1 Acute kidney injury

Acute Kidney Injury

Definition:
▪ Acute kidney injury (AKI) formerly referred to as acute renal
failure (ARF).

▪ It is defined according to the RIFLE criteria:

▪ The Pediatric RIFLE criteria —

▪ The RIFLE criteria consists of three graded levels of injury

as follows:

1. Risk — estimated creatinine clearance decrease by

25% or urine output <0.5 mL/kg per hour for 8 hours

2. Injury — estimated creatinine clearance decrease by

50 percent or urine output <0.5 mL/kg per hour for 16
hours

3. Failure — estimated creatinine clearance decrease by

75% or estimated creatinine clearance <
2
35ml/min/1.73 m or urine output < 0.3 mg/kg/h for 24
h or Anuria for 12 h

4. Loss — Persistent failure >4 weeks

5. ESRD — persistent failure > 3 months

▪ AKI results in the disturbance of renal physiological functions

including:

Impairment of nitrogenous waste product excretion.

Loss of water and electrolyte regulation.

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Loss of acid-base regulation.

Classification and causes

• The causes of AKI can be categorized as prerenal, renal, or
postrenal.

a. Prerenal —

i. Prerenal azotemia results from either:

1. Volume depletion due to:

a. Bleeding (surgery, trauma,

gastrointestinal bleeding).

b. Gastrointestinal (vomiting, diarrhea).

c. Urinary (diuretics, diabetes insipidus).

d. Cutaneous losses (burns).

2. Decreased effective arterial pressure:

a. Heart failure.

b. Shock.

c. Cirrhosis.

b. Intrinsic renal disorders —

i. Vascular :

1. Vascular causes of AKI include:

a. Thrombosis (arterial and venous).

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b. Hemolytic-uremic syndrome.

c. Malignant hypertension.

d. Vasculitis.

ii. Glomerular :

1. The principal glomerular cause of AKI is acute

glomerulonephritis, which is commonly
postinfectious.

2. AKI can be observed with most of the

glomerulonephritides that can occur in
childhood.

iii. Tubular and interstitial disease :

1. Acute tubular necrosis (ATN) results from

ischemia due to decreased renal perfusion or
injury from tubular nephrotoxins (eg.
aminoglycosides, amphotericin B, and
contrast agent.)

c. Postrenal —

i. Postrenal AKI is due to bilateral urinary tract

obstruction unless there is a solitary kidney.

ii. In neonates, urinary tract obstruction, due to

posterior urethral valves is the most common cause
of postrenal failure.

History and Clinical Presentation

▪ The assessment is directed towards:

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• Identifying the underlying cause.

• Distinguishing between prerenal and intrinsic ARF

• Discriminating between ARF and chronic renal failure (CRF).

▪ Identifying the underlying cause (table 1,2)

▪ A history of vomiting, diarrhea, hemorrhage, sepsis and/or decreased

oral intake resulting in hypovolemia, associated with decreased urine
output suggests AKI due to 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 due to
prerenal disease or ATN.

▪ Bloody diarrhea with oliguria or anuria is consistent with the hemolytic-

uremic syndrome.

▪ A history of pharyngitis or impetigo, a few weeks prior to the onset of

gross hematuria suggests post-infectious glomerulonephritis.

▪ Nephrotic syndrome, heart failure, and liver failure may result in

edema and other signs of specific organ dysfunction.

▪ Hemoptysis in the presence of renal impairment suggests a diagnosis

of pulmonary-renal syndrome, which includes Goodpasture's
syndrome or Wegener's granulomatosis.

▪ Skin findings, such as purpura, malar rash, or petechiae, and/or joint

pain favor a diagnosis of systemic vasculitis, such as systemic lupus
erythematosus or Henoch Schönlein purpura.

▪ Anuria or oliguria in a newborn suggests a major congenital

malformation or genetic disease, such as posterior urethral valves,
bilateral renal vein thrombosis, or autosomal recessive kidney
disease.

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▪ In the hospital, ATN resulting from hypotension (due to sepsis or

intraoperative events) or from the administration of nephrotoxic
medications (such as aminoglycosides or amphotericin-B) is the
common cause of AKI

Table 1. Relevant history in patients with suspected acute renal failure

Table 2: Relevant physical signs in acute renal failure

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▪ Distinguishing between prerenal and intrinsic ARF

Table. 3 Urinary indices in acute renal failure

▪ Distinguishing between ARF and CRF

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Table.4 Clinical and investigative tools differentiating acute renal

failure from chronic renal failure

Evaluation and Diagnosis

✓ Laboratory Evaluation:

• Urinalysis :

▪ The urinalysis is the most important noninvasive test in the

diagnostic evaluation.

▪ A normal or near-normal urinalysis, characterized by few

cells with little or no casts or proteinuria, suggests prerenal
disease, urinary tract obstruction, and some cases of ATN.

