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Acute renal failure

Educational resources for renal medicine

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

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 and other classifications) for milder degrees. 

Traditionally and usefully divided into (see figure):

  • Prerenal failure (see below) accounts for the majority in hospital
  • Post-renal - i.e. obstruction accounts for a lot.  See obstruction page
  • Renal - intrinsic renal disease disease - glomerulonephritis and interstitial nephritis - accounts for a minority, but needs active treatment to recover renal function. 


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 that you can't see in a biopsy.

Rarely a single cause

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 impairment, 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 just because of renal failure directly, but also 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). But carefully - over-hydrated patients with established AKI have significantly worse outcomes.  


Important investigations in ARF

  • Urinalysis - heavy proteinuria suggests glomerular disease.  Haematuria may suggest kidney inflammation if taken before catheterisation.  Urine infection can complicate the picture. 
  • Ultrasound - immediately diagnoses/excludes obstruction, identifies chronic scarring, missing kidneys etc.
  • Chest X-ray
  • Cultures of blood, urine, any wounds or drains. Infection is very common as cause and complication.
  • In more detail - including additional tests if intrinsic renal disease seems likely - Tests in acute renal failure (edren handbook)


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:
  • Pulmonary oedema (urgent)
  • Severe hyperkalaemia despite medical management
  • Symptomatic, or very poor biochemical results, and unlikely to recover renal function quickly
  • Pericarditis
  • Need for high fluid intake (e.g. for nutrition) during oliguria

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. Hyperkalaemia (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. 

 

After AKI/ ATN

A polyuric phase is typical in simple AKI in previously healthy kidneys, but not universal. It is usually stated that urine at this point has higher electrolyte losses than usual. This may be true, but don't perpetuate polyuria by giving massive sodium loads in 'replacement'. 

Recovery of kidney function after AKI may be incomplete, and if GFR was reduced before the event, further damage may be permanent. Poor outcomes are more likey with increasing severity and duration of the insult, duration of oliguria, patient age.


Further info:


Anaemia <<  |  Textbook  |  >> Angiotensin

 

 
Page last modified 01.12.2016, 20:57 by Administrator. edrep and edren are produced by the Renal Unit at the Royal Infirmary of Edinburgh and Univ. Edinburgh. CAUTIONS and Contact us. Note that the information published here is primarily intended for education, not for clinical care.