Focus on: RenalPrevention of acute kidney injury in the intensive care unit
Introduction
Acute Kidney Injury (AKI) is a relatively common condition in the intensive care unit (ICU) and is associated with an increased risk of mortality despite the ability to support the functions of the kidneys by means of renal replacement therapy (RRT). Studies looking at mortality in patients in intensive care have demonstrated 60% mortality.1 The recent National Confidential Enquiry into Patient Outcomes and Deaths (NCEPOD) has highlighted the problem of AKI in the UK associated with acute hospital admissions and reported that only 50% of patients received what could be classed as good care. The report claims that a fifth of patients could have been prevented from developing AKI.2 Acute kidney injury is more likely to occur in certain groups which include the elderly and those with pre-existing medical conditions such as hypertension and diabetes. However many of these patients have risks which can be modified to prevent injury to the kidney.
Within the ICU it has been demonstrated that AKI is an independent risk factor for mortality, which contrasts with the previously held view that patients die with rather than because of AKI. This view may be due to the relative ease with which RRT can now be provided, although the NCEPOD report demonstrated that some patients with AKI never received RRT. A clear correlation between the degree of AKI and worse patient outcomes (length of stay and mortality) in ICU has been demonstrated (Table 1).3 It is therefore intuitive that the prevention of AKI should be associated with a reduction in both mortality and morbidity and an improvement in patient care.
Until recently there was no standard definition of what constituted acute kidney injury (AKI), which has limited the general applicability of clinical trials aimed at looking at prevention and treatment of the disease. Recently two very similar definitions and staging systems for AKI have been proposed by the Acute Dialysis Quality Initiative group (ADQI) and the Acute Kidney Injury Network (AKIN).4 The application of these staging systems should provide a better basis for studies which aim to investigate the prevention of AKI in patients. It is important to recognize that the prevention of any insult to the kidney is important particularly in vulnerable patients on the ICU.
Acute kidney injury can be due to pre-renal, intrinsic renal and post-renal causes and methods to minimise kidney damage can be aimed at these three areas. The cause of kidney injury in critical care is often multi-factorial secondary to ischaemia and sepsis causing hypo-perfusion of the kidneys and acute tubular necrosis (ATN). However patients with sepsis can develop AKI without any other obvious cause and animal studies of AKI secondary to sepsis alone have suggested that hypo-perfusion of the kidney does not always occur.5 It is well recognised that histopathological examination of the kidney in patients with AKI does not always demonstrate frank proximal tubule cell necrosis.6 It has been suggested that sublethal cell injury occurs and contributes to proximal tubule cell dysfunction in the absence of obvious cell necrosis.
Section snippets
Prevention of acute kidney injury
The cornerstones of preventing AKI are the maintenance of an adequate circulating volume, an adequate perfusion pressure and the avoidance of further insults to the kidney. It has long been known that if renal blood flow falls below a given level glomerular filtration rate will fall and this can clearly be linked to the development of AKI from the RIFLE criteria. This should be achieved by adequate fluid resuscitation and then the use of inotropes or vasopressors.
The surviving sepsis guidelines7
Nephrotoxic drugs
Acute kidney injury can be caused by a wide range of drugs, the avoidance of these drugs, where clinically appropriate or the alteration of their dosage can reduce the incidence of AKI. Some drugs which are nephrotoxic should be avoided in patients with or at risk of AKI. This is most important for non-steroidal anti-inflammatory drugs which in an unwell hypovoleamic patient play a significant role in causing hypo-perfusion of the kidney. Angiotensin converting enzyme (ACE) inhibitors should
Radio-contrast induced nephropathy
This is a common cause of AKI in hospital,16 its mechanism is unclear but appears to due to a combination of direct renal tubular epithelial cell toxicity and renal medullary ischaemia. A transient decrease in glomerular filtration rate occurs in almost all patients after exposure to contrast media. The degree of injury depends upon the presence of patient risk factors which include; diabetes mellitus, pre-existing renal disease, other drugs being taken, hypovolaemia and factors related solely
Dopamine
Dopamine is a catecholamine that is vasodilatory at low doses, It is believed to exert its action predominantly on dopaminergic receptors at low doses 2.5–5 μg/kg/min commonly referred to as “renal dose” dopamine. At higher doses it has a beta and alpha effect. It was a long held view that dopamine was helpful in the treatment and prevention of AKI. This was based on initial animal studies which experimentally induced AKI which was treated with dopamine. Glomerular filtration rate, renal
Relief of ureteric obstruction
Post renal kidney injury can be caused by obstruction of the urinary tract which can be readily identified on ultrasound and treated, by the insertion of a nephrostomy. Early recognition and treatment of obstruction can result in rapid improvement in AKI and the potential for complete recovery. The NCEPOD AKI study recommended that radiological services should be available 24 h a day in hospitals to provide this important diagnostic and therapeutic intervention.
Conclusion
Acute Kidney Injury is a significant cause of morbidity and mortality in the critically ill patient. The NCEPOD report highlights that this is a condition which in a significant number of people is largely avoidable- by adequate volume expansion, stopping nephrotoxic drugs and early senior medical involvement. As yet there is no treatment which has reliably been shown to prevent or alter the course of AKI, once obstruction has been ruled out. Emphasis must therefore be to improve the early
Conflict of interest statement
The author of the above manuscript has not declared any conflict of interest which may arise from being named as an author on the manuscript.
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Acute renal failure during intensive care - Prevention and treatment
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