QuestionSBA
QuestionChoice
Whilst a urine dip might be helpful in diagnosis if obstruction is not the cause, he has reported he has not passed urine for over 12 hours therefore obtaining a urine sample may not be possible without inserting a catheter
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Urine dip
QuestionChoice
This is not an unreasonable investigation, as patients with metastatic disease may present with cauda equina, however the bladder scan is not suggestive of urinary retention at a spinal level and therefore less likely than external compression of a ureter for example
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d
Magnetic resonance imaging (MRI) of the spine
QuestionChoice
Whilst a CT of his abdomen and pelvis would be useful in aiding diagnosis, at the moment his renal function is poor and contrast is best avoided
32564
b
Computerised tomography (CT) of abdomen and pelvis with contrast
QuestionChoice
A FAST scan is used to detect free fluid in the abdomen in a trauma situation and therefore is not indicated in this case
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e
Focussed abdominal scanning in trauma (FAST) scanning
QuestionChoice
This patient has a significant acute kidney injury, is anuric, and has a known intraabdominal malignancy. It is important to rule out a urological obstruction as cause for his presentation. The bladder scan does not show retention, however there may be an obstruction at the ureteric level
32563
a
Ultrasound renal tract
QuestionComment
What are the chances of both ureters being obstructed at the same time?
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Monoclonal Supine
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# Summary

Acute kidney injury (AKI) refers to a sudden deterioration in kidney function which may lead to oliguria, electrolyte imbalance, and accumulation of urea and other waste products. It is characterised by increased serum creatinine levels and reduced urine output. Causes are typically categorised as pre-renal, renal and post-renal, with most cases being pre-renal. Initial investigations include a urine dip, U&Es and a bladder scan. If there is no obvious cause, common next steps involve an ultrasound of the kidneys, ureters and bladder to look for post-renal causes (i.e. obstruction) and bloods to look for renal causes. Management involves treating the underlying cause as well as addressing complications such as hyperkalaemia.

# Definition

An acute kidney injury is characterised by a decline in renal function that happens rapidly (over hours to days). It is diagnosed based on the Kidney Disease: Improving Global Outcomes (KDIGO) criteria as below:

- Increase in serum creatinine by >26.5 mmol/l within 48 h, or
- Increase in serum creatinine > 1.5x the baseline within the last 7 days, or
- Urine output < 0.5 ml/kg/h for 6 hours

Unlike chronic kidney disease (CKD), AKI is typically reversible, at least in part. 

# Epidemiology

AKI is common, affecting approximately 20% of patients admitted to hospital and up to 50% of critically unwell patients in intensive care.

It is a marker of severe illness, with a 90-day mortality rate of approximately 25%. 

Patients at increased risk of AKI include:

- Patients with CKD
- Elderly patients
- Previous AKI 
- Malignancy
- Medical conditions increasing risk of urinary obstruction (e.g. benign prostatic hyperplasia)
- Cognitive impairment and disability (may be reliant on others for fluid intake) 
- Recent use of medications such as NSAIDs or ACE inhibitors
- Recent administration of iodine-containing contrast media

# Aetiology

Causes AKI are categorised into pre-renal, renal, and post-renal causes:

**Pre-renal causes** are the most common, and occur due to decreased renal perfusion e.g. due to:

- Hypovolaemia (e.g. dehydration, haemorrhage, gastrointestinal losses, burns)
- Renovascular disease (e.g. renal artery stenosis)
- Medications reducing blood pressure or renal blood flow (e.g. NSAIDs, ACE inhibitors, ARBs, diuretics)
- Hypotension due to reduced cardiac output (e.g. heart failure, sepsis)

**Renal causes** occur due to structural damage to the kidneys, which may affect:

- The glomeruli (e.g. acute glomerulonephritis, nephrotic syndrome)
- The tubules (e.g. acute tubular necrosis due to ischaemia or toxins, rhabdomyolysis)
- The interstitium (e.g. acute interstitial nephritis secondary to drugs)
- The renal vessels (e.g. renal vein thrombosis, vasculitis)


**Post-renal causes** involve obstructed to urinary flow anywhere along the urinary tract, which may be:

- Luminal (e.g. ureteric stones or a blocked catheter) 
- Intramural (e.g. urethral or ureteric strictures, ureteric carcinomas) 
- Due to external compression (e.g. an abdominal or pelvic tumour, benign prostatic hyperplasia)

# Classification

AKIs are staged according to the KDIGO criteria as follows:

**Stage 1 - any of:**

- Creatinine rise of 26 micromol/L or more within 48 hours
- Creatinine rise to 1.5-1.99x baseline within 7 days
- Urine output < 0.5 mL/kg/hour for more than 6 hours

**Stage 2 - any of:**

- Creatinine rise to 2-2.99x baseline within 7 days 
- Urine output < than 0.5 mL/kg/hour for more than 12 hours

**Stage 3 - any of:** 

- Creatinine rise to 3x baseline or higher within 7 days
- Creatinine rise to 354 micromol/L or more with either
- Acute rise of 26 micromol/L or more within 48 hours or
- 50% or more rise within 7 days 
- Urine output < than 0.3 mL/kg/hour for 24 hours
- Anuria for 12 hours

# Signs and Symptoms

An AKI may be asymptomatic and be detected on blood tests only, or may be diagnosed due to a fall in urine output.

