ACUTE KIDNEY

INJURY
Paediatric Lecture: EDSU, UZAIRUE
June 2024
Dr. Adetunji A.E
MBBS, FWACP (Paed), Cert Sub-Specialty
Paediatric Nephrology (SA)
Outline
Introduction
Epidemiology
Causes
Pathogenesis
Clinical Manifestations
Staging
Laboratory Findings
Treatment
Prognosis
Prevention
Reference
Introduction
Acute kidney injury (AKI) has been traditionally defined as an abrupt
loss of kidney function leading to a rapid decline in the glomerular
filtration rate (GFR), accumulation of waste products such as blood
urea nitrogen (BUN) and creatinine, and dysregulation of extracellular
volume and electrolyte homeostasis.

AKI embodies a continuum of renal dysfunction that ranges from a

small increase in serum creatinine to complete anuric renal failure.
 Epidemiology
The incidence of AKI varies from 2–5% of all hospitalizations to >
25% in critically ill infants and children.

The aetiology of AKI varies widely according to age, geographic

region, and clinical setting.

Functional AKI induced by dehydration is usually reversible with early

fluid therapy. However, the prognosis for patients with structural AKI
in the intensive care setting with multiorgan failure remains guarded.
Common Causes of Acute Kidney Injury
Prerenal
Dehydration
Gastroenteritis
Hemorrhage
Burns
Sepsis
Capillary leak
Hypoalbuminemia
Cirrhosis
Abdominal compartment syndrome
Cardiac failure
Anaphylaxis
Intrinsic Renal

Glomerulonephritis Cortical necrosis

Postinfectious/poststreptococcal Renal vein thrombosis
Lupus erythematosus Rhabdomyolysis
Henoch-Schönlein purpura Acute interstitial nephritis
Membranoproliferative Tumor infiltration
Anti–glomerular basement Toxin and drugs
membrane Tumor lysis syndrome
Hemolytic-uremic syndrome Vasculitis
Acute tubular necrosis
Postrenal
Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Ureterocele
Tumors
Urolithiasis
Urethral strictures
Hemorrhagic cystitis
Neurogenic bladder
Pathogenesis

AKI has been conventionally classified into three categories: prerenal,

intrinsic renal, and postrenal.
Prerenal AKI, also called prerenal azotemia, is characterized by a
diminished effective circulating arterial volume, which leads to
inadequate renal perfusion and a decreased GFR. Evidence of
structural kidney damage is absent. If hypoperfusion is sustained,
intrinsic renal parenchymal damage can develop.
Intrinsic renal AKI includes a variety of disorders characterized by
renal parenchymal damage, including sustained hypoperfusion and
ischemia.
Many forms of glomerulonephritis can also cause intrinsic AKI.
Severe and prolonged ischemic/hypoxic injury and,nephrotoxic insult
lead to acute tubular necrosis (ATN), seen most often in critically ill
infants and children.

Postrenal AKI includes a variety of disorders characterized by

obstruction of the urinary tract.
Relief of the obstruction usually results in recovery of renal function,
except in patients with associated renal dysplasia or prolonged urinary
tract obstruction.
Clinical Manifestations
Detailed history and examination:
Prerenal AKI: vomiting and diarrhea, tachycardia, dry mucous
membranes, and poor peripheral perfusion.
Intrinsic AKI: recent pharyngitis in a child who presents with
periorbital edema, hypertension, and gross hematuria, peripheral
edema, rales, and a cardiac gallop (acute postinfectious
glomerulonephritis).
Rash and arthritis might indicate systemic lupus erythematosus or
Henoch-Schönlein purpura nephritis.
Palpable flank masses may be seen with renal vein thrombosis,
tumors, cystic disease, or urinary tract obstruction.
A critically ill child with a history of protracted hypotension or with
exposure to nephrotoxic medications most likely has ATN.
Clinical Manifestations
Careful attention to volume status.
Neonate with a history of hydronephrosis seen on prenatal ultrasound
studies and a palpable bladder most likely has congenital urinary tract
obstruction, probably related to posterior urethral valves.
Kidney Disease: Improving Global Outcomes
(KDIGO) Staging of Acute Kidney Injury
Laboratory Findings
Electrolytes, urea and creatinine: hyponatremia (dilutional); metabolic
acidosis; elevated serum concentrations of blood urea nitrogen, creatinine,
uric acid, potassium, and phosphate (diminished renal function); and
hypocalcemia (hyperphosphatemia).

