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Acute Kidney Injury (AKI)

Terra Swanson


  • Definition based on 2012 KDIGO Guidelines: 
    • Rise in serum creatinine (sCr) > 0.3 mg/dL within 48 hours, or increase > 1.5 x baseline in 7 days  
    • Urine volume \<0.5 cc/Kg/H for at least 6 H

Framework for AKI

  • Pre-renal/hemodynamic AKI:

    • Volume depletion: GI losses, hemorrhage, burns, critical illness increased insensible losses 
    • Decreased effective circulating volume: cardiorenal, hepatorenal, hemodynamic effects of ACEi/ARB 
    • Afferent arteriole constriction [NSAIDs, Iodinated contrast] 
    • Renal vein thrombus 
  • Intra-renal: Glomerular, tubular, or interstitial diseases

    • ATN = Most common form of intrinsic AKI. Can be Ischemic or toxic
      • Toxins can be broken down further into endogenous (e.g. rhabdo) and exogenous (e.g. drugs)
    • Acute Interstitial Nephritis (AIN): Usually drug induced (NSAIDs, PPIs, beta lactam abx)  
    • Glomerulonephritis
    • Other causes:  
      • Crystalline nephropathy: IV acyclovir, tumor lysis, ethylene glycol 
      • Small vessel disease: MAHA, TTP, HUS
      • Large vessel disease: Aortic dissection, renal artery stenosis  
  • Post-renal: Can occur at any level of the GU system 

    • Ureteral: stones, external compression (malignancy, LAD, abscess) 
    • Bladder: neurogenic bladder, malignancy, obstructing blood clot 
    • Urethra: BPH, prostate cancer, prostatitis  
  • Pre-renal azotemia and acute tubular necrosis comprise the majority of inpatient acute kidney injuries


  • History and volume exam

  • Labs: CMP, urinalysis, protein/Cr ratio

  • 500cc-1L IV fluid challenge: If sCr improves to baseline in \<48H then the insult was likely pre-renal. If not, then look for other etiologies

  • Evaluate for obstruction: I/O cath, Foley, Post Void Residual >250 cc

  • Who needs a renal ultrasound? 

    • No obvious cause of AKI
    • Abrupt oliguria or anuria (think renal vein thrombus or obstruction)
    • High suspicion for bladder outlet obstruction (PVRs might give you same data) 
    • Add doppler to evaluate for renal artery stenosis (or if working up resistant hypertension) 
  • Urine Electrolytes 

    • FENa \<1% or FEUrea \<33% (if on diuretics) suggest pre-renal physiology
    • Caveat, only validated in oliguric patients and more difficult to interpret after fluids, diuretics, etc
    • Not needed in the initial work-up of all patients with AKI. If high suspicion for pre-renal etiology, trial fluid challenge and assess response first
  • Urine sodium can be used to assess Na avidity: UNa > 40 suggests ATN and UNa \< 20 suggests pre-renal


  • All causes

    • Minimize fluctuations in blood pressure
    • Consider holding anti-hypertensive medications, especially ACEi/ARB (remember to determine plan to resume at/after discharge)
    • Avoid unnecessary nephrotoxins
    • Dose-adjust medications for changing renal function
  • Pre-Renal

    • True volume depletion- Intravenous volume expansion
    • Cardiorenal syndrome- Decongestion/diuresis
    • Hepatorenal syndrome- See Hepatology section for more information
  • Post-renal

    • Relieve Obstruction: I/O cath, foley, Urostomy (Urology), percutaneous nephrostomy (IR)
    • Monitor for post-obstructive diuresis
  • Intra-renal

    • ATN- supportive care, monitor for post-ATN diuresis. If delayed recovery, may need outpatient dialysis
    • Glomerulonephritis- Consult AKI service for assistance with biopsy and selecting immunosuppressive agents if needed
    • AIN- Review meds, consult nephrology for possible biopsy and recommendations for steroids
  • Monitor for renal recovery 

    • Suspect concomitant ATN if sCr declines with volume expansion, diuresis, or relief of obstruction but remains a few points above baseline
  • When to consult Nephrology

    • Urgent indication for dialysis (see “Renal Replacement Therapy”)
    • Abrupt anuria
    • Cr worsening or urine output inadequate w/o clear cause
    • Need for kidney biopsy  

Additional Information

  • Rhabdomyolysis: UA positive for blood but no RBCs on microscopy

    • Toxic damage due to myoglobin
    • Serologic markers of muscle injury: elevated CK, AST>AST with normal ALK Phos 
    • Fluids adjusted to urine output goal of 200-300 mL/hr until CK declines
      • Consider isotonic bicarb for initial 1-2L of IVF urine alkalinization to reduce precipitation
    • Avoid calcium repletion for hypocalcemia unless symptomatic 
  • Post-obstructive diuresis 

    • Necessary process to clear accumulated uremic toxins
    • Replace ~50% of urine output to prevent pre-renal azotemia
    • Monitor calcium, phosphorus, and magnesium in severe post-obstructive diuresis

Contrast Induced AKI (CI-AKI)

Trey Richardson


  • When someone develops an AKI do your due diligence and evaluate for the usual causes of AKI, regardless of when they were given contrast

  • Mechanism of injury: direct toxic effect leading to tubular necrosis and arteriolar vasoconstriction leading to medullary ischemia

KDIGO Criteria for CI-AKI:

  • sCr increase by 0.5mg/dl or 25% increase in sCr from baseline 48 H after radiologic procedure where intravenous contrast was administered

Who is at risk for CI-AKI?

  • Normal kidney function: incidence of CI-AKI is 1-3%

  • Pre-existing CKD: Incidence of CI-AKI may be as high as 20% in patients with CKD 4-5

  • Other risk factors include: diabetes, heart failure, and advanced age

  • No real sCr or eGFR threshold below which iodinated contrast is contraindicated, especially in patients for whom imaging will alter management (e.g. acute stroke, PE, STEMI)

Risk reduction strategies

  • Volume expansion with isotonic crystalloid (PRESERVE Trial) in patients with AKI or eGFR \<30 ml/min/1.73m^2 who are clinically hypo or euvolemic

    • 1cc/kg/hr for 6-12 hours before/during and 6-12 hours after the procedure in patients at high risk for CI-AKI. This rate can be decreased based on the risk for hypervolemia
  • If the patient is volume overloaded, they probably should not receive volume expansion prior to a contrasted study

  • Never delay a necessary procedure out of concern for worsening renal function. If in doubt, talk to nephrology

Iodinated contrast in CKD-5/ESRD patients

  • Iodinated contrast does not need to be dialyzed immediately

  • Avoid giving if you are trying to preserve residual kidney function in ESRD on PD

Gadolinium contrast for MRI

  • Contraindicated in any AKI or if GFR \<30 in CKD given risk of nephrogenic systemic fibrosis.