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8

Acute Kidney Injury

Mark Bevan

Introduction

Acute kidney injury (AKI) is a term that has recently gained worldwide
acceptance to describe the condition formally known as acute renal failure.
AKI describes a condition ranging from mild but significant impairment
to outright failure of the kidney, and is a serious life-threatening condition
that has been poorly understood, documented and managed (NCEPOD,
2009). AKI is marked by a rapid but potentially reversible decline of kid-
ney function, which results in retention of nitrogen-based waste products
of metabolism such as urea and creatinine and in most cases a reduction
in urine output (Clarkson et al., 2008). It is worth noting that AKI is not
inevitable in acute or critical illness and in many cases is preventable, and
while it is commonly seen in acute care wards it can also be found in the
primary care environment (Hegarty et al., 2005). The ability to estimate
the incidence of AKI has been limited until fairly recently when there have
been attempts to provide a more realistic picture of the problem. Much of
this limitation has been associated with a lack of standard definition which
has caused much variance. For example, Feest et al. (1993) estimated the
Copyright © 2016. Macmillan Education UK. All rights reserved.

incidence to be 51 people per million population (pmp) but they use a cre-
atinine level of 500 μmol/L (normal range 60 to 125 µmol/L: Provan and
Krentz, 2002). In a Scottish study Khan et al. (1997) using a creatinine level
of 300 μmol/L saw the incidence rise to 620 pmp, with the elderly present-
ing a significant risk. Where a lower creatinine level is used as a marker of
AKI, unsurprisingly the incidence increases. Ali et al. (2007) found, using
creatinine levels of ≥ 150 μmol/L for males and ≥ 130 μmol/L for females,
an incidence of 1,811 pmp/year with a high incidence in patients (336
pmp/year) with underlying chronic kidney disease (CKD). An influential
study undertaken by Chertow et al. (2005) examined the effects of AKI on
19,982 patients and found that even a modest elevation of serum creatinine

214

Clarke, David, and Alison Ketchell. Nursing the Acutely Ill Adult, Macmillan Education UK, 2016. ProQuest Ebook Central,
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Created from sguluk on 2021-05-22 12:37:25.
Acute Kidney Injury 215

26.5–35.36 μmol/L led to a 70 per cent increase in risk for death compared
to those who had little or no rise in creatinine. Chertow et al. (2005) also
reported that those who developed AKI tended to be older and had a higher
severity of illness, and that AKI incidence was higher in those with cardio-
vascular disease, infectious diseases, endocrine and nutritional conditions,
respiratory disease, genitourinary disease, injuries and poisoning. What
this study demonstrated was that a small elevation in serum creatinine
increases the risk of death and as such the incidence and impact of AKI has
been significantly underestimated. What can be seen is an inverse relation-
ship between lower levels of elevated creatinine threshold and the higher
incidence of AKI. This means in reality that in previous years there has
been under-reporting; the apparent increase in patients diagnosed with AKI
reflects a change in acceptable diagnostic threshold with greater sensitivity
(Case et al., 2013), rather than an actual increase in AKI.
The study by Chertow et al. heralded the development of a standardised
definition as identified by the Acute Kidney Injury Network (AKIN) and
now endorsed by many bodies such as the Renal Association (UK), National
Institute for Health and Care Excellence (NICE) and the Kidney Disease
Improving Global Outcomes (KDIGO), though not without controversy.
According to NICE (2013) which echoes the AKIN (Mehta et al., 2007) cri-
teria, AKI occurs when there is:

a rise in serum creatinine of 26 micromol/l or greater within 48 hours; a 50%

or greater rise in serum creatinine known or presumed to have occurred within
the past 7 days; a fall in urine output to less than 0.5 ml/kg/hour for more than
6 hours in adults and more than 8 hours in children and young people and a 25%
or greater fall in eGFR in children and young people within the past 7 days (NICE,
2013: 176).

For full AKI staging criteria see Table 8.1.