▪ Muddy brown granular casts and epithelial cell casts are

highly suggestive of ATN.

▪ The finding of a red cell cast is diagnostic of

glomerulonephritis.

▪ The concurrent presence of hematuria with red cell casts,

dysmorphic red cells and heavy proteinuria is commonly
associated with AKI due to glomerulonephritis.

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▪ Pyuria with white cell and granular casts is suggestive of

tubular or interstitial disease or urinary tract infection.

▪ Hematuria and pyuria may be seen in acute interstitial

nephritis, glomerular disease, vasculitis, obstruction, and
renal infarction.

• Urine sodium excretion:

▪ The urine sodium concentration is usually above 30 to 40

mEq/L in ATN and below 10 mEq/L in the prerenal AKI.

• Fractional excretion of sodium (FENa) :

▪ The effect of variations in urine volume can be eliminated by

calculating the FENa

▪ This is defined by the following equation:

FENa = ([U/P]Na)/([U/P]Cr) × 100

▪ Where UCr and PCr are the urine and serum creatinine
concentrations, respectively, and UNa and PNa are the urine
and serum sodium concentrations, respectively.

▪ The FENa is a screening test that differentiates between

prerenal AKI and ATN in children.

▪ A value below 1 percent suggests prerenal disease, where

the reabsorption of almost all of the filtered sodium
represents an appropriate response to decreased renal
perfusion.

▪ A value between 1 and 2 percent may be seen with either

disorder.

▪ A value above 2 percent usually indicates ATN.

• Urine osmolality:

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▪ Loss of concentrating ability is an early and almost universal

finding in ATN with the urine osmolality usually being below
350 mosmol/kg.

▪ Urine osmolality above 500 mosmol/kg is highly suggestive

of prerenal disease.

• Serum creatinine concentration :

▪ Estimation of the glomerular filtration rate (GFR), usually by

the serum creatinine concentration.

▪ GFR is used clinically to assess the degree of renal

impairment and to follow the course of the disease.

✓ Renal imaging:

▪ Renal ultrasonography should be performed in all children

with AKI of unclear etiology.

▪ It can:

1. Document the presence of one or two kidneys.

2. Delineate renal size.

3. Help survey renal parenchyma.

4. It is particularly useful in diagnosing urinary tract

obstruction or occlusion of the major renal vessels.

✓ Renal biopsy —

▪ A renal biopsy is most commonly obtained when noninvasive

evaluation has been unable to establish the correct
diagnosis

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PREVENTION OF AKI

• General measures to help prevent AKI include:

▪ Vigorous fluid administration has been successfully

employed to prevent ARF in patients at high risk, including:

1. Cardiac surgery.

2. Renal transplantation.

3. Hemoglobinuria, myoglobinuria.

4. Early tumor lysis syndrome.

5. Administration of nephrotoxic agent such as

radiocontrast, cisplatin, and amphotericin.

▪ Close monitoring of serum levels of nephrotoxic drugs.

▪ Adequate fluid repletion in those with hypovolemia.

▪ Aggressive hydration and alkalinization of the urine prior to

chemotherapy.

Treatment

• The basic principles of the general management of the child with

AKI include:

▪ Maintenance of electrolyte and fluid balance

▪ Adequate nutritional support

▪ Avoidance of life-threatening complications

▪ Treatment of the underlying cause.

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• Hyperkalemia —

▪ Severe hyperkalemia (serum potassium levels above 7.0

mEq/L), manifested by electrocardiographic changes or
peripheral muscle weakness.

▪ Can be life-threatening and requires immediate attention.

▪ Acute management includes:

1. The administration of intravenous calcium to

stabilize the cardiac membrane.

2. Glucose/insulin infusion.

3. Sodium bicarbonate.

4. Beta agonists to promote extracellular potassium

movement into the cells.

5. Kayexalate, an anion exchange resin, can remove

excess potassium from the body.

6. Renal replacement therapy is required if medical

management fails to improve the patient's
hyperkalemia.

• Acidosis —

▪ Sodium bicarbonate should only be administered with life-

threatening acidosis or hyperkalemia.

▪ Serum bicarbonate levels of greater than 14 mEq/L and/or

arterial pH greater than 7.2 do not require immediate
intervention.

• Renal replacement therapy —

▪ Renal replacement therapy in children with AKI is

recommended for the following:
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1. Signs and symptoms of uremia

2. Azotemia (BUN greater than 80 to 100 mg/dL)

3. Severe fluid overload that is refractory to medical therapy

4. Severe electrolyte abnormalities (eg, hyperkalemia and

acidosis) that are refractory to supportive medical therapy

5. Need for nutritional support in a child with oliguria or anuria

• Modalities of replacement therapy:

1. Hemodialysis

2. Peritoneal dialysis

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