AKI

• An acute kidney injury (AKI) is caused by a rapid deterioration in kidney function - causing a sudden decrease in glomerular filtration rate
• GFR is maintained by sufficient blood flow into the kidneys, functioning nephrons and a clear pathway for outflow of urine from the kidney. If there are alterations to this system, an AKI can occur.
• AKI can have pre-renal, intra-renal and post-renal causes
• Pre-renal causes are the most common causes of AKI and are causes by hypoperfusion of the kidneys:

  • Absolute hypovolaemia - haemorrhage, over-diuresis, vomiting and diarrhoea
  • Sepsis
  • Heart failure
  • Cirrhosis
  • Drug induced- NSAIDs, ACE inhibitors and diuretics
  • Renal artery stenosis
• Intra-renal AKI occurs when there is a structural or functional change at the level of the nephron. This can occur independently or as a transformation of a pre-renal AKI

  • Acute tubular necrosis - most common cause of intrinsic AKI
  • Rhabdomyolysis
  • Glomerulonephritis
  • Acute interstitial nephritis
• Post-renal causes involve obstruction to the outflow of urine away from the kidney - obstructive uropathy:

  • Kidney stones
  • Tumours - bladder and prostate
  • Strictures of the ureters or urethra
  • Benign prostatic hyperplasia
• Acute tubular necrosis refers to damage and necrosis of the epithelial cells of the renal tubules, can occur due to:

  • Ischaemia due to hypoperfusion - dehydration, shock or heart failure
  • Nephrotoxins - gentamicin, radiocontrast agents
• Muddy brown casts on urinalysis confirm acute tubular necrosis. Renal tubular epithelial cells may also be seen.
• NSAIDs can be implicated in multiple causes of renal impairment and can cause pre-renal, intra-renal and post-renal AKI. NSAIDs should not be used in patients at risk of AKI.
• The NICE guidelines criteria for diagnosing an acute kidney injury are:

  • Rise in creatinine of more than 25 micromol/L in 48 hours
  • Rise in creatinine of more than 50% in 7 days
  • Urine output of less than 0.5 ml/kg/hour over at least 6 hours
• Risk factors for AKI:

  • Older age - above 65
  • Sepsis
  • CKD
  • Heart failure
  • Diabetes
  • Liver disease
  • Cognitive impairment - leading to reduced fluid intake
  • Medications - NSAIDs, gentamicin, diuretics, metformin and ACE inhibitors
  • Radiocontrast agents
• Symptoms of AKI:

  • Often asymptomatic - especially in the early stages
  • Nausea and vomiting
  • Suspected dehydration - dry mucous membranes, reduced skin turgor
  • Reduced urine output (oliguria) or changes to urine colour
  • Confusion, fatigue and drowsiness
• General Investigations for AKI:

  • Observations - tachycardia and hypotension in hypovolaemia
  • Check for signs of fluid overload - oedema / raised JVP
  • Signs of dehydration
  • Post void volume - obstruction
  • Renal tract USS if obstruction suspected
  • ECG - AKI can cause hyperkalaemia
  • Urine output monitoring
• Laboratory investigations for AKI:

  • U&Es - creatinine, blood urea nitrogen (BUN), calcium, phosphate, potassium and sodiun
  • FBC
  • LFTs for serum albumin
  • VBG for bicarbonate - will be low in AKI
  • CRP
  • Urinalysis if dip positive for blood, protein, leukocytes or nitrates
  • Serum creatine kinase if rhabdomyolysis is suspected
• Treating an acute kidney injury involves reversing the underlying cause and supportive management, for example:

  • IV fluids for dehydration and hypovolaemia
  • Withhold medications that may worsen the condition (e.g., NSAIDs and ACE inhibitors)
  • Withhold/adjust medications that may accumulate with reduced renal function (e.g., metformin and opiates)
  • Relieve the obstruction in a post-renal AKI (e.g., insert a catheter in a patient with prostatic hyperplasia)
  • Dialysis may be required in severe cases
• Calling ACE inhibitors nephrotoxic is incorrect. ACE inhibitors should be stopped in an acute kidney injury, as they reduce the filtration pressure. However, ACE inhibitors have a protective effect on the kidneys long-term. They are offered to certain patients with hypertension, diabetes and chronic kidney disease to protect the kidneys from further damage.
• Complications of AKI:

  • Fluid overload, heart failure and pulmonary oedema
  • Hyperkalaemia
  • Metabolic acidosis
  • Uraemia (high urea), which can lead to encephalopathy and pericarditis
• The kidney disease improving global outcomes (KDIGO) classification tool confirms AKI. There are additional criteria for staging AKI.
• Relevant imaging investigations include:

  • Post-void residual volume (PVR): can be assessed rapidly using a bedside bladder scanner
  • Ultrasound of the kidneys, ureters and bladder (KUB): assess kidney size, hydronephrosis, postrenal obstruction, renal lesions
  • CT non-contrast: radiopaque and non-radiopaque calculi, ureteric obstruction
  • CT urogram: investigate for urinary tract bleeding
  • CT triphasic kidneys: dedicated cross-sectional imaging for renal lesions (often used to clarify masses seen on ultrasound)
• Acute interstitial nephritis is a cause of intra-renal AKI:

  • Most often eosinophilic nephritis
  • Drug induced e.g. NSAIDs, penicillin
  • Infection induced e.g. TB, legionella
  • Immune mediated e.g. sarcoidosis, SLE or IgG-related disease
• A renal biopsy can be considered for suspected intra-renal AKI or suspected rapidly progressive glomerulonephritis (RPGN). 
• Renal replacement therapy (RRT) is indicated in more severe cases of AKI:

  • Metabolic acidosis pH < 7.15 or worsening acidaemia
  • Refractory electrolyte abnormalities (hyperkalaemia >6.5mmol)
  • Presence of dialysable toxins (toxic alcohols, aspirin, lithium)
  • Refractory fluid overload (diuretic resistant fluid overload in setting of AKI)
  • End-organ uraemic complications (e.g. pericarditis, encephalopathy, uraemic bleeding)
• Complications:

  • Fluid overload (leg oedema, pulmonary oedema, pleural effusions)
  • Electrolyte derangement (hyperphosphatemia, hyperkalaemia)
  • Acid-base disorder (metabolic acidosis)
  • End-organ complications of uraemia
  • Chronic kidney disease (CKD)
  • End-stage renal disease (ESRD)
  • Death