Standardisation of AKI criteria means that more consistent and mean-
Copyright © 2016. Macmillan Education UK. All rights reserved.

ingful information is forthcoming, providing a more accurate picture. Case

et al. (2013) identified the incidence of AKI in intensive care (ICU) patients
ranging from 20 to 50 per cent. Case et al. (2013) also reported AKI as a
significant risk factor for death associated with a mortality of greater than
50 per cent. In relation to urology patients, Caddeo et al. (2013) reported
587 episodes of AKI in 410 patients which correspond to 6.7 per cent of the
total hospitalised urology patients. They also reported that males were four
times more likely to get AKI and the mean age was 73 years. One-third of
the patients developed AKI during the course of their elective admission.
Mortality rates were identified at 7.8 per cent with the majority of deaths
being in non-elective patients and mortality increased with the severity of

Table 8.1 Criteria for diagnosis of acute kidney injury

AKI stage Serum creatinine criteria Urine output criteria

1 Increase in serum creatinine of 26 Less than 0.5 mL/kg/hour for

µmol/litre or more within 48 hours more than 6 hours
OR
1.5 to 2-fold increase from baseline

2 Increase in serum creatinine to more Less than 0.5 mL/kg/hour for

than 2 to 3-fold from baseline more than 12 hours

3 Increase in serum creatinine to more Less than 0.3 mL/kg/hour

than 3-fold from baseline for 24 hours or anuria for
OR 12 hours
Serum creatinine more than 354 µmol/
litre with an acute increase of at least
44 µmol/litre

Source: Adapted from Mehta et al. (2007)

AKI. A study of ten acute medical units in England and Scotland over two
24-hour periods highlighted the prevalence of community-acquired AKI at
17.7 per cent with sepsis, hypovolaemia, CKD and diabetes mellitus identi-
fied as major risk factors (Finlay et al., 2013). Perhaps a more telling picture
of AKI incidence is provided by Challiner et al. (2014) who performed a
retrospective audit on 745 case records of unselected emergency admissions.
What they found was an AKI incidence of 25.4 per cent, with one-third of
AKI being present on admission and two-thirds developing post admission.
Where baseline kidney function was known at admission AKI was reported
as even higher at 38.1 per cent. Patients with AKI spent more than twice as
long in hospital and severity of AKI correlated with longer stay in hospital,
Copyright © 2016. Macmillan Education UK. All rights reserved.

use of ICU and risk of mortality (Challiner et al., 2014).

What this indicates is that AKI is no longer seen as a rare organ failure
but is very common in hospitals, ranging from 13 to 18 per cent (Challiner
et al., 2014; NICE, 2014). In this case nearly 1 in 5 patients in hospital will
have or have acquired AKI and 1 in 4 emergency admissions will have AKI.
Minor changes in creatinine (≥25 μmol/L) demonstrate a failing kidney and
this is correlated to increase in likelihood of death. Up to 30 per cent of
AKI episodes are avoidable if health care professionals do what is expected
of them (NCEPOD, 2009). Therefore early detection of AKI cannot be
neglected and understanding it and its effective prevention and manage-
ment becomes a priority.

Aim and Learning Outcomes

Aim
The aim of this chapter is to explore the priorities of early accurate assess-
ment and prevention of AKI and nursing and medical management of the
individual presenting with AKI.

Learning Outcomes
At the end of this chapter the reader will be able to:

1. Define AKI and distinguish between the differing manifestations of AKI.

2. Identify and explain the pathophysiological basis of the presenting signs
and symptoms of AKI.
3. Identify and explain the immediate nursing and medical assessment,
specific monitoring and key investigations required to enable an accurate
and timely diagnosis.
4. Explore the evidence basis for immediate priorities of medical and nurs-
ing management, with a particular focus upon pharmacological and
invasive interventions.
5. Appreciate the role of different health professionals in acute assessment
and management of AKI.
6. Recognise the common complications associated with AKI.

The Case Scenario: The Presenting Complaint

Ralph is an 80-year-old man who lives in an elderly care home. He is usually

mobile and self-caring. The staff at the home report that over the past four days
Copyright © 2016. Macmillan Education UK. All rights reserved.

