Acute Kidney Injury


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






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



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 (FENa <1%)
  • Treatment:
    • Treat underlying cause, eliminate offending agent
    • NS to restore blood volume and pressure (don’t give if edema)


2. Renal: 2nd 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 (FENa >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




  • 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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