This assignment focuses on the topic of Acute Kidney Injury (AKI). It aims to identify a robust definition of AKI, and will open a discussion around epidemiological factors, aetiology, clinical signs/symptoms, investigations and pharmacological interventions. It will also outline psychosocial outcomes of the disorder.
Acute Kidney Injury refers to the spectrum of disorders implicated by impaired renal functions. It is defined fundamentally as an immediate or abrupt decline in kidney function, which results in the retention of urea and nitrogenous waste products (Azotaemia), irregular fluid volume and a decrease in electrolyte control (Singbartl and Joannidis, 2015). In addition, National Institute for Health and Care Excellence (NICE) guidance suggests that a diagnostic of acute kidney injury is assessed by measuring creatinine levels with or without urine output (Nice.org.uk, 2013).
In recent years a definition of Acute Renal Failure (ARF) has progressed through several classifications whereby the term AKI surfaced. With advances in technology and greater life expectancy, guidelines were redefined and used by research experts in nephrology such as; Risk, Injury, Failure, Loss of function and End-stage kidney disease (RIFLE) in 2004, Acute Kidney Injury Network (AKIN) in 2007 to Kidney Disease: Improving Global Outcomes (KDIGO) in 2012. These tools were used collaboratively in an attempt to have a standardised approach to managing AKI and predicting mortality rates in patients (Basile, Anderson and Sutton, 2012).
KDIGO introduced AKI staging system which identifies levels of severity (AKI 1-3), i.e stage 1 defining a rise of serum creatinine greater than 26 umol/L or 1.5 to 1.9 times the baseline serum creatinine, stage 2 being two to three fold from the baseline and stage 3 being an increase of 3 fold from baseline (Summary of Recommendation Statements KDIGO, 2012). Not only does the staging system recognise serum creatinine levels, it assesses urine output of less than 0.5ml per kg/body weight/per hour, initially over 6 hours to 12 hours and 24 hours identifying stage of severity. Presentation of oliguria and creatinine or both will determine which stage the patient will be managed for.
Whilst the use of the staging system is fundamental, additional review of patients admitted to hospital is crucial. A report by the National Confidential Enquiry into Patient Outcome and Death (NCEPOD) identified the care of patients who died with a diagnosis of AKI. It states that approximately 50% of patients who received care in a hospital setting were considered as “good”. Furthermore it identifies that post admission, 60% of patients at risk of AKI were predictable and 21% was avoidable. This highlighted inadequate identification of AKI and management of patients thus exposing them to a higher mortality rate (Stewart, 2009). It is now acknowledged that small rises in serum creatinine are associated with higher levels of mortality, providing rationale and recognition of a less severe impairment, early management and prevention of further damage (Lameire et al., 2013).
The prevalence of AKI varies, although common, it is difficult to ascertain an exact incidence rate due to the level of inaccuracies of definitions and classifications (Anathhanam and Lewington, 2013). However, it is recognised that these NHS resources and services cost around £434 million and £620 million per annum, which is more than associated cost of providing services in breast, lung or skin cancer combined (Nice.org.uk, 2013). In addition NICE approximates that 13% – 18% of patients admitted to hospital in developed countries have a diagnosis of AKI with the majority of elderly impacted (Nice.org.uk, 2013).
The broader term for AKI is multi-factorial, causes are identified into three classifications; pre-renal, intrinsic and post-renal. Pre-renal kidney injury is marked as the most prevalent form of kidney injury accounting for approximately 95% of hospital acquired cases (Lameire, Van Biesen and Vanholder, 2005).
The causes of pre-renal injury are highly associated with a decrease in blood flow such as hypovolaemia, haemorrhage, impaired perfusion due to heart failure and decreased vascular volume because of increased vascular capacity in relation to sepsis or anaphylaxis (Prowle et al., 2009). The kidney requires around 25% of cardiac output and a mean arterial pressure of around 70 mmHg to function adequately, therefore requires optimum heart function (Byrne and Murphy, 2008). Whilst the kidneys are volume responsive, some vasoactive mediators play an important role in relation to function. Diagnostic imaging and pharmacological interventions may inhibit perfusion in the kidneys, thus causing intra renal vasoconstriction and ischemic changes (Porth, 2015).
Intrinsic damage is associated with damage to the glomeruli and renal tubules of the kidney. The aetiology of this is that often they cause permanent damage, even with correction therapy may not return to normal function (Thomas, 2013). Intra-renal injury are often associated with patients who have major surgery, hypovolaemia, burns, sepsis, vascular inflammation (vasculitis) and glomerulonephritis. As the tubular structures of the nephron are subjected to injury, they are often ischemic or have cellular death, which is known as Acute Tubular Necrosis (Porth, 2015). This sloughing and necrosis of the tubules are not the only factor of intrinsic damage, they are consequences of the combined insult from pre and post causes leading to a reduced glomerular filtration rate (Makris and Spanou, 2016). Post renal refers to impairments or obstruction to flow of urine from both kidneys or a single kidney. The obstructions can occur anywhere from the renal tubules to urethral outlet and usually a result of intrinsic factors such as renal calculi (kidney stones) and transitional cell carcinoma. Extrinsic factors include inflammation or enlargement of surrounding area such as prostatic carcinomas or abdominal aneurysms (Caddeo et al., 2013).
Whilst impaired kidney functions are subject to pre, intrinsic and post renal causes, there are a number of clinical signs and manifestations that a patient may present with in AKI. These signs and symptoms will depend on severity, rate of decline and cause of kidney malfunction. Initially patients with mild or moderate AKI are asymptomatic, however a reduction in urine output may indicate a precursor to impaired kidney function and dehydration (Mehta et al., 2007). In addition it is important to recognise that body weight is considered when assessing urine output as stated in guidelines as 0.5ml per kg/body weight/per hour (KDIGO, 2012). Early symptoms of AKI include oedema, a patient may present with swollen limbs or ankles due to compromised regulatory mechanisms, namely renal obstruction and circulating cellular products such as serum potassium, sodium and water (Malkina, 2017). When elevated levels of urea nitrogen flow in the blood (BUN), urea decomposes into ammonia and stimulates the gastrointestinal mucosa, causing nausea and vomiting (Murphy and Byrne, 2010).
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