Acute Kidney Injury
Definition
Acute kidney injury (AKI) implies an acute decline in kidney function, leading to a rise in serum creatinine and/or a fall in urine output. The Kidney Disease: Improving Global Outcomes (KDIGO) system for the diagnosis and staging of AKI is widely used to define AKI. This is defined by a rise in serum creatinine (SCr) of ≥ 26.5 μmol/L within 48 hours or SCr rises ≥ 1.5 fold from the reference value, which is known or presumed to have occurred within the preceding 7 days, or urine output of < 0.5ml/kg/h for 6 hours.
| Stage | Serum creatinine (SCr) criteria Urine output criteria |
|---|---|
| 1 | 1.5 to 1.9 times baseline or ≥ 26.5 μmol/L increase in ≤ 48h <0.5 mL/kg/h for 6 – 12 hours |
| 2 | 2.0 to 2.9 times baseline <0.5 mL/kg/h for ≥ 12 hours |
| 3 | ≥ 3.0 times baseline or increase in SCr ≥ 26.5 μmol/L to ≥ 354 <0.3 mL/kg/h for ≥ 24 hours
μmol/L or initiation of renal replacement therapy irrespective of or anuria for ≥ 12 hours stage |
Causes of AKI
A basic way of categorising AKI is based on whether the underlying pathology is pre-renal, renal or post-renal. Pre- and post-renal are the most common causes, while renal causes tend to be the most complex.
Pre-Renal
- Absolute decrease in effective blood volume: haemorrhage or volume depletion
- Relative decrease in effective blood volume: cardiac failure, sepsis, decompensated liver disease
- Arterial stenosis or occlusion of renal artery
- Vasomotor: secondary to drugs such as non-steroidal anti-inflammatories, ACE-inhibitors or angiotensin receptor blockers
Intrinsic Renal
- Vasculitic: this may be due to vasculitis, thrombotic microangiopathies or malignant hypertension
- Acute glomerulonephritis
- Acute interstitial nephritis which may be drug associated
- Acute tubular necrosis. This may be ischaemic, secondary to drugs, as well as contrast agents. It may also be secondary to haemoglobinuria, myoglobinuria, myeloma casts or Intratubular crystals Post-Renal
- Bladder outlet obstruction
- Bilateral ureteral obstruction
Investigations in AKI
Most investigations in the first instance are routine, with knowledge of specialist tests required, in particular when intrinsic renal causes of AKI are suspected.
Blood tests
- U&Es, LFTs, CRP, FBC, Clotting Screen, Blood Culture (if Sepsis suspected). CK and bone profile. A viral screen may be required in specific cases.
- Urinalysis:
- Marked haematuria may suggest glomerulonephritis, renal tract malignancy or bleeding disorder. Heavy proteinuria suggests glomerular disease.
- Protein creatinine ratio and albumin creatinine ratio are useful in the presence of proteinuria.
- Casts or dysmorphic red cells suggest glomerulonephritis.
- Leucocytes suggest infection/interstitial nephritis.
- Crystals may be observed in drug-induced or uric acid nephropathy.
Imaging
- A renal tract ultrasound is the first line imaging investigation. It is often used if there is no clear cause of AKI or if pyelonephritis or pyonephrosis or urinary tract obstruction is suspected
Special Tests
- Immunological tests are performed once common causes of AKI have been excluded or if there is a clinical suspicion based on history.
- Kidney Biopsy is also used for definitive diagnosis in some cases.
Management
Immediate management is supportive and guided by the cause.
Key points in the management are
- Regular assessment and optimisation of volume status
- Suspend nephrotoxic drugs and adjust doses of therapeutic drugs according to renal function
- Screen for infections and treat promptly if present
- Ensure adequate nutritional support
- Monitor urinary output and arrange urgent imaging tests if urinary tract obstruction is suspected
- Manage complications such as hyperkalaemia, pulmonary oedema, uraemic complications and acideamia
Refer the following life-threatening complications for emergency renal replacement therapy (RRT):
- Refractory hyperkalaemia (potassium >6.5 mmol/L)
- Refractory metabolic acidosis (pH <7.15)
- Refractory volume overload with or without pulmonary oedema
- End-organ complications of uraemia (e.g. pericarditis, encephalopathy, uraemic bleeding) or other end-organ involvement (e.g. neuropathy, myopathy)
- Severe AKI and poisoning/drug overdose (e.g. secondary to ethylene glycol, lithium).
References
1. Lewington A, Kanagasundaram S. Acute Kidney Injury. BMJ Best Practice. Nov 2022. https://bestpractice.bmj.com/topics/en-gb/3000117. Last accessed 10 December 2022. 2. Steddon S, Ashman N, Chesser A, Cunningham J, 2014. Oxford Handbook of Nephrology and Hypertension, 2ⁿᵈ Edition, Oxford University Press, Oxford.
3. Walker B, College N, Ralston S, Penman I, 2014. Davidson’s Principles and Practice of Medicine, 22ⁿᵈ Edition, Churchill Livingstone Elsevier, Edinburgh.
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