Acute Kidney Injury

Dana Baba
Previously called acute renal failure.

Definition of AKI: Sudden deterioration in renal function

results in the inability of kidneys to maintain fluid ,electrolyte
and homeostasis.

other definition :AKI is defined as a decrease in glomerular

filtration rate (GFR), which traditionally is manifested by an
elevated or a rise in serum creatinine from baseline, and/or a
reduction in urine output.
 P-RIFLE
classification AKIN classification

KDIGO
 Pediatric Modified Criteria
pRIFLE (Pediatric Risk, Injury, Failure, Loss, End Stage Renal Disease)
AKIN Classification
The Kidney Disease: Improving Global
Outcomes (KDIGO) Classification
Types according to Urine output
Anuria – No urine output.

Oliguria – Urine output <1 mL/kg per hour in infants, and in children and adults, urine output
<0.5 mL/kg per hour for greater than six hours.

Non-oliguria – Urine output for greater than six hours of >1 mL/kg per hour for infants and
>0.5 mL/kg per hour for children and adults.

Polyuria – Urine output of greater than 3 mL/kg per hour. Some patients with a urinary
concentrating defect will present with polyuric AKI, particularly those with acute tubular
necrosis and those with nephrotoxic AKI.
Etiology: General Approach
Though likely multifactorial, can be divided into:

Pre-renal --> MC in pediatrics due to hypovolemia (caused by reduce renal

perfusion),GFR is reduced and renal tubular function is intact.

Renal(intrinsic)-->Intrinsic or intrarenal AKI is characterized by structural damage to

the renal parenchyma. The most common causes of intrinsic disease are prolonged
hypoperfusion, sepsis, nephrotoxins, or severe glomerular diseases.
Post-renal-->Postrenal or obstructive AKI is typically the result of congenital or
acquired anatomic obstructions to the lower urinary tract.
Etiologic Classification
Biomarkers of AKI — Because serum creatinine is often a delayed and
imprecise test for AKI, research has focused on identifying biomarkers
that accurately predict AKI in the early stages of injury.

• Urinary Neutrophil Gelatinase-Associated Lipocalin (NGAL)

• Urinary Interleukin 18
• Urinary Kidney Injury Molecule 1 (KIM-1)
• Cystatin C
 Epidemiology of AKI
• Incidence US: 0.8/100 000
• 7% of hospitalized patients. More common
• 36-67% of critically ill patients, depending on the definition.
• 5-6% of ICU patients with AKI require RRT.
• Mortality in critically ill patients with AKI requiring RRT 50-70%.
Normal Creatinine Varies by age, gender and muscle mass.
 Acute Tubular Necrosis
Describes an end effect of tubular damage.
• Secondary to perfusion insults
• Secondary to toxins

Change in blood flow, obstruction and passive filtrate backflow into tubular cells can cause
a cycle leading to further death.
Symptoms of acute tubular necrosis include:
 A small amount of urine output.
 Swelling and fluid retention.
 Nausea and vomiting.
 Trouble waking up/drowsiness.
 Feeling sluggish.
 Confusion.
Acute Interstitial Nephritis
• Symptoms
• Blood in the urine, Fever, Increased or decreased urine output, Mental status changes (drowsiness,
confusion, coma)Nausea, vomiting, Rash, Swelling of any area of body and Weight gain (from retaining
fluid).

• Drug (71%)-1/3 antibiotics

Penicillin, cephalosporins, NSAID, sulfonamides, cipro, rifampin, PPIs
, allopurinol and more.

• Infection(15%)
Strep, legionella, leptospirosis, CMV, EBV and many.

• Tubulointerstitial Nephritis and uveitis TINU (5%).

• Autoimmune
• Idiopathic
Nephrotoxins
• Vascular effect
-ACEi, cyclosporine, tacrolimus. (decrease GFR) dilatation of efferent arteriole that decrease
intraglomerular pressure so decrease perfusion.
Give with caution

• Tubular effect
o Proximal: aminoglycosides, amphotericin B, cisplatin, immunoglobulins,
contrast
o Distal: NSAIDs, ACEi, lithium, cyclophosphamide
o Obstruction: sulfa, acylovir, methotrexate

• AIN
Post-renal causes
Two kidneys - distal or bilateral proximal obstruction
Single kidney - obstruction anywhere
• Posterior urethral valves
• Ureteropelvic junction obstruction
• Ureterovesicular junction obstruction
• Ureterocele
• Stones
• Tumour
• Hemorrhagic cystitis
• Neurogenic bladder
DIAGNOSIS
The current diagnosis of AKI is made clinically based on the presence of
characteristic signs and symptoms, and laboratory findings indicative of
an acute change in kidney function.

