids and electrolytes may be lost.
Prepared by Dr. Shams
18
 Intrinsic Renal AKI or Structural AKI includes sustained hypoperfusion and ischemia.
 Ischemic/hypoxic injury and nephrotoxic insults lead to ATN and are the most common causes of intrinsic AKI in
the US
 Mechanism leading to ischemic AKI include Hypotension, Vasodilation or constriction, renal artery obstruction and
impaired renal blood flow.
 In ATN, examination may be normal except for dehydration.
 Nephrotoxic agents cause uniform epithelial damage in the proximal tubules without disruption of tubular
basement membrane

Prepared by Dr. Shams

19
 Post-Renal AKI includes a variety of disorders characterized by the obstruction of the urinary tract.
 In a patient with two functional kidneys, obstruction must be bilateral to result in AKI.
 Relief in obstruction usually results in recovery of renal function except for prolonged obstruction or renal
dysplasia.
 In neonates and infants congenital conditions such as posterior urethral valves and bilateral ureteropelvic junction
obstruction accounts for the majority of cases of AKI.

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HISOTRY: A careful taken history is critical in defining the cause of AKI.

o Previous infection, Neurogenic bladder, Single kidney
o Exposure to NSAIDS, β-lactam antibiotics, Acyclovir, Aminoglycosides,
Amphotericin-B, Cisplatin
o Gross hematuria: AGN (tea colored), renal calculi (bright red blood)
o Trauma: crush injury,
o An infant with a 3 day H/O vomiting & diarrhea most likely has
Prerenal AKI but HUS must also be considered.
o A 6 years old child with a recent pharyngitis who present with
periorbital edema, hypertension & gross hematuria most likely has
intrinsic AKI.
o A critically ill child with a H/O protracted hypotension or with
exposure to nephrotoxic medications most likely has ATN.
o A neonate with a H/O hydronephrosis & a palpable bladder most likely
has Congenital Urinary Tract Obstruction.

Prepared by Dr. Shams

21
SIGNS & SYMPTOMS:
 Fever, rash, bloody diarrhea, pallor, severe vomiting or diarrhea,
abdominal pain, hemorrhage, shock, anuria, polyuria
 Tachycardia, dry mucus membrane & poor peripheral perfusion
suggest inadequate circulatory volume and the possibility of
Prerenal AKI.
 Hypertension, Peripheral edema, rales & a cardiac gallop suggest
volume overload & possibility of Intrinsic AKI.
 Palpable flank masses may be seen with renal vein thrombosis,
tumors, cystic disease or urinary tract obstruction.
PHYSICAL EXAM:
General: weight and hydration status; shock, edema (calculation
of percent fluid overload based on body weight), jaundice
Lungs: rales
Heart: gallop
Abdomen/pelvis: mass
Skin: rash, petechiae
Joints: arthritis
Prepared by Dr. Shams
22

DIFFERENTIAL DIAGNOSIS OF AKI

 Chronic kidney disease: insidious, associated with poor
growth, normocytic anemia, hyperparathyroidism
 Azotemia (elevated BUN): hyper-catabolic states
including corticosteroid therapy or upper GI bleeding
 Elevated creatinine: caused by rhabdomyolysis, drugs
(trimethoprim-sulfamethoxazole, cimetidine)

Prepared by Dr. Shams

23 DIAGNOSTIC TESTS & INTERPRETATION

Initial Tests (screening, lab, imaging)

All patients with AKI should have a urinalysis with microscopic exam, serum chemistries and a CBC:
– Urinalysis:
Specific gravity (>1.020 suggests Prerenal AKI),
Proteinuria (>3+ structural, glomerular AKI),
Eosinophiluria (AIN),
Pyuria (pyelonephritis),
Granular casts (functional, ATN),
Pigmenturia (ATN),
Erythrocyte casts (glomerulonephritis, AIN, ATN)
– Serum chemistries: hyponatremia, acidosis, hyperkalemia, hypocalcemia, hyperphosphatemia
– CBC: microangiopathic hemolytic anemia, thrombocytopenia (i.e. HUS), eosinophilia (i.e., AIN)
Selected patients require further studies, including serologies, urine electrolytes, imaging, and renal biopsy
– Serologies: hypocomplementemia, Antineutrophil cytoplasmic antibodies, antinuclear antibodies (AGN)

