Acute Kidney Injury (AKI)

Nephrology Editors: Madison Bandler, Rachel Brown
Reviewed by: Ed Gould, MD and JP Arroyo, MD, PhD
Section Editors: Piera Sosa, Rachel Brown

Background

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

Stages of AKI

  • Based on 2012 KDIGO Guidelines:

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)
  • Note, risk of need for RRT and risk of death increases with increased stage

Framework for AKI

  • Pre-renal/hemodynamic AKI:
    • Volume depletion: GI loss, 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
    • Note, when prerenal AKI is prolonged it can lead to intrinsic ATN
  • Intra-renal: glomerular, tubular, or interstitial diseases
    • 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., staphylococcal infections (especially in diabetics), streptococcal infections, legionella)
    • Glomerulonephritis
    • Other causes:
      • 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
  • 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 o In rare instances, retroperitoneal fibrosis
    • Note, when postrenal AKI is prolonged/untreated it can lead to irreversible intrinsic kidney disease
  • Pre-renal azotemia and acute tubular necrosis comprise the majority of inpatient AKI

Evaluation

  • History (carefully evaluate all medications taken + contrast exposure) and volume assessment (physical exam, CXR, TTE)
  • Labs: CMP, urinalysis, urine 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
  • 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 (PVRs might give you same data)
    • Note, add doppler to evaluate for renal artery stenosis (or if working up resistant hypertension)
  • Urine electrolytes
    • FENa <1% or FEUrea <35% (if on diuretics) suggest pre-renal physiology
      • 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
      • Less specific in patients with CKD
    • 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. If UOsm>SOsm = water retention. Role in AKI in clinical trials still unclear.

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>ALT with normal ALK Phos
    • 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
  • 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
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