Acute Kidney Injury (AKI)

Nephrology Editors: Julien Tremblay, Brianna Cathey
Reviewed by: JP Arroyo, MD, PhD and Trey Richardson, MD
Section Editors: Alana Jones

Background 

  • Definition: Rise in serum creatinine (sCr) ³ 0.3 mg/dL within 48 hrs or increase ³ 1.5x baseline in 7d 
  • Urine volume <0.5 mL/Kg/H for 6 hours (2012 KDIGO Guidelines):

Stages of AKI

Serum Creatinine

Urine Output
Stage 1 Increase of ≥ 0.3 mg/dl (≥26.5 μmol/L) or 1.5 - 1.9x baseline 0.5 ml/kg/h for > 6 hours
Stage 2 2.0 - 2.9x baseline 0.5 ml/kg/h for > 12 hours
Stage 3 > 3.0x baseline, or increase in serum creatinine to >4.0 mg/dl, or initiation of RRT < 0.3 ml/kg/h for 24 hours or anuria for 12 hours
  • Patients should be staged based on criteria that gives them highest stage (sCr v UOP) 
  • Framework for AKI 
  • Can be broken down into 3 major categories
    • 1. Pre-renal/hemodynamic 
      • Causes: 
        • Volume depletion (GI loss, hemorrhage, burns, critical illness) 
        • Decreased effective circulating volume (cardiorenal, hepatorenal, ACEi/ARB effects) 
        • Afferent arteriole constriction (NSAIDs, iodinated contrast) 
        • Renal vein thrombus 
        • Note, prolonged prerenal AKI can lead to intrinsic ATN 
    • 2. Intra-renal 
      • Comprises glomerular, tubular, or interstitial diseases 
      • Causes: 
        • ATN = Most common form of intrinsic AKI. Can be ischemic or toxic 
        • Toxins: endogenous (e.g. rhabdo) and exogenous (e.g. drugs) 
        • Acute interstitial nephritis (AIN): usually drug induced (i.e. NSAIDs, PPIs, beta lactam abx), though can also be secondary to autoimmune disorders (i.e. SLE, Sjögren’s) Infection associated – e.g. staph (especially in diabetics), strep, legionella 
        • Glomerulonephritis 
      • Other causes (less common): 
        • Crystalline nephropathy: IV acyclovir, tumor lysis, ethylene glycol 
        • Small vessel disease: MAHA, TTP, HUS 
        • Large vessel disease: Aortic dissection (leading to renal infarction), renal artery aneurysm or other renal artery abnormality. Note, these would suggest bilateral renal involvement or patient with only one functioning kidney 
        • Cholesterol emboli: Embolization of cholesterol crystals into the kidneys, which can happen after arterial catheterization. 
    • 3. Post-renal 
      • Causes: 
        • Ureteral: stones, external compression (malignancy, LAD, abscess) 
        • Bladder: neurogenic bladder, malignancy, obstructing blood clot 
        • Urethra: BPH, prostate cancer, prostatitis 
        • retroperitoneal fibrosis (rare)

Initial Evaluation 

  • History (carefully evaluate all medications taken + contrast exposure) and volume assessment (physical exam, CXR, TTE) 
  • Labs: CMP, urinalysis, urine lytes, urine protein/Cr ratio 
  • FENa <1% or FEUrea <35% (if on diuretics) suggest pre-renal physiology 
  • Urine sodium can be used to assess Na avidity: UNa > 40 suggests ATN and UNa < 20 suggests pre-renal. - Urine osmolality can be used as a surrogate marker for Na/volume avidity. UOsm>SOsm = water retention 
  • Rhabdomyolysis: UA positive for blood but no RBCs on microscopy, Serologic markers of muscle injury, elevated CK, AST>ALT with normal ALK Phos 
  • Fluid challenge if high suspicion for pre-renal (0.5-1L). 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 
    • Renal ultrasound: usually to evaluate for post renal or renal vascular etiologies and not warranted unless any of the following: 
      • No obvious cause of AKI is identified 
      • Abrupt oliguria or anuria (think renal vein thrombus or obstruction) 
      • High suspicion for bladder outlet obstruction (get PVR) 
      • Add doppler to evaluate for renal artery stenosis (or if working up resistant HTN)

Management 

For all causes: 

  • Minimize fluctuations in blood pressure 
  • Consider holding anti-hypertensive medications, especially (ACEi/ARB) 
  • Avoid unnecessary nephrotoxins 
  • Dose-adjust medications 

Pre-renal: 

  • True volume depletion: IV volume expansion 
  • Cardiorenal syndrome: decongestion/diuresis 
  • Hepatorenal syndrome: see Hepatology section 

Post-renal: 

  • Relieve obstruction (I/O cath vs foley) 
  • Consider involving urology/IR (e.g. for urostomy, percutaneous nephrostomy) 
  • Monitor for post-obstructive diuresis to clear uremic toxins 
  • Replace ~50% of urine output to prevent pre-renal azotemia 
  • Monitor K, Ca, Phos, Mg in severe post-obstructive diuresis (hyperkalemia can linger) 
    • Intra-renal: 
      Based on etiology 
  • ATN: Supportive care. Monitor for post-ATN diuresis 
  • Rhabdo: 
  • Fluids adjusted to urine output goal of 200-300 mL/hr until CK declines (monitor for volume overload while on fluids) 
  • Consider isotonic bicarb for initial 1-2L of IVF-> urine alkalinization reduces precipitation 
  • Avoid calcium repletion for hypocalcemia unless symptomatic 
  • 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 
  • Infection associated: treat the infection 
  • Monitor for renal recovery: Suspect concomitant ATN if sCr decreases 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 without clear cause 
  • Need for kidney biopsy (i.e., RPGN, nephrotic syndrome)
Last updated on