AKI Unit 2

Urine Output Definitions…

1. Anuric < 50 mL/day

2. Oliguric < 500 mL/day

3. Non-oliguric > 500 mL/day

KDIGO Staging of AKI…Stage 1

• SCr Criteria: SCr increase ≥ 0.3 mg/dL OR 1.5-1.9 times from baseline

• Urine: < 0.5 mL/kg/h for 6-12 hours

KDIGO Staging of AKI…Stage 2

• SCr Criteria: SCr increase 2-2.9 times from baseline 

• Urine: < 0.5 mL/kg/h for ≥ 12 hours

KDIGO Staging of AKI…Stage 3

• SCr Criteria: 

  • SCr increases three times from baseline 

  • SCr ≥ 4 mg/dL 

  • Need for Renal replacement therapy 

  • eGFR < 35 mL/min/1.73 in patients < 18 years

• Urine Criteria

  • Anuria ≥ 12 hours

  • < 0.3 mL/kg/h for ≥ 24 hours

Limitations to Staging Criteria…

→ biomarkers of SCr and urine output HAVE LIMITATIONS 

1. SCr

   1. Lag in SCr rise (48-72 hours from time of injury) 

   2. Baseline SCr must be known 

2. Urine Output

   1. Non-specific marker 

   2. Depends on volume, diuretic use, or cause of AKI

Risk Factors for AKI

1. Age, volume status 

2. COMORBID CONDITIONS

   1. CKD

   2. DM

   3. HTN

   4. Coronary artery disease 

   5. Congestive heart failure 

   6. Liver 

3. Proteinuria 

4. Medication and nephrotoxic exposure 

5. Surgery 

6. Sepsis 

Causes of Pre-Renal AKI

VOLUME DEPLETION

• HEMORRHAGE

• Decreases effective perfusion volume

• Vasodilation (sepsis)

• Diuretics 

• Thirst, hypotension, tachycardia 

Decreased Cardiac Output

• Congestive heart failure 

• Myocardial infarction 

• Cardiac surgery 

Functional: NSAIDs, ACEi

Pre-renal AKI labs…

1. Urine sodium < 20 

2. Urine osmolality:serum osmolality > 1.5

3. BUN:SCr > 20 

4. Low fractional excretion of sodium (FeNa)

   1. Pre-renal failure < 1%

Pre-renal AKI management: 

GOAL: restore renal blood flow by increase intravascular volume

1. Hemorrhage 

   1. → packed red blood cells 

2. Plasma losses (burns) or volume loss 

   1. → crystalloids OR colloid solutions 

3. Improve cardiac output (hypotension) 

   1. → positive inotropes, vasopressors 

Tubular Damage/Acute Tubular Necrosis Causes: INTRINSIC AKI

→ majority of intrinsic AKI (85%)

• 50% from renal ischemia 

• 35% from direct tubular toxins

Tubules are highly susceptible to ischemic damage 

1. Nephrotoxins:

   1. Antibiotics 

   2. Chemotherapy 

   3. Contrast 

2. Renal Hypoperfusion 

   1. Hypovolemic status 

   2. Low cardiac output 

   3. Sepsis 

Nephrotoxins

1. Antibiotics 

2. Chemotherapy 

3. Contrast 

FOUR PHASES OF ATN:

1. Initiation: renal tubular epithelial cell injury (vasoconstriction and ischemia)

   1. Leads to GFR reduction 

2. Extension: continued cell injury and inflammatory response 

3. Maintenance: 

   1. GFR reaches lowest points 

   2. Initial recovery of kidneys 

4. Recovery:

   1. new tubule cells regenerated 

ATN Labs and Urinarlysis…

• Color and appearance: muddy brown (RBC and WBC casts)

• Granular or epithelial cell casts 

• Urine : serum osmolality < 1.3

• BUN : SCr = 15

• FeNa > 2%

ATN Management

→ improve urine output 

→ restore kidney function 

→ improve survival

POST-RENAL AKI: causes

→ accounts for 5% of all cases of AKI 

• Bladder outlet obstruction

  • BPH, cancer, surgery 

• Ureteral obstruction 

  • Nephrolithiasis 

Post-Renal Failure Labs and Urinalysis 

• Urine sodium > 40 

• BUN : Scr ration = 15 

• Some cellular debris in urine 

• Urine : serum osmolality < 1.5

• FeNa: variable

Post-Renal Failure Management

• Removal of obstruction 

• Alpha, beta blockers for BPHS

• Catheterization 

• Percutaneous nephrostomy 

Complications of AKI

1. Volume overload and edema 

2. Electrolyte imbalance 

3. Acid-base disorder

4. Malnutrition 

5. Drug-dosage adjustment 

Renal Replacement Therapy? 

→ intermittent hemodialysis (IHD)

• Short treatment session 3-4 hours 

• Rapid removal of volume and small solutes

• Can cause hypotension

→ continuous renal replacement therapy 

• Reserved for unstable patients 

• More solute removal 

• Less hypotension risk  

Volume Overload…

1. Clinical Presentation: peripheral and pulmonary edema 

2. Management: 

• fluid restriction

• limit sodium intake 

• Loop diuretics 

3. Diuretic resistance: bioavailability of the drug is reduced 

• Continuous instead of intermittent for more consistent concentration  

• Combination therapy → synergy with diuretic at distal tube 

Drug Dosing in AKI…

1. Pharmacokinetic alterations 

2. Estimate of renal function 

3. Volume of distribution (drug’s normal Vd and patient’s volume status)

4. Type of Renal Replacement Therapy  

5. Drug monitoring/therapeutic window 

6. Individualized approach