Prepared by Dr. Shams

24 DIAGNOSTIC TESTS & INTERPRETATION
Fractional excretion of sodium (FENa)
– Can be useful to assess tubular function; FENa = [(UNa / PNa) / (Ucreat/ Pcreat)] × 100
– The FENa should not be obtained after diuretics are administered;
FENa >2: ATN; FENa <1: AGN, Prerenal
– FENa can be <1% despite ATN in case of radiocontrast nephropathy or pigment nephropathy.
Fractional excretion of urea (FEUrea)
– Less affected by diuretics
– FEUrea = [(UUrea / PUrea) / (Ucreat / Pcreat)] × 100
FEUrea <35: Prerenal AKI; FEUrea >50: ATN
Chest Radiograph: cardiomegaly or pulmonary edema (fluid overload)
Renal US: hydronephrosis, trabeculated bladder (i.e., obstruction), increased echogenicity (i.e., ATN, AIN, AGN, HUS),
abnormal Doppler study (renal venous thrombosis)

Prepared by Dr. Shams

 25
 Anemia
(SLE, Renal Vein Thrombosis, HUS)
 Leukopenia (SLE, Sepsis)
 Thrombocytopenia
(SLE, Renal Vein Thrombosis, HUS, Sepsis)
 Metabolic acidosis
 Elevated BUN, Serum Creatinine,
Hyperkalemia, Hyperphosphatemia
(DIMINISHED RENAL FUNCTION)
 Hyponatremia (dilutional)
 Hematuria, Proteinuria & RBC Casts
or Granular Urinary Casts
(INTRINSIC AKI)
 WBC Casts, Low Grade Hematuria &
Proteinuria
( TUBULOINTERSTITIAL DISEASE)

NOTE: Serum Creatinine is an insensitive & delayed measure of decreased kidney function following AKI!

Prepared by Dr. Shams

26
ACUTE
GLOMERULO
HYPOVOLEMIA ATN INTERSTITIAL OBSTRUCTION
NEPHRITIS
NEPHRITIS
Bland, may have hyaline Broad, brownish WBCs, Eosinophils,
Sediment RBCs, RBCs Casts Bland or Bloody
casts granular casts Cellular casts
Minimal but may be
Increased,
Protein None or Low None or Low increased with Low
>100mg/dL
NSAIDS
Urine Sodium <20 (acute)
<20 >40 >30 <20
(mEq/L) >40 (few days)
Urine Osmolality
>400 <35 <350 >400 <350
(mOsm/Kg)
Fractional
<1 (acute)
Excretion of <1 >2 varies <1
>1 (few days)
Sodium %

Prepared by Dr. Shams

27

Renal Biopsy is indicated in AKI in the

following cases:
1. Rapidly progressive or non-resolving
glomerulonephritis
2. AKI associated with underlying systemic
disorder e.g. lupus erythematosus, HSP
3. Suspected interstitial nephritis
4. Clinical diagnosis of ATN or HUS, if
significant dysfunction persists beyond
2-3 weeks
5. Underlying cause of AKI not apparent
on clinical features and investigations

Prepared by Dr. Shams

Fluid Repletion:
 Pre-renal ARF responds to fluid replacement
 Dehydration is corrected by infusion of 20-30 ml/Kg or
normal saline or Ringer’s lactate over 45-60 minutes. (30min)
 Incase of hemorrhage, blood transfusion should be
performed.
 Potassium shouldn’t be administered until urine flow is
established.
 Patients with renal hypo-perfusion responds to fluid with
urine output (~2ml/Kg over 2-3 hours)
 Furosemide (1-2 mg/Kg IV) may be given if no diuresis
despite correction of dehydration. Bumetanide (0.1mg/Kg)
may be given as an alternative to furosemide.
 To increase the cortical blood flow, administer dopamine
(2-3μg/Kg/min in conjunction with diuretic therapy.
 Mannitol may be effective in pigment (myoglobin,
hemoglobin) induced renal failure.
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Fluid Restriction:
 Intake-Output monitoring, daily weight
gain, physical examination and serum
sodium guide fluid management.
 Fluid retention from excessive oral or
parenteral fluids leads to edema,
hypertension and heart failure.
 Daily fluid requirement is restricted to
300-400 ml/m²
 A rapid weight loss and rising sodium
suggests inadequate fluid replacement
while absence of weight loss and low
serum sodium indicates fluid excess.

