Seminar on Management of

Acute Kidney Injury

Moderator Dr. Yemisrach T (MD,Pediatrician)

Presented by Dr. Deginet T(Intern)
Hidar/2015 EC
 Outline

• Definition
• Clinical features
• Diagnosis
• Management of AKI

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 Introduction
Anatomy
 Cortex
 Medulla

Functions
 Excretion
 Regulation
 Endocrine function
 Metabolic function

Nephron is structural
and functional unit.

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 Introduction

Acute kidney injury (AKI) is-

 An 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 homeostasis.
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 Cont. …
• A classification system proposed by the Kidney Disease Improving
Global Outcomes (KDIGO) AKI Consensus Conference takes both
serum creatinine and urine output criteria into account to define and
stage AKI

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 Acute Renal Disease: 3 Categories

1. Prerenal
2. Intrinsic Renal
3. Postrenal

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 Pathogenesis
 AKI has been conventionally classified into three
categories:
 prerenal, intrinsic renal, and postrenal
 Common Causes of Acute Kidney Injury are-

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 Cont. …

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 Prerenal AKI
 Characterized by a diminished effective circulating
arterial volume, which leads to inadequate renal
perfusion and a decreased GFR.
 If the underlying cause is reversed promptly, renal
function returns to normal.
 Structural kidney damage is absent.

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 Intrinsic renal AKI
 Characterized by renal parenchymal damage,
 Ischemic/hypoxic injury and nephrotoxic insults are
the most common causes, leads to ATN
 Glomerulonephritis can also cause intrinsic AKI,

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 Cont. …
Tumor lysis syndrome is a specific form of AKI
related to spontaneous or chemotherapy-induced
cell lysis,
– In patients with lymphoproliferative
malignancies.
– Primarily caused by obstruction of the tubules
by uric acid crystals

• Acute interstitial nephritis is a result of a

hypersensitivity reaction to a therapeutic agent or
various infectious agents

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 Postrenal AKI
 Characterized by obstruction of the urinary tract,
 In neonates and infants, congenital conditions,
such as posterior urethral valves and bilateral
ureteropelvic junction obstruction, account for the
majority of cases,
 Relief of the obstruction usually results in recovery
of renal function,

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 Clinical Manifestations and Diagnosis
 A carefully taken history is critical in defining the
cause of AKI.
 The physical examination must be thorough, with
careful attention to volume status.

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 Laboratory Findings
 Laboratory abnormalities can include
– Anemia
– Leukopenia
– Thrombocytopenia
– Hyponatremia
– metabolic acidosis
– Elevated serum concentrations of BUN, creatinine, uric
acid, K+ , and phosphate; and hypocalcemia
(hyperphosphatemia)
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 Cont. …
– Serum C3 level may be depressed
– Antibodies may be detected
– Hematuria, proteinuria, and red blood cell or granular urinary
casts
– WBC and WBC casts
– Urinary eosinophils

– Urinary indices
– Chest radiography
– Renal ultrasonography
– Renal biopsy
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 Cont. …

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 Management of AKI

 In a newborn with suspected posterior urethral

valves, a bladder catheter should be placed,
 when initially evaluating, determination of the
volume status is important,
 If no volume overload or cardiac failure, IV
administration of isotonic saline, 20 mL/kg over
30 min
 During blood loss or hypoproteinemia, colloid
solutions are required

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 Cont. …
• After resuscitation hypovolemic patients void
within 2 hr; if failure suggests intrinsic or
postrenal AKI.
• Hypotension caused by sepsis requires vigorous
fluid resuscitation followed by a continuous
infusion of vasopressors.

• Diuretic therapy considered, Furosemide (2-4

mg/kg) as a single IV dose. Bumetanide (0.1
mg/kg) as an alternative .

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 Cont. …
 If urine output is not improved, then a continuous
diuretic infusion may be considered to increase renal
cortical blood flow, many clinicians administer
dopamine (2-3 µg/kg/min) in conjunction with
diuretic therapy,

 If there is no response to a diuretic challenge,

diuretics should be discontinued and fluid restriction
is essential.

