Acute Kidney Injury (AKI)


  • Increase in serum creatinine by 26.5 micromol/l over 48h; or
  • Increase in serum creatinine >1.5 times baseline within 7 days
  • Urine volume <0.5 ml/kg/h for 6 hours


Risk Factors

  • CKD (eGFR less than 60 ml/min/1.73m2, CKD stage 3-5)
  • Previous AKI
  • Sepsis
  • Heart failure
  • Liver disease
  • Diabetes
  • Hypovolaemia
  • Drugs: NSAIDs, aminoglycosides (gentamicin), ACE inhibitors, ARBs, diuretics. (Metformin is not nephrotoxic but is exclusively excreted via the kidneys; administration in AKI causes lactic acidosis)
  • Iodinated contrast within the past week
  • Pathologies causing renal out-flow obstruction
  • >65 years



  • Pre
    • Dehydration/hypovolemia
  • Intra
    • Glomerular disease: glomerulonephritis, thrombosis, haemolytic uraemic syndrome.
    • Tubular injury: ATN, nephrotoxins (aminoglycosides, radiocontrast media, myoglobin, cisplatin, heavy metals, light chains in myeloma kidney).
    • Acute interstitial nephritis: NSAIDs, Paracetamol, infection or autoimmune disease
    • Vascular disease: vasculitis (usually associated with ANCA)
    • Eclampsia
  • Post
    • Intrinsic or extrinsic obstruction of urinary out-flow tract



  • Urine dipstick – refer to nephrology for investigation of glomular nephritis if positive for protein and blood
  • USS – within 6h when pyonephritis expected; within 24h when no cause evident/obstruction possible
  • Immunology
    • Free kappa/lambda light chain assay, serum protein electrophoresis, Bence Jones’ proteinuria: immune paresis, monoclonal band on serum protein electrophoresis, and Bence Jones’ proteinuria suggest myeloma.
    • ANA: positive in systemic lupus erythematosus (SLE) and other autoimmune disorders, anti-double-stranded DNA antibodies more specific for SLE
    • ANCA: c-ANCA and anti-PR3 associated with Wegener’s granulomatosis; p-ANCA and anti-MPO associated with microscopic polyangiitis
    • Complement concentrations: low in SLE, acute post-infectious glomerulonephritis, cryoglobulinaemia
    • anti-GBM antibodies: Goodpasture’s syndrome.
    • Antistreptolysin O and anti-DNase B titres: high after streptococcal infection.
  • CK (rhabdomyalis)
  • New biomarkers: cystatin C, NGAL, KIM-1, IL-18. None currently in routine use



guideline NICE Acute Kidney Injury, CG 196, 2013

guideline Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2: 1–138




ICU-Acquired Weakness


Clinically detected weakness in critically ill patients in whom there is no plausible aetiology other than critical illness. Incidence is about 40-50% in patients who develop MOF, severe sepsis and require prolonged ventilation. Hyperglycaemia is an additional risk factor. Steroids, aminoglycosides, NMBD… are all suggested as potential risk factors.



  • Critical Illness Polyneuropathy (CIP)
  • Critical Illness Myopathy (CIM) – this is further classified histologically:
    • Cachectic Myopathy
    • Thick Filament Myopathy
    • Necrotizing Myopathy
  • Critical Illness Neuromyopathy (CINM)



All of:

  • Weakness following critical illness
  • Generalized, symmetrical, flaccid weakness, with cranial nerve spearing
  • Causes not related to underlying critical illness

And either:

  • Mean muscle power <4/5 in all testable muscle groups, on >2 occasions separated by >24 h
  • Ventilator dependence



  • Hypothesised to be a “peripheral neuromuscular failure” due to the inflammatory cytokines, and poor macro & microvascular perfusion implicated in other organ failures.
  • Atrophy and denervation due to lack of use



paperFrom the NEJM Critical Care review series: ICU-Acquired Weakness and Recovery from Critical Illness. N Engl J Med 2014; 370:1626-1635

paperIntensive care unit-acquired weakness, Appletin & Kinsella, CEACCP 2012