Acute renal failure (ARF), and Acute kidney injury (AKI)

Go straight to: what do people with ARF die of?

A sudden deterioration of kidney function. ARF and AKI really mean the same thing.  AKI has grades (e.g. RIFLE criteria) for milder degrees. 

Traditionally and usefully divided into (see figure):


Pre-renal ARF and acute tubular necrosis

Pre-renal ARF is associated with reduced renal blood flow caused by hypotension or hypovolaemia. For a variable time this is reversible. Reversible oliguria (<500mls urine/24h) is characterised by low urinary sodium, and high urinary urea and osmolality, though these may be altered by diuretics, and are in any case an imperfect guide. When prolonged, acute tubular necrosis (ATN) may occur. On a renal biopsy, tubules are dilated and cells necrotic (mitotic figures can be seen as recovery occurs), but the physiological state also includes dramatic changes in renal blood flow.

In practice, ATN and pre-renal failure short of ATN are usually associated with other risk factors such as sepsis, or exposure to predisposing or nephrotoxic drugs (notably NSAIDs, ACE inhibitors, diuretics; aminoglycoside antibiotics, vancomycin) or other toxins (e.g. myoglobin in rhabdomyolysis). It is more likely in the presence of pre-existing renal disease and in the elderly, and usually occurs in the context of other severe illnesses. Mortality of over 50% for ATN occurring in hospital is usual, not because of renal failure directly, but mainly because of its association with failure of other organs and with severe sepsis.

Renal artery (or aortic) occlusion is true pre-renal failure, in the absence of signs of shock.  There are usually other signs of vascular occlusion.


Approach to the patient with oliguria

Most of this also applies anyone with new renal failure, whether or not they are oliguric.

  1. Is oliguria real – is output recorded and reliable?   If complete anuria, obstruction (check for bladder) or vascular cause particularly likely.
  2. Assess circulatory state – blood pressure (versus patient’s normal), JVP, perfusion. Lying and standing BP can be informative.
  3. Fluid balance – in and out over last 48h or longer. Extra losses? (vomiting, diarrhoea, fever, drains)
  4. History or evidence suggestive of urinary tract obstruction?
  5. Exposure to nephrotoxic drugs and other toxins (consider muscle lysis – rhabdomyolysis)
  6. Evidence for renal inflammation – urinary red cells, protein, or white cells in the absence of infection.
    Previous samples (and pre-catheterisation samples) often best.
  7. Regardless of cause, optimise circulation (fluid replacement; ?inotropic agents)


Important investigations in ARF


Management of established acute renal failure

  1. Control intake of fluid (daily requirement if euvolaemic = losses + 500mls ‘insensible’ loss if afebrile), sodium, potassium. Learn more about fluid prescribing.
  2. Nutrition: low protein but high calories
  3. Indications for dialysis or other renal replacement therapy:

Dialysis: peritoneal dialysis is now rarely used in ARF. Haemodialysis may need to be given frequently (e.g. daily) in order to prevent large fluid swings and give enough biochemical clearance. Slow continuous treatments (haemodialysis or haemofiltration) are often used in an intensive care or high dependency setting.  Prescribing dialysis in ARF from the EdRen Handbook

 

What do people with ARF die of?

Without dialysis (or other type of RRT), the causes of death in acute renal failure are

  1. Hyperkalaemis (see Hyperkalaemia page)
  2. Pulmonary oedema
  3. Infection - renal failure is an immunosuppressed state, and intravascular catheters, oedema etc put patients at great risk of bacterial infections
  4. Uraemia - the malnutrition, coma, fits etc you read about in textbooks

Note that uraemia is fourth!  Dialysis is a great treatment for 1 and 2 and prevents 4.  Careful conservative management can prevent 1-3 and delay 4, allowing recovery to occur. 

 


Further info:

 

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