Acute Kidney Injury

Case presentation
Aug.2019
Case
A 70 yrs old female patient , w/ Hx of diabetes ( last HbA1c 8 ,
On insulin ) and HTN ( on captopril and diuretic ) , REF-HF
( EF <40%)

Presented to OPC with Hx of 10 days LL swelling , from knee

down
Her Hx dates back to 3 months ago and the patient complains of
Orthopnea ( sleeps on 3 pillows , PND )
On routine blood test , her Sr Cr increased to 1.4 ( 0.6 before )
On P/E
Unremarkable
Vitals At day of admission : BP 130/90 , HR 110 , afebrile

General COA , Fatigue and generalized weakness , Dyspnea

Eye No jaundice ( liver dx) , no band keratopathy ( Multiple myeloma ) , no keratitis , uveitis
vasculitis )

ENT No hearing loss ( Alport ) , no mucosal ulceration( Wegner )

Skin No maculopapular Rash ( AIN)

Chest Normal S1 , S2 . No added murmur , No friction rub
GAEB , No lung crackles
Abdomen No visible pulsation ( Atheroemboli ) , no tenderness ( Nephrolithiasis )
Limbs Pitting edema from knee down On Both legs . No discoloration , skin changes , Pulses Intact
Labs :

CBC KFT LFT Electrolytes Urine analysis

Hb 11.2 Urea Na 142
MCV 89 Cr Cl K 4.5
WBC 5k On 31/7  0.6 Glu 92
On 1/8  1.4
Insert Image

By definition : A K I is
• Serum Cr increase • Decreased urine
by > 0.3 mg/dl output <0.5 ml/kg
within 48 hrs over 6 hrs

It can present Asymptomatic

incidentally on labs
high Cr, high BUN and hyperkalemia.
on U/A
albuminuria or abnormal urine sediment
Related to diminished kidney function
Edema , HTN , anuria
Evaluate your patient
LOOK for etiology / Cause

Reach your Diagnosis

Through
History
P/E
Labs
Imaging ?!
 • Timing of Cr elevation ( events )
History • Drugs ( Nephrotoxic medication)
Physical examination
Labs
• Past medical
Imaging • HTN ,Diabetic
• Past Surgical
• Post surgery

Up to date
 • Signs of volume depletion
History • Hypotensive , Tachy , Pallor , dizziness

Physical Examination • Typical drug rash

Labs • Suggest AIN
Imaging
• Blue toes
• suggest cholesterol emboli.
• Significant volume overload and signs of heart
failure
• suggest cardiorenal syndrome
• Ascites and jaundice
• suggest liver disease with portal hypertension and
hepatorenal syndrome.

Up to date
 • Cbc
• KFT
History • LFT
Physical examination
• EGFR
Labs Urine analysis:
And urine analysis 1. urine dipstick( PH, albumin, glucose, Hbg, leukocyte
Imaging esterase) ,
2. Microscopic examination of the urine sediment
3. Urine volume:
oliguria <500 ml/day
Anuria <50 ml/day
4. Hematuria glomerular disease or vasculitis
5. Pyuria AIN

Up to date
 Not indicated

History
Physical examination
Unless you want to Asses urinary
Labs tract obstruction renal ultrasound
Imaging • Urolithiasis  Ct without contrast
( Hx of flank pain )

!! Avoid MRI

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 Management

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Management
• Admission
• ABC / Stable /Check vitals
• Triage / Referral
• Assess fluid status
• Fluid resuscitation
• Treat underlying etiology

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Copyrights apply
 • Patients with stage 2 or 3 AKI as per the KDIGO
ER referral criteria

• Patients with stage 1 AKI who have an unclear

etiology, patients who have an unknown duration
or trajectory of elevated creatinine, or if they
have a concomitant, uncontrolled comorbid
condition (eg, acute on chronic exacerbation of
heart failure, diabetic ketoacidosis

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 Renal
Urgent • Hypervolemia w/ pulmonary edema

Replacement • Severe Hyperkalemia

• >6.5 mEq/L,

• hyperkalemia associated with symptoms or signs (ie, cardiac

conduction abnormalities, muscle weakness)
• hyperkalemia >5.5 mEq/L if there is ongoing tissue breakdown (eg,
rhabdomyolysis) or ongoing potassium absorption (eg, significant
gastrointestinal bleeding)

• Life threatening Uremic symptoms

• Toxin exposure

• Metabolic acidosis <7.1 pH

Up to date
Hyperkalemic Pulmonary edema
emergency We use 80 to 200 mg of intravenous (IV)
furosemide and monitor for an increase in
urine output
( We consider a urine output of greater than
200 mL within two hours of the furosemide
dose as adequate )

Up to date
Management
• Identify etiology of AKI
• Treat reversible cause ( Hypotension , Urinary Tract obstruction )
• X insult
• Medication : NSAIDS , ACE , ARBs , nephrotoxins (eg, aminoglycoside
antibiotics, amphotericin, tenofovir, nephrotoxic chemotherapy)
• Dosing adjustment based on GFR
• Hypotension ( identify and correct )
• Volume assessment – Primary aim of therapy

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Volume assessment

Hypovolemia Hypervolemia
oliguria ,hypotension , suggestive Hx Critically ill under obligate fluid intake (ATN ) ,
HF (cardio-renal ) , aggressive IV fluid

1 to 3 liters of crystalloid with assessment of

clinical response ( we continue maintenance
isotonic fluids at 75 mL/hour or greater
depending upon the ongoing losses. )
> Improve renal perfusion
>prompt drugs excretion
Goal MAP > 65 mmHg
In diuretic-naïve patients, we start with 80 mg
of intravenous (IV) furosemide and assess for
response. Patients who were on diuretics prior
to the onset of AKI should receive a dose that is
at least double their prior (home) dose.

Up to date
Manage complications

Hyperkalemia Hyperphosphatemia
Restrict dietary phosphorous to <2 g
per day
. Phosphate binders in pts :-
. o phosphate concentration >5.5 mg/dL
o enteral feeding (eating or receiving tube
feeds)
Acid base disorders o likely prolonged course of AKI
o severe hypocalcemia
o continued release of intracellular
phosphate such as rhabdomyolysis and
tumor lysis syndrome
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F/U
• Serum creatinine, electrolytes, total serum calcium, phosphate, and
albumin should be measured daily in stable patients

• Monitor daily weights, fluid intake, and urine output in order to assess
daily fluid balance

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American Family
physician