Acute kidney injury (AKI), previously termed acute renal failure, describes a reduction in renal function following an insult to the kidneys. In years gone by the kidneys were very much a neglected organ in acute medicine - the recognition of decreasing renal function was often slow and action limited. Around 15% of patients admitted to hospital develop AKI.

Causes of AKI are traditionally divided into prerenal, intrinsic and postrenal causes

Prerenal

One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.

Examples

• Hypovolaemia secondary to diarrhoea/vomiting
• Renal artery stenosis

Intrinsic

The second group of causes relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.

Examples

• Glomerulonephritis
• Acute tubular necrosis (ATN)
• Acute interstitial nephritis (AIN), respectively
• Rhabdomyolysis
• Tumour lysis syndrome

Postrenal

The third group relates to problems after the kidneys. This is where there is an obstruction to the urine coming from the kidneys resulting in things 'backing-up' and affecting the normal renal function. An example could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by benign prostatic hyperplasia.

Examples

• Kidney stone in ureter or bladder
• Benign prostatic hyperplasia
• External compression of the ureter

Who is at an increased risk of AKI?

One of the keys to reducing the incidence of AKI is identifying patient who are at increased risk. NICE support this approach and have published guidelines suggesting which patients are at greater risk.

Risk factors for AKI include:

• Chronic kidney disease
• Other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
• History of acute kidney injury
• Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
• Use of iodinated contrast agents within the past week
• Age 65 years or over

oliguria (urine output less than 0.5 ml/kg/hour)

• Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer

Basic steps

• Final pathway is tubular cell death.
• Renal medulla is a relatively hypoxic environment making it susceptible to renal tubular hypoxia.
• Renovascular autoregulation maintains renal blood flow across a range of arterial pressures.
• Estimates of GFR are the best indices of renal function. Useful clinical estimates can be obtained by considering serum creatinine, age, race, gender and body size. eGFR calculations such as the Cockcroft and Gault equation are less reliable in populations with high GFRs.
• Nephrotoxic stimuli such as aminoglycosides and radiological contrast media induce apoptosis. Myoglobinuria and haemolysis result in necrosis. Overlap exists and proinflammatory cytokines play and important role in potentiating ongoing damage.
• Post-operative renal failure is more likely to occur in patients who are elderly, have peripheral vascular disease, high BMI, have COPD, receive vasopressors, are on nephrotoxic medication or undergo emergency surgery.
• Avoiding hypotension will reduce the risk of renal tubular damage.
• There is no evidence that administration of ACE inhibitors or dopamine reduces the incidence of post-operative renal failure.

Urine analysis

• urine dipstick
  • urinary tract infection: leucocytes +/- nitrites
  • glomerulonephritis: haematuria + leucocytes
  • acute interstitial nephritis: leucocytes by themselves
• microscopy, culture and sensitivity
  • if any evidence of UTI on the urine dipstick
• protein:creatinine ratio if glomerulonephritis is suspected

Bloods

• urea and electrolytes
  • important to detect hyperkalaemia as this may require urgent treatment
• as a minimum a FBC, CRP and bone profile should also be performed
• if the cause is not known further blood tests should be considered including:
  • creatinine kinase
• ANA
• ANCA
• anti-GBM
• complement levels
• immunoglobulin levels
• antistreptolysin O titre
• HIV

Ultrasound

• an ultrasound scan should be performed in new cases of AKI
• if obstructive uropathy or pyelonephritis is suspected this should be performed urgently
  • UK guidelines suggest this should be performed within 24 hours if obstruction is suspected or there is no identifiable cause.

Prerenal uraemia - kidneys hold on to sodium to preserve volume


*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100

**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100

NICE recommends that we can use a variety of different criteria to make an official diagnosis of AKI. They state:


Once diagnosed, AKI can be staged using the KDIGO classification:

The management of AKI is largely supportive. This means patients require careful fluid balance to ensure that the kidneys are properly perfused but not excessively to avoid fluid overload. It is also important to review a patient's medication list to see what treatments may either be exacerbating their renal dysfunction or may be dangerous as a consequence of renal dysfunction. The table below gives some examples of common drugs:


Treatments which are not recommend include the routine use of loop diuretics (to artificially boost urine output) and low-dose dopamine (in an attempt to increase renal perfusion). There is however a role for loop diuretics in patients who experience significant fluid overload.

Specialist input from a nephrologist is required for cases where the cause is not known or where the AKI is severe.

All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist.

Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, acidosis or uraemia.

Whilst most patients with AKI recover their renal function there are many patients who will have long term impaired kidney function due to AKI. As well as long-term morbidity, AKI may also result in acute complications including death. Whilst exact figures are difficult to calculate NICE estimate that inpatient mortality of AKI in the UK might typically be 25-30% or more.