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 Cont. …
 Patients with a relatively normal intravascular
volume should initially be limited to 400
mL/m2 /24 hr (insensible losses) plus an amount
of fluid equal to the urine output for that day.

 Extrarenal (blood, GI tract) fluid losses should be

replaced,

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 Cont. …

Hyperkalemia (serum potassium level >6 mEq/L)

– Exogenous sources of potassium should be
eliminated,
– Sodium polystyrene sulfonate resin
(Kayexalate), 1 g/kg, should be given orally or
by retention enema.

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 Cont. …
 In more severe hyperkalemia (>7mEq/L);
– Calcium gluconate 10% solution, 1.0 mL/kg IV,
over 3-5 min
– Sodium bicarbonate, 1-2 mEq/kg IV, over 5-
10 min
– Regular insulin, 0.1 U/kg, with glucose 50%
solution, 1 mL/kg, over 1 hr,

 If hyperkalemia is persistent and not responding

to the above medical managements, it should be
managed by dialysis.
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 Cont. …
Acidosis
– If it is severe (arterial pH < 7.15; serum
bicarbonate < 8 mEq/L) or contributes to
hyperkalemia, treatment is required.
• Bicarbonate (slowly).
– Rapid correction of acidosis can precipitate
hypocalcemia.

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 Cont. …
Hypocalcemia
Primarily treated by lowering the serum
phosphorus level.
Low-phosphorus diet
Phosphate binders
 Sevelamer (Renagel),
 Calcium carbonate and
 Calcium acetate

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 Cont. …
Hyponatremia
Fluid restriction
Hypertonic (3%) saline limited to patients with
symptomatic hyponatremia (seizures, lethargy)
or with a serum Na level <120 mEq/L.
• Acute correction of serum sodium to
125mEq/L accomplished using the following
formula:
– mEq sodium required= 0.6Wt (125 –
Serum[Na])

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 Cont. …
GI bleeding
Oral or IV H2-blokers (ranitidine)
Hypertension
Fluid and salt restriction
Diuretics
Calcium channel blockers
Βeta blockers
Vasodilators (for urgency and emergency)

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 Cont. …

Neurologic symptoms
 in AKI can include headache, seizures, lethargy,
and confusion (encephalopathy).
– Diazepam if seizure
– Treat the precipitating cause.

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 Cont. …
Anemia
 If Hb is <7g/dl, transfusion is needed.
In hypervolemic patients
– Slow (4 – 6hr) transfusion with packed RBC
(10ml/kg )
– The use of fresh washed red blood cells
minimizes the acute risk of hyperkalemia and
chronic risk of sensitization.
In the presence of severe hypervolemia or
hyperkalemia, blood transfusions are most
safely administered during dialysis or
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 Cont. …
Nutrition
In most cases, sodium, potassium, and
phosphorus should be restricted.
Protein intake should be restricted moderately
while maximizing caloric intake to minimize the
accumulation of nitrogenous wastes.
In critically ill patients with AKI, parenteral
hyperalimentation with essential amino acids
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 Dialysis
Indications for 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
Neurologic symptoms (altered mental status, seizures)
Blood urea nitrogen >100-150 mg/dl (or lower if rapidly rising)
Calcium: phosphorus imbalance, with hypocalcemic tetany

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 Prognosis
 Mortality rate is variable and depends entirely on
the nature of underlying disease process.
 Recovery of renal function is likely after :
– Prerenal causes,
– ATN,
– Acute interstitial nephritis,
– TLS
 Recovery of renal function is unusual after:
– Most types of RPGN,
– bilateral renal vein thrombosis,
– bilateral cortical necrosis.

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 Sequelae of AKI

 Chronic renal failure

 Hypertension

 Renal tubular acidosis

 Urinary concentrating defect

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 Reference
• Nelson Text book of pediatric 21th ed.

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 THANK YOU

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