Understanding acute kidney injury

Understanding Acute Kidney Injury

A young man was presented to ED with confusion and a profound metabolica acidosis after ingesting around 400ml of ethylene glycol-based anti-freeze. His GCS deteriorated and he required intubation. He was commenced on iv ethanol and commenced on haemodiafiltration. He initially had a polyuric acute kidney injury, but became anuric after 24 hours. His acidosis normalised within 36 hours, and his creatinine peaked at 549. His urine output improved after a week of oligoanuria and his creatinine reached a baseline of around 150.

What are the diagnostic criteria for acute kidney injury?

Prad Shanmugasundaram

It has become increasingly clear that patients suffering a new deterioration in renal function from their baseline suffer from deficits in their quality of care and have poorer outcomes than patients without acute renal impairment. An NCEPOD report in 2009 reviewed the care of patients who died in hospital with a primary diagnosis of acute kidney injury (AKI). They found that AKI was poorly assessed and recognised, and that its complications were both avoidable and managed badly in around a fifth of patients. Around 12% of patients received RRT. Of the remaining patients, the NCEPOD advisors felt that around 8% of them should have received RRT. Only 50% of AKI care was considered good by the advisors to NCEPOD (1).

Acute kidney injury is the accepted term that has come to encompass and replace acute renal failure (ARF). Astonishingly, there was never an accepted consensus definition of ARF and the term was used variably for reduced or absent urine output, rising or elevated serum urea or creatinine levels, or deteriorating eGFR. This led to confusion and variation in virtually all aspects of ARF including incidence and outcome investigations.

In 2004 the Acute Dialysis Quality Initiative group proposed the RIFLE criteria that aimed to address some of these shortcomings (2). These criteria of three highly sensitive severity classes of Risk, Injury, and Failure defined on the basis of the severity of changes in serum creatinine, GFR or urine output, and two highly specific outcome classes, Loss and End Stage Renal Disease (ESRD) defined by the duration of the loss of kidney function. Validation studies of the RIFLE criteria show that increasing severity of renal impairment defined by RIFLE stage leads to increased risk of death. A study by Uchino et al. investigated a hospital cohort of over 20000 patients over a 3 year period to examine the predictive ability of the RIFLE classification (3). They found a significant increase in hospital mortality with increasing RIFLE class, with RIFLE F patients having ten times the hospital mortality rate of those with RIFLE-I, who themselves had twice the mortality of those with RIFLE-R classification renal impairment. RIFLE-R patients had mortality in excess of three times higher than patient without renal impairment.

In 2007, an international multidisciplinary collaborative group was formed to improve outcomes in their newly proposed term: acute kidney injury (4). They recognised that while highly sensitive, the RIFLE criteria may omit small changes in creatinine that have been shown to affect outcome. The AKIN group modified the RIFLE criteria and proposed a system to stage AKI. They proposed a 3 stage system mapping closely to the R-I-F categories from the RIFLE system.

Most recently in 2012, the Kidney Disease: Improving Global Outcomes (KDIGO) group aimed to harmonise these systems by defining AKI as any of: increase in serum creatinine by 26.5 micromol/l within 48 hours; increase in serum creatinine to >1.5 times baseline within the preceding 7 days; or urine volume <0.5ml/kg/hour for 6 consecutive hours. They also advocated the AKIN staging system for severity. These recommendations are largely expected to be adopted by the worldwide renal medical community (5).

The KDIGO AKI guidelines also included a number of recommendations involving patients requiring RRT. The most significant changes that may result from their recommendations are that they advocate using regional citrate anticoagulation as a first-line option for continuous RRT over heparin-based anticoagulation; they prioritise sites for vascular access for RRT (right internal jugular> femoral veins> left internal jugular> dominant subclavian vein> non-dominant subclavian vein); and they recommend using bicarbonate-based buffering dialysate and replacement fluid rather than lactate. Many of these recommendations were echoed by the Acute Kidney Injury guidelines released by The Renal Association (6).

All the recent guidelines have reinforced the lack of evidence for diuretics and dopamine, and have reinforced that crystalloids appear to be ‘winning’ the long-standing rivalry with colloids. One treatment that is showing promise is fenoldopam, a pure dopamine type-1 receptor agonist which avoids the systemic alpha and beta adrenergic effects of dopamine. Several small studies have suggested a protective effect against developing AKI including sepsis (7,8). There are no large scale randomised controlled trials showing benefit yet, but a meta-analysis of the beneficial effects of fenoldopam in critically ill patients concluded that fenoldopam reduces mortality and the need for RRT in these patients (9). The guidelines have stopped short of recommending its use until further evidence comes to light.


1. NCEPOD Report. Acute Kidney Injury – Adding Insult to Injury. 2009. http://www.ncepod.org.uk/2009aki.htm
2. Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care 2004; 8: R204–212.
3. Uchino S, Bellomo R, Goldsmith D, et al. An assessment of the RIFLE criteria for acute renal failure in hospitalized patients. Crit Care Med 2006; 34: 1913–1917.
4. Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007; 11: R31.
5. Kidney Disease: Improving Global Outcomes. Clinical practice guideline on acute kidney injury. 2011. http://www.kdigo.org
6. Lewington A, Kanagasundaram S. Acute Kidney Injury Clinical Practice Guidelines. The Renal Association 2011. http://www.renal.org/clinical/guidelinessection/acutekidneyinjury.aspx
7. Morelli A, Ricci Z, Bellomo R, et al. Prophylactic fenoldopam for renal protection in sepsis: a randomized, double-blind, placebo-controlled pilot trial. Crit Care Med 2005; 33: 2451–2456.
8. Tumlin JA, Finkel KW, Murray PT, et al. Fenoldopam mesylate in early acute tubular necrosis: a randomized, double-blind, placebo-controlled clinical trial. Am J Kidney Dis 2005; 46: 26–34.
9. Landoni G, Biondi-Zoccai GGL, Tumlin JA et al. Beneficial impact of fenoldapam in critically ill patients with or at risk for acute renal failure: a meta-analysis of randomised clinical trials. Am J Kidney Dis 2007; 49 (1): 56-68

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