Acute Kidney Injury

Definition:

Rapid decline in kidney function + increase in serum creatinine (50%, or 0.5-1.0 mg\dL increase)

 

Classification:

 

Presentation:

Oliguric (<400 mL\day) \anuric\non-oliguric (>400 mL\day), wt gain, edema, azotemia

 

Categories:

1. Prerenal: most common

• Pathophysiology: decrease in renal blood flow
  • True volume depletion: lack of oral intake, vomiting, diarrhea, GI bleeding, diuretics, hyperglycemia, DI
  • Reduction in effective circulating volume: CHF, cirrhosis, hepatorenal syndrome, Nephrotic syndrome, sepsis\shock,
  • Medications: diuretics, ACEI\ARBs (dilate efferent), NSAIDs (constrict afferents)
  • Reversible (unless persistent hypoperfusion -> ischemia -> ATN)
• Investigation:
  • Oliguria (<400 mL\day)
  • Increased BUN\Cr ratio (>20:1), due to increased water and urea reabsorption
  • Increased urine osmolality (>500 mOsml\kg)
  • Low urine sodium (<20 mEq\L)
  • Low urine fractional excretion of sodium (FE_Na <1%)
• Treatment:
  • Treat underlying cause, eliminate offending agent
  • NS to restore blood volume and pressure (don’t give if edema)

 

2. Renal: 2^nd most common

• Pathophysiology: damage to renal parenchyma
  • Tubular ds (ATN): can be due to ischemia (shock, sepsis, hemorrhage, HF) and nephrotoxins (Meds: antibiotics ‘aminoglycosides and vancomysin’, NSAIDs, radiocontrast, myoglobinuria ‘muscle damage, strenuous exercise, rhabdomyolysis’, hemoglobinuria ‘hemolysis’, chemo ‘cisplastin’)
  • Glomerular ds (GN)
  • Vascular ds: renal artery occlusion, TTP, HUS
  • Interstitial ds: allergic interstitial nephritis (due to hypersensitivity to meds)
• Investigations:
  • Decreased BUN\Cr ratio (<20:1), bc urea is less absorbed here compared w\ prerenal
  • Decreased urine osmolality (<350 mOsm\kg), bc impaired renal water reabsorption
  • High urine sodium (>40 mEq\L)
  • High urine fractional excretion of sodium (FE_Na >2-3%)

• Treatment:
  • Supportive, eliminate offending agent
  • If oligouric -> furosemid

 

3. Postrenal: least common

• Pathophysiology: urinary tract obstruction -> increase tubular pressure -> ↓GFR
  • Reversible if obstruction is relieved. If not -> ATN
  • MCC: BPH -> urethral obstruction
  • Obstructing nephrolithiasis
  • Obstructing neoplasm
  • Retroperitoneal fibrosis
  • Renal vein thrombosis
• Investigations:
  • Ultrasound: test of choice
• Treatment:
  • Bladder cath -> decompress compression

 

Diagnosis of acute kidney injury in general:

• Blood work: high BUN and Cr, electrolyte (K, Ca, PO), CBC
• Urine volume, urinalysis, urine sediment, urine chemistry
• Foley cath (rule out bladder outlet obstruction)
• Fluid challenge (rule out prerenal)
• Imaging: US (post renal obstruction and hydronephrosis)
• Renal biopsy (if sus GN or acute allergic interstitial nephritis)
• Renal arteriography

 

Complications:

• Volume overload -> pulmn edema -> give furosemide
• High anion gap metabolic acidosis w\ hyperkalemia
• Can’t form active vit D + PTH resistance -> Hypocalcemia
• Water intake is more than output or volume depleted patients consuming hypotonic solutions -> Hyponatremia
• Uremia
• Infection (multifactorial\uremia impairing immunity): pneumonia, UTI, wound infec, sepsis

 

 

Random notes:

• Most common cause of AKI in hospital setting is? Acute tubular necrosis, followed by prerenal causes
• Rhabdomyolysis: muscle breakdown (e.g. trauma, seizures, snake bites) -> release of muscle fiber content into blood stream (myoglobin) -> nephrotoxicity and AKI. High CPK and K. Treat with IV fluid, mannitol (osmotic diuretic), and bicarbonate (drives K back into cells)
• Course of ATN: oliguric phase -> diuretic phase -> recovery phase

 

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References:

• Step up to medicine
• Master the boards
• Kaplan step 2 videos and lecture notes
• Toronto notes
• Step up to USMLE step 2