Acute Kidney Injury

Acute kidney injury
- AKI -
Ammar Aladaileh
Definition
• Deterioration in renal function over a period of hours to days with
subsequent inability to clear water, electrolytes, and nitrogenous
wastes, and dysregulation of normal acid-base status
• Diagnosis:
1. Greater than 0.3 mg/dL rise in serum creatinine from baseline over
48 hours or a rise of 50% or more in 1 week
2. Urine output less than 0.5 mL/kg/h for 6 hours.
Pathophysiology
1. Pre-renal AKI: Decrease renal perfusion
2. Intrarenal AKI: Damage to the kidney (Glomerulonephritis, interstitial
nephritis, acute tubular necrosis)
3. Postrenal AKI: obstruction of the urine output from the kidney
1. Prerenal AKI
• Mechanism: Decrease perfusion to the kidney > Activate RAAS >
reabsorption of sodium and water (urine contains low sodium
concentration)
Note: urea is reabsorbed too with free water.
• Causes:
1. Systemic: dehydration, hemorrhage, heart failure or sepsis.
2. Local (decrease perfusion only to the kidney): NSAIDs, hepatorenal
syndrome (spasm).
- Most important clue: history and exam.
2. Intrarenal AKI
• Damage to the kidney > inability of kidney to concentrate the urine “inability to absorb
the sodium” (high sodium in the urine).
• Causes:
1. Glomerular disease: rapidly progressive glomerulonephritis ..etc.
2. Acute tubular necrosis: ischemic (severe and prolonged causes of prerenal or
embolism) or toxigenic.
3. Toxins (medications, contrast, hemoglobin, rhabdomyolysis, urate, or myeloma cast).
4. Acute interstitial nephritis: (Antibiotics, PPIs and NSAIDs)
• Most important investigation: urinalysis
3. Postrenal AKI
• Obstruction of the flow of urine. (backward
pressure >decrease GFR)
• Causes:
1. Benign prostatic hyperplasia
(suprapubic swelling)
2. Bilateral kidney stone
3. Abdominal or pelvic tumor
4. Renal vein thrombosis
• Most important Investigation: Imaging
(Ultrasound or CT scan)
History taking
• Urinary symptoms: Oliguria, color of the urine? (hematuria, cola, brown.. Etc.),
loin or suprapubic pain, difficulty urination or drippling.
• Determination of the cause:
MAIN THING TO LOOK: hx of medications.
1. Prerenal: history of vomiting diarrhea, heart failure, liver cirrhosis or sepsis
OR ANY HYOPTENSIVE EPISODE. History of NSAIDs.
2. Intrarenal: skin rash, arthritis, arthralgia, fever or weight loss (glomerular
disease) jaundice, fatigue, myalgia (rhabdo or hemolytic anemia) history of
contrast or invasive procedure.
3. Postrenal: history of these diseases.
• Looking for complications:
1. Overload: peripheral edema, shortness of breath, orthopnea
2. Hyperkalemia and acidosis: fatigue and weakness
3. Hypertensive emergency: blurry vision, headache or seizure
Physical examination
• Vitals: looking for hypertension or hypotension (test orthostatic) (prerenal).
High RR or low O2 saturation indicates pulmonary edema.
• General manifestations: dehydration vs euvolemia vs overload, asterixis (uremia)
respiratory distress, jaundice & anemia (hemolysis) or rashes.
• Chest: crackles, S3, friction rub.
• Abdomen: costovertebral tenderness, suprapubic swelling (urethral obstruction).
Investigations
• CBC: eosinophilia (AIN), anemia (hemolytic or CKD)
• KFT: to confirm diagnosis and to differentiate between
prerenal AKI (>20 urea: creatinine ratio) and ATN (<20 urea:
creatinine ratio)
• Urinalysis: FENa (<1% suggests prerenal and >2% suggests
ATN), Osmolality (>500 suggests prerenal)
Casts:
1. Granular: ATN
2. RBCs and dysmorphic RBCs: glomerulonephritis
3. WBCs and eospinphiluria: AIN
• LFT (including bilirubin), LDH and haptoglobin: hemolytic
anemia
• CPK: for rhabdomyolysis if suspected
• Ultrasound & CT scan: for evaluation of postrenal causes of
AKI
Investigations for complications
• ECG & cardiac monitoring: hyperkalemia
ECG Changes: 1. Peaked T wave 2. Prolonged QRS 3. Prolonged PR interval
• ABG: metabolic acidosis
Severe hyperkalemia: sine wave
Treatment of complications
1. Hyperkalemia (normally 3.5-5.5 mEq/L)
• According to level (>6.5 mEq/L) and ECG changes.
• Treatment:
1. Calcium gluconate: to stabilize the heart
2. insulin + glucose: shifting of K+ intracellularly with glucose
3. Albuterol
4. Furosemide: increase excretion of potassium
5. Dialysis: if refractory or life-threatening.
Treatment of complications
2. Overload: diuretics (furosemide) if not responding dialysis
3. Metabolic acidosis: bicarbonate infusion if not responding
dialysis
4. HTN: Fenoldopam is a good choice to dilate the renal
vessels and to treat hypertension.
5. Uremia (pericarditis, asterixis or encephalopathy): dialysis
Treat the underlying cause
• Prerenal: IV fluid, inotropes if HF, liver transplant for hepatorenal syndrome.
• Postrenal: relieve the obstruction (urologist consultation).
Indications of dialysis
AKI vs CKD
1. Baseline creatinine
2. Anemia
3. Size of the kidney: atrophic in CKD (except DM, amyloidosis and PCKD)
4. Presence of uremia manifestations on the presentation.

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