Causes of Acute Kidney Injury

and Christopher Isles²

(1)

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK

(2)

Dumfries and Galloway Royal Infirmary, Dumfries, UK

Q1What is meant by the term acute kidney injury?

AKI describes conditions in which the kidney loses function over hours and days rather than months and years (this makes it distinct from chronic kidney disease). AKI is usually but not always associated with oliguria, defined as urine volume less than 0.5 ml/kg/h (approximately 30 ml/h). Consensus definitions proposed by the Acute Dialysis Quality Initiative (ADQI) and the Acute Kidney Injury Network (AKIN) have been merged to produce a new definition and staging system as shown in the box below:

Box 10.1 Definitions of AKI

Stage	Serum creatinine criteria	Urine output criteria
1	Increase ≥26 umol/l or increase 1.5–1.9× from baseline	<0.5 ml/kg/h for >6 consecutive hours
2	Increase 2–2.9× from baseline	>12 h
3	Increase ≥3× or increase ≥354 umol/l or RRT irrespective of stage	<0.3 ml/kg/h for >24 h or anuria for >12 h

The baseline creatinine is the lowest value within 3 months of the episode of AKI. If a baseline is not available, and AKI is suspected, then repeat the creatinine in 24 h. If there is no baseline within 3 months and the patient recovers then you can use the lowest creatinine during recovery to stage the severity of AKI retrospectively

Q2 Give a clinical approach to the diagnosis of unexplained renal failure.

There are numerous ways of doing this. The ‘pre-renal, renal, post-renal’ approach is a good place to start but still requires a way of remembering what are the pre-renal, renal and post-renal causes (Fig. 10.1).

Fig. 10.1

Causes of acute kidney injury

The lists given in standard textbooks are usually long and are sometimes unhelpful in that they do not differentiate causes of acute kidney injury that are extremely common from those that are vanishingly rare. A practical way of approaching the diagnosis of acute kidney injury is to consider the following five questions:

Box 10.2 The Five Clinical Questions of AKI

Q1 Is it acute, acute on chronic or chronic presenting acutely?
Q2 Are there risk factors for acute tubular necrosis?
Q3 Is there evidence of obstruction?
Q4 Is there renal inflammation?
Q5 Are there any pointers to other causes of AKI?

Q3 How can you tell if AKI is acute or acute on chronic?

This question is usually answered by reviewing previous blood results. Most would agree that if a patient has had a serum creatinine greater than 150 μmol/l for over 3 months before presentation with AKI, then this is likely to be acute on chronic kidney disease. In the absence of previous blood results renal ultrasound can assess for chronicity. A renal ultrasound which shows bilateral small kidneys (each less than 9 cm in bipolar diameter) implies CKD.

Q4 What is meant by chronic presenting acutely?

Chronic Kidney Disease Presenting Acutely (CKDPA aka “Crash Landing”) is important to recognise because these patients may require dialysis within a week of first presentation and have little time to prepare for the demanding treatment that lies ahead. We describe a case below:

Case Report

A 17-year-old girl presented to her general practitioner with 4 weeks of progressively worsening nausea and vomiting, superimposed on a few months of general malaise. Initially she vomited twice a day but by the end of the 4 weeks she was vomiting all the time. This was associated with epigastric pain, anorexia and weight loss of approximately 1 stone. Her symptoms did not respond to omeprazole and led to referral for endoscopy. While awaiting her endoscopy, her general practitioner noted that she looked pale and sent off bloods, which revealed haemoglobin, 46 g/l with serum potassium, 8.2 mmol/l, serum bicarbonate, 11 mmol/l, blood urea, 93.3 mmol/l and serum creatinine, 3,737 μmol/l. She had her first dialysis that evening. Renal biopsy showed that the cause of her renal failure was chronic interstitial nephritis. She remained dialysis dependent and subsequently received a live donor transplant from her mother.Reproduced from Wolfe M, et al. Chronic kidney disease presenting acutely: presentation, clinical features and outcome of patients with irreversible chronic kidney disease who require dialysis immediately. Postgrad Med J. 2010;86:405–8, with permission from BMJ Publishing Group Ltd

The clue to the diagnosis is the severity both of the anaemia and the uraemia. The only way the haemoglobin could have fallen this far or the urea to have risen that high without presenting earlier is for the chronic kidney disease to have evolved slowly over a period of months or years.

Q5 What do you understand by the term acute tubular necrosis (ATN)?

ATN is what happens if we fail to restore renal perfusion quickly enough in a patient with pre-renal ARF. A patient with ATN usually becomes dialysis dependent for a period of time until the tubules regenerate. This can take anything from 3 days to 3 months depending on the severity of the insult.

Q6 What are the four main risk factors for acute tubular necrosis?

Essentially these are the pre-renal causes of AKI which together account for the majority of cases of AKI. You can assess the four reversible factors by asking the following questions:

Are they dry?

Are they wet?

Are they infected?

Are they taking a nephrotoxic drug?

Patients with AKI commonly have more than one pre-renal cause for their kidney injury. Sepsis and nephrotoxic drugs are discussed in more detail here, with ‘dry’ (i.e. hypovolaemia of any cause) and ‘wet’ (i.e. cardiac failure and other pathologies associated with ECF overload) being covered in the chapters on fluid management and cardiorenal failure. We recognise that not all nephrotoxins cause pre-renal AKI (e.g. gentamicin) but it is convenient nevertheless to think of them as a group of reversible causes.

Q7 Give ten important nephrotoxins.

Medical students often start answering this question by naming gentamicin. This commonly causes AKI at high serum levels but is not an important cause of AKI in the population because its use is limited to a small group of extremely sick patients in hospital. The top ten frequently encountered nephrotoxic drugs are probably:

Box 10.3 Commonly Encountered Nephrotoxins

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