Signs and symptoms include edema, fluid overload, decreased or no

urine output, gross hematuria and/or hypertension.
Five Key Steps in Evaluating AKI
1. Obtain a thorough history and physical.
2. Do everything you can to accurately assess volume status
3. Always order a renal ultrasound
4. Look at the urine
5. Review urinary indices
 Laboratory findings
Serum creatinine — The most common laboratory test used to identify reduced glomerular filtration rate
(GFR) as an indication of AKI is serum creatinine
Urinalysis - An abnormal urinalysis provides supportive diagnostic evidence for AKI.
NORMAL:
-pre-renal
(may be concentrated)
-post-renal (granular casts)
-acute tubular necrosis ATN. (granular casts)
ABNORMAL:
-brown granular/epithelial
casts = ATN
red cell casts = Glomerulonephritis
pyuria, white cell casts (mainly neutrophils) = UTI or glomerulonephritis (post-infection)
Fractional Excretion of Sodium
FENa compensates for the urine output…
Urinary-Na x Plasma-Cr
Plasma-Na x Urinary-Cr
can also be thought of as
UNa/PNa
UCr/PCr
<1% --> pre-renal disease
1-2% --> ??
>2% --> ATN
Bloodwork
CBC: look for MAHA, thrombocytopenia
Extended lytes. Renal injury can result in:
• Hyperkalemia
• Hyperphosphatemia
• Hypocalcemia
• Metabolic acidosis
Other options, depending on history: ANCA,
ANA, ASOT, complement, drug levels
Imaging
Ultrasound - in all children if etiology unclear
• Number of kidneys
• Size of kidneys
• Obvious parenchymal damage
• Obstruction
• Stone
• Thrombus/vessel occlusion
Renal biopsy
Only when diagnosis remains unknown, or there is a failure to respond
to treatment or in cases of rapid progressive course
Renal Options:
Replacement • Continuous renal replacement therapy
Therapy-RRT
• Peritoneal dialysis
• Hemodialysis
Prognosis
Mortality: 60% (critically ill)
20-25% go on to have some degree of chronic renal issues
TREATMENT - Medical Management
• Obstruction- PUV: bladder catheterisation should be placed
immediately for drainage
• volume status : If there is no volume overload or cardiac failure,
isotonic saline 20 mL/kg over 30 min
• After volume resuscitation, hypovolemic patients generally void
within 2 hr; failure to do so suggests intrinsic or postrenal AKI
• Hypotension caused by sepsis: vigorous fluid resuscitation followed
by norepinephrine infusion
• Furosemide (2-4 mg/kg) and mannitol (0.5 g/kg) may be
administered as a single IV dose
Hyperkalemia
1. Stop Exogenous sources of potassium (dietary, intravenous fluids, total parenteral nutrition)
2. Increase K loss by GI: Sodium polystyrene sulfonate resin (Kayexalate), 1 g/kg, should be
given orally or by retention enema.
3. More severe elevations in serum potassium (>7 mEq/L), ECG changes • Calcium gluconate
10% solution, 1.0 mL/kg IV, over 3-5 min
4. Shift of K into intracellular spaces:
• Sodium bicarbonate, 1-2 mEq/kg IV, over 5-10 min
• Regular insulin, 0.1 units/kg, with glucose 50% solution, 1 mL/kg, over 1 hr
• β-adrenergic agonists
5. Persistent hyperkalemia should be managed by dialysis.
Metabolic Acidosis
• We should correct if pH< 7.15 and bicarbonate <12
• IV then oral
• Correction of metabolic acidosis with intravenous bicarbonate can
precipitate tetany in patients with renal failure as rapid correction of
acidosis reduces the ionized calcium concentration
Other targets of managements in AKI
• Hypertension
• Anemia
• GI protection
• hyperphosphatemia
• Neurological disorders
• Dialysis
• Nutritional support
Indication of Dialysis
1. Oliguria progress to anuria.
2. Volume overload with evidence of hypertension and/or pulmonary
congestion or edema refractory to diuretic therapy
3. Persistent hyperkalemia
4. Severe metabolic acidosis unresponsive to medical management
5. Uremia (encephalopathy, pericarditis, neuropathy)
6. Blood urea nitrogen >100-150 mg/dL (or lower if rapidly rising)
7. Calcium: phosphorus imbalance, with hypocalcemic tetany that
cannot be controlled by other measures