Acute Kidney Injury

Reviewed and revised 7 August 2015

OVERVIEW

  • AKI is the entire spectrum of disease (mild -> severe), and can be defined as an abrupt (1 to 7 days) and sustained (more than 24 hours) decrease in kidney function
  • Mortality of critically patients with acute renal failure is high (50%–60%)
  • Renal recovery in survivors may be as high as 90% but as many as 50% of survivors do not return to baseline function

Spectrum as classified according to the RIFLE criteria

  • Risk
  • Injury
  • Failure
  • Loss
  • End-stage
RIFLE criteria

INCIDENCE + PROGRESSION

  • common (35-65%) of ICU admissions
  • 5-20% general hospital admissions
  • mortality significantly increases in patients with AKI

RISK FACTORS

  • sepsis
    – > age (especially > 62 years)
  • race (black)
    – > severity in APACHE III or SOFA score
  • pre-existing chronic kidney disease
  • admission to a non-ICU ward
  • surgical patients
  • cardiovascular disease
  • emergency surgery
  • on MV

CAUSE

Pre-renal

  • volume responsive AKI -> monitor haemodynamics and challenge with volume
  • sepsis-induced AKI
  • hypotension – manage aggressively
  • renovascular disorders

Renal

  • nephrotoxins
    — allopurinol, aminoglycosides, amphotericin, frusemide, NSAIDS, ACE-I, organic solvents, contrast, sulfondamides, thiazides, herbal medicines, heavy metals, pentamidine, paraquat
  • glomerular disease
  • HUS
  • crystal nephropathy
  • tubulointerstitial disease
  • rhabdomyolysis

Post-renal

  • obstruction at any post-renal site (e.g. tumour, clot, papillary necrosis, foreign body, post-surgical, blocked IDC)
  • abdominal compartment syndrome

Can also be categorised as:

  • volume-responsive (50%)
  • sepsis-induced (contributes to 50%)
  • hypotension-related (Rx with fluids and noradrenaline)
  • post-operative (combination of the above, with possible vascular or post-renal factors)

CONSEQUENCES OF AKI

AKI is a systemic disorder!

  • Volume overload – CHF, HTN, decreased Q
  • Metabolic acidosis
    – hyperchloraemia
    — accumulation of organic anions – PO4
    — decreased Alb -> decreased buffering
    — impaired insulin action -> hyperglycaemia
    — catcholamine resistance (bAR downregulation)
    — increased iNOS
  • Electrolytes – increased K+ and low Na+
  • Pulmonary oedema – low albumin -> decreased oncotic pressure + volume overload
  • ALI – neutrophil activation and sequestration in the lung
  • Uraemia
  • Immune – decreased clearance of oxidant stress, tissue oedema, WCC dysfunction – increased risk of infection
  • Haematological – decreased RBC synthesis and increased destruction of RBC -> anaemia, decreased EPO, vWF -> bleeding
  • GI – GI oedema -> compartment syndrome, decreased nutritional absorption, gut ischaemia -> peptic ulcer disease
  • Pharmacology – increased Vd, decreased bioavailablity, albumin, decreased elimination -> under dosing or toxicity

Reasons for Dialysis/Ultrafiltration (UFAKE or AEIOU)

  • Uraemic encephalopathy or uraemic pericarditis
  • Fluid overload
  • Acidosis
  • K+
  • Extras (TNT = tox, Na (hi/low), temperature)
  • Acidosis
  • Electrolyte abnormalities-hyperkalemia
  • Ingestion of toxic substances like toxic alcohols, lithium, potassium, theophyline, barbiturates, valproate
  • Overload fluid (unresponsive to diuretics)
  • Uremia symptoms (pericarditis, encephalopathy)

MANAGEMENT

Specific therapy for AKI

  • rule out obstructive causes and decompress (e.g. IDC, SPC, stent, nephrostomy)
  • optimize preload and renal perfusion using hemodynamic monitoring +/- ino-pressors
  • glomerular disease
    -> confirm diagnosis
    -> specific treatment with immunosuppressive drugs
  • interstitial nephritis (look for white cells, red cells, and white cell casts in urine sediment; eosinophiluria in 2/3)
    -> treat infection (e.g.Legionella, leptospirosis, Streptococcus, CMV)
    -> treat autoimmune disease
    -> discontinue causative agent (e.g. antibiotics, allopurinol diuretics, PPIs, NSAIDs, indinavir, 5-aminosalicylates)
  • abdominal compartment syndrome
    -> measure pressure (likely if IAP > 25 mmHg)
    -> decompress
  • CRRT (intermittent haemodialysis is usually not appropriate in critically ill patients as cannot tolerate haemodynamic instability)

References and Links

LITFL

Journal articles and Textbooks


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

One comment

  1. Great blog with very nice information! We have been looking for this type of information. Thanks a lot for sharing this kind of information. Keep posting!

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