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Diet:
 Patients with AKI are usually catabolic.
 Proteins, Carbohydrates, Fats, Vitamins
and micronutrients are provided.
 A diet containing 1-1.2 g/Kg of protein in
infants and 0.8-1.2 g/Kg in older children
and minimum 60-80 Kcal/Kg is
recommended.
 In most cases, sodium, phosphorous and
potassium should be restricted.

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General Measures:
 Urine should be collected by condom drainage,
catheterization isn’t preferred.
 Prophylactic antibiotics aren’t recommended.
 Nephrotoxic drugs should be avoided.
 Diuretics don’t affect renal function but may
transiently improve urine output.
 Dopamine in low dose causes renal vasodilation
& may induce natriuresis and diuresis. It has no
effect on outcome of AKI and may cause transient
tachyarrhythmia or tissue ischemia.
 In AKI, rapid development of hyperkalemia
(>6mEq/L) can lead to cardiac arrhythmia,
cardiac arrest and death.

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In AKI, dialysis support may be necessary for up to 12 weeks.
Dialysis should begin early to prevent life-threatening
complications.
Indications for Dialysis in AKI include the following:
I. Anuria/Oliguria
II. Volume overload with the evidence of Hypertension or
Pulmonary edema
III. Persistent hyperkalemia (>6.5mEq/L)
IV. Severe metabolic acidosis (NaHCO₃ <10-12 mEq/L)
V. Uremia (encephalopathy, pericarditis, neuropathy)
VI. Caclium:Phosphorus imbalance with hypocalcemic tetany
VII. Hyponatremia (<120mEq/L) or Hypernatremia

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 Common Complications of Acute Kidney Injury
CARDIO-
METABOLIC GASTROINTESTINAL NEUROLOGIC HEMATOLOGIC INFECTIOUS OTHER
PULMONARY

Hyperkalemia Pulmonary Nausea Neuromuscular Anemia Pneumonia Hiccups

Metabolic Acidosis Edema Vomiting irritability Bleeding Septicemia ↑ PTH
Hyponatremia Arrhythmias Malnutrition Asterixis Urinary ↓Total T₃
Hypocalcemia Pericarditis Hemorrhage Seizures tract ↓Total T₄
Hyperphosphate Pericardial Mental status infections Normal
mia effusion changes thyroxine level
Hypomagnesemia Hypertension
Hyperuricemia Myocardial
infarction
Pulmonary
embolism

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1. Fluid Over load
 Fluid restriction
 Insensible loss estimation (300-400ml/m²/day)
 5% dextrose for insensible losses and N/5 for urine output
Note: Prefer oral to parenteral fluids
2. Pulmonary Edema
 Oxygen therapy
 Furosemide 2-4 mg/Kg IV
 Bumetanide 0.1mg/Kg as an alternative to furosemide
Note: Monitor using CVP

3. Neurological Symptoms; include headache, seizures, lethargy & encephalopathy.

 Benzodiazepines are the most effective agents in acutely controlling seizures.

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4. Metabolic Acidosis; is common because of retention of hydrogen ions,
phosphate & Sulphate. Treatment is indicated in case of severe acidosis i-e
arterial pH <7.15; NaHCO₃ < 8 mEq/L or significant hyperkalemia.
Acidosis is corrected partially parenterally & remaining orally.
Sodium bicarbonate (IV or Oral) is given as following:
Body weight (kg) x base deficit x 0.3
Note: watch for fluid overload, hypernatremia, hypocalcemia, consider dialysis
5. Hyperkalemia: In AKI, rapid development of hyperkalemia (>6mEq/L) can
lead to cardiac arrhythmia, cardiac arrest and death.
 Calcium gluconate (10%) 0.5-1 ml/Kg over 5-10 min IV
Stabilizes cell membranes and prevents arrhythmias
 Salbutamol 5-10mg Nebulized
Shifts potassium into cells
 Dextrose (10%) 0.5-1 g/Kg and insulin o.1-0.2 U/Kg IV
Insulin take potassium into cells
 Sodium bicarbonate (7.5%) 1-2 ml/Kg over 15 min
Shifts potassium into cells but is less efficient
 Calcium or sodium resonium (Kayexalate) 1g/Kg
Given orally or rectally, can be repeated 4-8 hours
 Furosemide (1 to 2 mg/kg) if renal function is adequate
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6. Hyponatremia
 Fluid restriction
 In case of seizures, 3% saline 6-12 mL/Kg over 30-90 min
Note: hyponatremia is usually dilutional;
12mL/Kg of 3% saline raises sodium by 10 mEq/L