The presence of hematuria, proteinuria, and red blood cell or granular

urinary casts suggests intrinsic AKI, in particular glomerular disease and
ATN.
Anemia (the anemia is usually dilutional or hemolytic
Other laboratory findings will depend on the underlying aetiology: low C3
in post infectious AGN, SLE.
Ultrasound studies may show features of congenital urinary tract
obstruction, probably related to posterior urethral valves.
Laboratory Findings
Renal ultrasonography can reveal hydronephrosis and/or hydroureter,
which suggest urinary tract obstruction, or nephromegaly, consistent
with intrinsic renal disease.

Chest radiography may reveal cardiomegaly, pulmonary congestion

(fluid overload), or pleural effusions.

Renal biopsy can ultimately be required to determine the precise

cause of AKI
Serum creatinine is an insensitive and delayed measure of decreased
kidney function following AKI.

Other biomarkers under investigation include changes in

Plasma Neutrophil gelatinase–associated lipocalin and cystatin C
levels, and
Urinary changes in neutrophil gelatinase-associated lipocalin,
interleukin 18, and kidney injury molecule-1.
Treatment

Medical Management
General measures:
Relief the obstruction in patient with urinary tract obstruction
Strict input and output (urine, stool… output) monitoring
Daily weight measurement
Daily serum electrolytes, urea and creatinine
Restrict salt and water intake as necessary
Close monitoring of vital signs
Fluid intake, urine and stool output, body weight, and serum
chemistries should be monitored on a daily basis.
Specific measures:
Determination of the volume status is of critical importance at initial
evaluation:
o No evidence of volume overload or cardiac failure, the intravascular volume
should be expanded by intravenous administration of isotonic saline, 20
mL/kg over 30 min. additional fluid boluses may be required in severe
hypovolemia.
o Colloid-containing solutions are not required for volume expansion except in
blood loss or hypoproteinemia.
o Determination of the central venous pressure may be helpful.
o After volume resuscitation, hypovolemic patients generally void within 2 hr
otherwise think of intrinsic or postrenal AKI.
o Consider diuretic therapy only after the adequacy of the circulating blood
volume has been established. Furosemide (2-4 mg/kg) or Bumetanide (0.1
mg/kg) can be given as a single intravenous dose.
o If urine output is not improved, then a continuous diuretic infusion may be
considered.
Treatment
o Dopamine (2-3 μg/kg/min) in conjunction with diuretic therapy can be used to
increase renal cortical blood flow.
o There is little evidence that diuretics or dopamine can prevent AKI or hasten
recovery.
o Mannitol may be effective in the prevention of pigment (myoglobin,
hemoglobin)-induced renal failure.
o Hypotension caused by sepsis requires vigorous fluid resuscitation followed
by a continuous infusion of vasopressors.
o If there is no response to a diuretic challenge, diuretics should be discontinued
and fluid restriction is essential.
o Fluid restriction if there is no response to diuretic challenge
Treatment
o In relatively normal intravascular volume, fluid for that day should initially be
limited to 400 mL/m2 /24 hr (insensible losses) plus previous day urine output.
Other fluid losses should be replaced, milliliter for milliliter.
o Markedly hypervolemic patients can require further fluid restriction, omitting the
replacement of insensible fluid losses, urine output, and extrarenal losses.
Treatment of electrolyte derangement:
Hyperkalemia (serum potassium level > 6 mEq/L) can lead to cardiac
arrhythmia, cardiac arrest, and death. The earliest electrocardiographic
change seen in patients with developing hyperkalemia is the
appearance of peaked T waves. This may be followed by widening of
the QRS intervals, ST segment depression, ventricular arrhythmias,
and cardiac arrest.
o Procedures to deplete body potassium stores should be initiated when the serum
potassium value rises to > 6.0 mEq/L:
o Stop exogenous sources of potassium (dietary, intravenous fluids, total parenteral
nutrition)
o Sodium polystyrene sulfonate resin (Kayexalate), 1 g/kg, should be given orally or
by retention enema.
o Serum potassium (>7 mEq/L) requires emergency measures in addition to
Kayexalate. The following agents can be given while preparing for dialysis:
o Calcium gluconate 10% solution, 100 mg/kg/dose (maximum 3000 mg/dose). It
counteracts the potassium-induced increase in myocardial irritability but does not
lower the serum potassium level.
o Sodium bicarbonate, 1-2 mEq/kg intravenously, over 5-10 min
o Regular insulin, 0.1 units/kg, with glucose 50% solution, 1 mL/kg, over 1 hr
o Nebulize with β-adrenergic agonists.

 Administration of sodium bicarbonate, insulin, or glucose lowers the serum potassium

level by shifting potassium from the extracellular to the intracellular compartment.

