Material For Cme - AKI

Acute Renal Failure
Muhammad Hazim bin Azizul
AKI Definition
AKI is defined as any of the following
(Not Graded):
Increase in SCr by > 0.3 mg/dl (>26.5
micrmol/l) within 48 hours; or
Increase in SCr to>1.5 times baseline,
which is known or presumed to have
occurred within the prior 7 days; or
Urine volume <0.5 ml/kg/h for 6 hours.
Acute kidney injury stages

AKI
STAGE
Serum creatinine criteria
Urine output
criteria
Increase in serum creatinine of 26

micromol/litre or more within 48 hours
OR
1.5 to 2-fold increase from baseline
Less than 0.5 ml/kg/hour

for more than 6 hours*
Increase in serum creatinine to more

than 2 to 3-fold from baseline

for more than 12 hours
Increase in serum creatinine to more

than 3-fold from baseline
OR
Serum creatinine more than 354
micromol/litre with an acute increase of
at least 44 micromol/ litre

for 24 hours or anuria for
12 hours
Risk factors
Chronic kidney disease (or history of)

Diabetes
Heart failure
Sepsis
Hypovolaemia
Age 65 years or over
Use of drugs with nephrotoxic potential (for
example, NSAIDs, ACE inhibitors)
Use of iodinated contrast agents within past week
Oliguria
Symptoms or history of urological obstruction
Etiology
Prerenal Azotemia
renal hypoperfusion in which the integrity of renal tissue
is preserved
blood flow is inadequate filtration is less effective
decrease in renal function
clinical evidence of " true" hypovolemia (eg, hemorrhage,
vomiting, diarrhea, diuresis, burns, hyperpyrexia)
decreased " effective" circulatory volume (eg, cardiac or
liver failure, sepsis).
Definitive diagnosis rests on rapid recovery of glomerular
filtration rate after the restoration of renal perfusion
Etiology
Intrinsic Renal Azotemia
glomeruli acute poststreptococcal
glomerulonephritis, idiopathic rapidly progressive
glomerulonephritis, and systemic lupus
erythematosus.
kidney's interstitium acute allergic interstitial
nephritis, infections, or infiltration from diseases
such as sarcoidosis and lymphoma.
Tubules usually necrosis secondary to long
periods of hypotension, nephrotoxic drugs
(antibiotics such as aminoglycoside and radiological
contrast agents)
Etiology
Postrenal Etiologies
Obstructive uropathy - most common in
males and patient with recurrent urinary
tract infection.
Level of obstruction - ureter, bladder, and
urethra.
Clinical features - dysuria, frequency,
hesitation, gross hematuria, pain in the
costovertebral angle and groin, and anuria.
Relevant history
Urine output history:
Oliguria generally favors AKI.
Abrupt anuria suggests acute urinary
obstruction, acute and severe
glomerulonephritis, or embolic renal artery
occlusion.
A gradually diminishing urine output may
indicate a urethral stricture or bladder outlet
obstruction due to prostate enlargement.
Relevant history
Prerenal failure
commonly p/w
symptoms related to
hypovolemia:
thirst, decreased
urine output,
dizziness, and
orthostatic
hypotension.
volume loss from
vomiting,
diarrhea,
sweating,
polyuria, or
hemorrhage
Intrinsic renal
failure
Nephritic syndrome
of hematuria,
edema, and
hypertension
indicates a
glomerular etiology
for AKI. Query about
prior throat or
skin infections.
Acute tubular
necrosis (ATN) period of
hypotension
exposure to
nephrotoxins should
include a detailed
list of all current
medications and
any recent
radiologic
Postrenal failure
prostatic obstruction
and symptoms of
urgency,
frequency, and
hesitancy in
elderly.
Flank pain and
hematuria should
raise a concern
about renal calculi
Physical Examination
Hydration status
Septic looking
Clinical features of heart failure
Investigations
BUN
Electrolytes
Blood gases - Acidosis
Ufeme
US KUB
Management
Maintenance of volume homeostasis and
correction of biochemical abnormalities
remain the primary goals of treatment:
Correction of fluid overload with frusemide
Correction of severe acidosis with
bicarbonate
Correction of hyperkalemia
Correction of hematologic abnormalities
(eg, anemia) such as transfusions
Management
Monitory closely hydration status:
Lungs - crepitations
Urine output
Cvp monitoring
Prevention of contrast-induced
nephropathy
NaHCO3
isotonic NaHCO3 solution should be
administered before and after the
procedure.
N-acetylcysteine
oral N -acetylcysteine at a dosage of 1200
mg every 12 hours.
administered to high-risk patients the day
before a contrast study is performed and is
continued the day of the procedure.
Management
If post renal cause
Refer to urology
Indications for dialysis (ie, renal

replacement therapy) in AKI
Volume expansion that cannot be
managed with diuretics
Hyperkalemia refractory to medical
therapy
Correction of severe acid-base
disturbances that are refractory to
medical therapy
Severe azotemia (BUN >80-100)
Uremia
Case study
A 50-year-old patient is seen in the ED for treatment of bi-lobar
pneumonia. He has poorly controlled diabetes. On admission, his
BUN is 18.9, probably reflecting dehydration from 4 days of illness,
but his serum creatinine is 247, representing underlying kidney
disease, which is probably a result of his longstanding diabetes.
On day 1 of admission, despite receiving 2 L of fluid in the ED, his
BUN rises to 21 and his creatinine rises to 265. It is of concern that
his creatinine and BUN are increasing, despite the fluid challenge.
Over the day, his urine output, falls to 500 mL over a 24-hour
period.
On day 2, he develops shortness of breath and lower-extremity
edema. The fluids are discontinued, and labs reveal that his
creatinine has risen to 556 and his BUN has increased to 32. He
fails to respond to diuretics. The man promptly undergoes
hemodialysis
The END

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Acute Renal Failure

Muhammad Hazim bin Azizul

Acute kidney injury stages

Serum creatinine criteria

Increase in serum creatinine of 26

Less than 0.5 ml/kg/hour

Increase in serum creatinine to more

Less than 0.5 ml/kg/hour

Increase in serum creatinine to more

Less than 0.3 ml/kg/hour

Chronic kidney disease (or history of)

Indications for dialysis (ie, renal

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