7. Severe Anemia; is generally mild (Hb=9-10mg/dL)

primarily results from volume expansion.
 In HUS, SLE, active bleeding or prolonged AKI can require
transfusion of Packed red cells 3-5 mL/Kg if Hb levels falls
below 7g/dL.
Note: Monitor BP and fluid overload

8. Hyperphosphatemia
 Phosphate binders (Sevelamer, Calcium carbonate,
acetate, aluminum hydroxide)
Note: avoid high phosphate products: milk products and
high protein diets
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9. Hypocalcemia
 Primarily treated by lowering the serum phosphate.
 Calcium shouldn’t be given intravenously, except in tetany to
avoid deposition of calcium salts into tissues.

10. Hyponatremia
 Most commonly dilutional
 Hypertonic (3%) saline should be limited to symptomatic
hyponatremia (seizure, lethargy) or serum sodium level
<120mEq/L by using the following formula:
mEq Na required = 0.6 х weight (kg) × (125- serum Na in mEq/L)

11. GI Bleeding
 GI bleeding is due to uremic platelet dysfunction, increased
stress and heparin exposure if treated with dialysis.
 Oral or parenteral H2 blockers such as ranitidine is commonly
administered.

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12. Hypertension
 Results from hyperreninemia, associated with expansion of extracellular volume.
 Most common in AKI patients with GN or HUS
 Symptomatic: Sodium nitroprusside 0.5-8 μg/Kg/min infusion
Furosemide 2-4mg/Kg IV
Nifedipine 0.3-0.5mg/Kg oral/sublingual
 Asymptomatic: Nifedipine, amlodipine, prazosin, labetalol, clonidine
 Salt & water restriction may be useful.
 Isradipine (0.05-0.15 mg/Kg/dose) may be used for rapid reduction in BP.
 Longer acting oral agents such as calcium channel blockers
(amlodipine 0.1-0.6 mg/Kg/24hr QD or divided BID) or
β blockers (labetalol 4-40mg/Kg/24hr divided BID or TID) may be helpful.
 Children with hypertensive urgency or emergency should be treated with
continuous infusion of Nicardipine (0.5-5 μg/Kg/min),
Sodium nitroprusside (0.5-10 μg/Kg/min) & labetalol (0.25-3 mg/Kg/min).

Note: in emergency, reduce BP by one-third during first 6-8 hrs,

One-third over next 12-24 hrs and the final one-third slowly over 2-3 days.
Prepared by Dr. Shams 38
 FOLLOW-UP RECOMMENDATIONS
The likelihood of recovery from AKI depends on the underlying cause.
AKI may result in full recovery or incomplete recovery leading to
chronic kidney disease. In severe cases, non-recovery may lead to end-
stage renal disease.
Long-term follow-up to monitor renal function is recommended.

PROGNOSIS
The mortality rate increases in patients with multisystem organ failure despite good supportive care. AKI is
independently associated with increased mortality in ICU patients. The mortality rate is variable and depends
entirely on the nature of the underlying disease process.
o Post infectious glomerulonephritis have a very low mortality rate (<1%)
o AKI with multiple organ failure have a very high mortality rate (>50%)
o Recovery of renal function is likely AKI resulting from Prerenal causes, ATN, acute interstitial nephritis or
tumor lysis syndrome.
o Complete recovery is unusual in AKI resulting form rapidly progressive glomerulonephritis, bilateral renal
vein thrombosis or bilateral cortical necrosis.

Prepared by Dr. Shams 39

Definition: Urine output < 0.5 mL/Kg/hr or serum creatinine > 1.2 mg/dL
Important causes include:
a. Perinatal hypoxemia associated with birth asphyxia or RDS
b. Hypovolemia
c. Sepsis
d. Delayed initiation and inadequacy of feeding
e. Increased insensible losses (phototherapy, radiant warmers)
f. Nephrotoxic medications (aminoglycosides, indomethacin, maternal intake
of ACE inhibitors, nimesulide)
g. Renal vein thrombosis in infants with diabetic mothers, server birth asphyxia,
dehydration, polycythemia and catheterization of umbilical veins
Management :
Principles of management is similar to that for older children.
Fluid should be limited to insensible (30 mL/Kg/day for full-term, 50-100 mL/Kg/day for
preterm neonates)
Systolic BP > 95 – 100 mmHg may need treatment.

Prepared by Dr. Shams 40

Prepared by Dr. Shams
[email protected]