 Because the duration of action of these emergency measures is just a few hours,
persistent hyperkalemia should be managed by dialysis.
Treatment
 Mild metabolic acidosis is common in AKI because of the retention
of hydrogen ions, phosphate, and sulfate, but it rarely requires
treatment. If acidosis is severe (arterial pH < 7.15; serum bicarbonate
< 8 mEq/L).
o It can be corrected partially by the intravenous route with bicarbonate
to raise the arterial pH to 7.20 (which approximates a serum
bicarbonate level of 12 mEq/L).
o Complete correction can be accomplished by oral administration of
sodium bicarbonate after normalization of the serum calcium and
phosphorus levels.
Treatment
Hypocalcemia is primarily treated by lowering the serum phosphorus
level. Calcium should not be given intravenously, except in cases of
tetany, to avoid deposition of calcium salts into tissues.
o Low-phosphorus diet, and
o Oral phosphate binders will increase the GI phosphate excretion.e.g.
sevelamer (Renagel), calcium carbonate (Tums tablets or Titralac
suspension), and calcium acetate (PhosLo). Aluminum-based binders
should be avoided because of the risk of aluminum toxicity.
Hyponatremia: commonly dilutional, that must be corrected by fluid
restriction rather than sodium chloride administration.
o Administration of hypertonic (3%) saline should be limited to:
Symptomatic hyponatremia (seizures, lethargy) or
Serum sodium level < 120 mEq/L.
o Acute correction of the serum sodium to 125 mEq/L (mmol/L) should be
accomplished using the following formula:
mEq sodium required = 0.6×weight in kg × (125-serum sodium in mEq/L)

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
can be used to prevent it.
Hypertension can result from hyperreninemia associated with the
primary disease process and/or expansion of the extracellular fluid
volume especially in acute glomerulonephritis or HUS.
o Salt and water restriction is critical, and
o Diuretic administration may be useful
o Hypertensive urgency or emergency should be treated with continuous
infusions of nicardipine (0.5-5.0 μg/kg/min), sodium nitroprusside
(0.5-10.0 μg/kg/min), labetalol (0.25-3.0 mg/kg/hr), or esmolol (150-
300 μg/kg/min) and converted to intermittently dosed
antihypertensives when more stable.
o Longer-acting oral agents such as calcium channel blockers
(amlodipine, 0.1-0.6 mg/kg/24 hr qd or divided bid) or β blockers
(labetalol, 4-40 mg/kg/24 hr divided bid or tid) may be helpful as
maintenance agents.
Neurologic symptoms (headache, seizures, lethargy, and confusion
(encephalopathy)):
o Causes: hypertensive encephalopathy, hyponatremia, hypocalcemia, cerebral
hemorrhage, cerebral vasculitis, and the uremic state.
o Benzodiazepines to control the seizures
o Subsequent therapy is directed towards the cause

Anemia of AKI is generally mild (hemoglobin 9-10 g/dL) and

primarily from hemodilution.
o Children with HUS, SLE, active bleeding, or prolonged AKI can require
transfusion of packed red blood cells , caution must be taken to prevent further
risk of volume expansion (it can be safely done during dialysis).
o The use of fresh, washed red blood cells minimizes the acute risk of
hyperkalemia, and the chronic risk of sensitization.
Nutrition is of critical importance in AKI.
o In most cases, sodium, potassium, and phosphorus should be
restricted.
o Protein intake should be moderately restricted while maximizing the
caloric intake to minimize the accumulation of nitrogenous wastes.
o Parenteral hyperalimentation with essential amino acids should be
considered in critically ill patients.
Dialysis
Indications for dialysis in AKI include the following:
o Anuria/oliguria
o Volume overload with evidence of hypertension and/or pulmonary edema
refractory to diuretic therapy
o Persistent hyperkalemia
o Severe metabolic acidosis unresponsive to medical management
o Uremia (encephalopathy, pericarditis, neuropathy)
o Calcium:phosphorus imbalance, with hypocalcemic tetany that cannot be
controlled by other measures.
o Inability to provide adequate nutritional intake because of the need for severe
fluid restriction.
Types:
o Intermittent hemodialysis
o Peritoneal dialysis
o Continuous renal replacement therapy (CRRT)
Prognosis
The mortality rate is variable and depends entirely on the nature of the
underlying disease process rather than on the renal failure itself.
o Postinfectious glomerulonephritis have a very low mortality rate (<1%)
o AKI related to multiorgan failure have a very high mortality rate (>50%).

The prognosis for recovery of renal function depends on the disorder

that precipitated AKI.
Prevention
Using 5 levels of prevention
General health promotion
Specific protection
Early diagnosis and prompt treatment
Limitation of disability
Rehabilitation
Reference
Acute Kidney Injury. Prasad Devarajan. Nelson Textbook of Pediatrics. 21 st
edition. Editors: Robert M. Kliegman, Joseph W. ST Geme, Nathan J. Blum,
Samir S. Shah, Robert C. Tasker, Karen M. Wilson, Richard E. Behrman.
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