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

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

• CCC — RIFLE Criteria and AKIN Classification

Journal articles and Textbooks

• KDIGO Clinical Practice Guidelines for Acute Kidney Injury. Kidney International Supplements 2012;2:1
• Kellum, J. A., et al (2010) “Continuous Renal Replacement Therapy” Oxford University Press, pages 3-9 [Google Books Preview]