Symptoms may be seen especially in severe cases where uraemia occurs, and include:

- Nausea and vomiting 
- Fatigue
- Confusion
- Anorexia
- Pruritus 

On examination, look for:

- Hypertension (a complication of AKI)
- Bladder distension due to urinary retention
- Hypotension and dehydration (in many pre-renal causes)
- Signs of fluid overload (e.g. raised jugular venous pressure, pulmonary and peripheral oedema) as a complication of AKI
- Signs related to the underlying cause (e.g., fevers in sepsis, rashes in vasculitis)
- Pericardial rub (in uraemic pericarditis)

# Investigations

**Bedside tests:**

- **Urinalysis** - urine dip may show blood and protein in glomerular disease, increased white blood cells may suggest infection or interstitial nephritis
- **ECG** to screen for complications of hyperkalaemia
- **Blood gas** to look for acidosis as a complication of AKI, allows rapid potassium measurement

**Blood tests:**

- **U&Es** to get creatinine for diagnosis (compare to baseline if available) and check for hyperkalaemia
- **Full blood count** may show anaemia in vasculitis or raised white cells in infection
- **LFTs** may be deranged in severe hypotension causing ischaemic hepatitis 
- **Clotting** as a baseline in case a renal biopsy is later required (rare)
- **Bone profile** to screen for hypercalcaemia (seen in myeloma which can cause renal AKI)
- **Creatinine kinase** to look for rhabdomyolysis
- **CRP** may be raised in infection or vasculitis

**Imaging:**

- **Bladder scan** if urinary retention is suspected
- **Ultrasound KUB (kidneys, ureters and bladder)** if a post-renal cause is suspected, may show hydronephrosis. The next line of imaging would be a **CT KUB** as this is a more sensitive modality.

If initial investigations do not reveal a cause, bloods for an acute **renal screen** may be done, including:

- ANA
- Double-stranded DNA
- Anti-nuclear cytoplasmic antibodies
- Anti-GBM antibodies
- Erythrocyte sedimentation rate
- Serum immunoglobulins
- Serum electrophoresis
- Serum free light chains
- Complement levels (C3 and C4)
- HIV screening
- Hepatitis B and C serology

If the diagnosis is still unclear and a renal cause is suspected, a **renal biopsy** may be indicated.

# Management

- The key to AKI management is identification and treatment of the underlying cause
- The **most common cause of AKI is dehydration,** and so for many patients IV fluid resuscitation will be required 
- Careful assessment of fluid status is crucial though, as in certain cases where the patient is fluid overloaded diuretic treatment rather than fluids may be required
- Fluid balance should be monitored closely with consideration of catheterisation to monitor urine output 
- A catheter may be the definitive treatment in some cases (e.g. post-renal AKI due to urethral obstruction)
- Screen for complications of AKI (e.g. hyperkalaemia, acidosis, pulmonary oedema) and instigate treatment promptly
- Involve the renal team early in severe or complicated AKIs, where the cause is unclear or where a renal cause is suspected
- Review regular medications and **suspend any nephrotoxic drugs** (e.g. NSAIDs, aminoglycosides, ACE inhibitors, ARBs) and review those that may cause complications in cases of renal impairment (e.g. opiates, metformin)
- Low-risk patients with an uncomplicated stage 1 or 2 AKI may be considered for discharge if there is an identifiable cause that can be managed in the community
- The following should prompt referral for consideration of renal replacement therapy with dialysis or haemofiltration (remembered by the AEIOU mnemonic): 
	- **A**cidosis (severe metabolic acidosis with pH of <7.20)
	- **E**lectrolyte imbalance (resistant hyperkalaemia)
	- **I**ntoxication (AKI secondary to certain drugs or poisons)
	- **O**edema (refractory pulmonary oedema)
	- **U**raemia (uraemic encephalopathy or pericarditis)

# NICE Guidelines

[NICE CKS - Acute Kidney Injury](https://cks.nice.org.uk/topics/acute-kidney-injury/) 

[NICE: Acute kidney injury: prevention, detection and management](https://www.nice.org.uk/guidance/ng148) 

# References

[KDIGO - AKI guideline](https://kdigo.org/guidelines/acute-kidney-injury/) 

[Patient UK - Acute Kidney Injury](https://patient.info/doctor/acute-kidney-injury-pro)
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Quesmed Tutorial: Renal and Electrolytes
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An ultrasound is performed in an anuric patient with a known intra-abdominal malignancy to assess for potential causes of urinary obstruction, such as tumor compression, hydronephrosis, or metastatic involvement of the urinary tract.
An 83 year old male with metastatic colorectal cancer presents to the emergency department with abdominal pain. He reports not passing urine for the last 12 hours. On examination he has moist mucous membranes, his JVP is not raised and his abdomen is diffusely tender without being peritonitic. Bladder scan shows a volume of 20ml.


His admission bloods are as follows:


||||
|--------------|:-------:|---------------|
|Haemoglobin|83  g/L|(M) 130 - 170, (F) 115 - 155|
|White Cell Count|16.5x10<sup>9</sup>/L|3.0 - 10.0|
|Platelets|235x10<sup>9</sup>/L|150 - 400|
|Sodium|134 mmol/L|135 - 145|
|Potassium|5.4 mmol/L|3.5 - 5.3|
|Urea|14 mmol/L|2.5 - 7.8|
|Creatinine|300 µmol/L|60 - 120|
|C Reactive Protein|15 mg/L|< 5|


What is the most important next investigation?
a