Ralph has become increasingly lethargic and drowsy following treatment for a
chest infection (treated with oral Amoxicillin® 500 mg three times daily for seven
days). He was found on the floor of his room by morning staff; they are unsure
of how long he had been lying there. He has been taking no food and very
little fluids and has had several episodes of vomiting over the past two days. On
examination Ralph is drowsy but responsive to questioning, though a little diso-
rientated. He is also irritable and has a headache. His skin is dry, he has a minor
petechial rash on his upper chest and lower neck and has an unproductive cough.
He complains of anorexia, nausea and has vomited once (100 mL bile-stained
fluid). His bladder is not palpable.

The Case Scenario continued

His vital signs were recorded as:

Pulse: 110 beats/minute sinus tachycardia
Blood pressure (BP): lying = 90/40 mmHg; standing = 80/40 mmHg
Jugular venous pressure (JVP): unrecordable
Oxygen saturations (SpO2): 92 per cent on room air
Temperature: 37.7 °C
Glasgow Coma Scale: 14 (E4, V4, M6)
Weight: 75 kg
Ralph’s past medical history reveals:
Type 2 diabetes mellitus since age 65
Osteoarthritis of left hip
Hypertension since age 60
Urinary hesitancy awaiting urological investigation
Ralph’s current medication is:
Metformin® 2 g divided with meals
Bendrofluazide® 5 mg daily
Ibuprofen 400 mg eight-hourly
A provisional diagnosis of AKI is made.

Consider the following:

1. With reference to the underlying pathophysiology describe what is meant

by AKI.
2. What are the common signs and symptoms associated with AKI?
3. What further investigations need to be carried out to identify a definitive
diagnosis?
Copyright © 2016. Macmillan Education UK. All rights reserved.

Acute Kidney Injury

The medical review of Ralph’s clinical features suggests that he has AKI.
However, unless one knows how to interpret these clinical features it will
not be clear how this conclusion was made. One way in which to make
sense of these clinical features is to start with some indication of the causes
of AKI. Initial assessment should be comprehensive to help determine the
cause of AKI and to ensure appropriate treatment (Stevens et al., 2008), and
should include physical assessment and investigations (Table 8.2).
AKI has many causes but is generally classified into three groups, known as
pre-renal, intrinsic and post-renal. While each group is discrete in its content

Table 8.2 Summary of the assessment of the AKI patient

Assessment Content

History Presenting condition, symptoms, past medical history,

drug history, family history, social history

Clinical examination Vital signs (BP, P, resps)

Level of consciousness
Intravascular volume (skin turgor, mucous membranes, BP
lying and standing, orthostatic pulse change)
JVP
Pulse oximetry
CVP, pulmonary artery catheter
Peripheral capillary return
Weight
Systems: cardiovascular, respiratory, gastrointestinal,
neurological, dermatological eyes, nails, oedema

Urine Output, volume

Appearance and content (cells, crystals, blood, protein,
glucose, pH, ketones, SG)
Culture
Biochemistry: sodium, protein, creatinine clearance

Blood Estimated GFR: creatinine

Biochemistry: sodium, potassium, chloride, bicarbonate,
calcium, phosphate, pH, magnesium, urea
Blood gases
LFTs: CK, amylase, albumin
Cholesterol
Immunology
Culture

ECG LVF, dysrhythmia, MI

Imaging Ultrasound, X-ray, CT scan, MRI, urography, nuclear

medicine, angiography, cystoscopy

it is worth noting that there may be considerable overlap, especially with pre-
renal and intrinsic causes. The causes of AKI are summarised in Figure 8.1.

Pre-renal AKI
The causes of pre-renal AKI can be identified from the term ‘pre-renal’,
occurring before the kidney, whereby AKI is a secondary event, with the pri-
mary event occurring elsewhere in the body. In order to understand how an

Acute Kidney Injury

(AKI)

Pre-Renal AKI Intrinsic AKI Post-Renal AKI

Hypovolaemia
Reduced Rental Perfusion Internal Obstruction
Hypotension External Obstruction

Glomerular injury Tubular Injury Interstitial Injury Vascular Injury

Glomerulonephritis Toxins Toxins Inflammation
Thrombosis Ischaemia Infection Thromboembolism

Figure 8.1 Causes of acute kidney injury

illness or disease elsewhere in the body can affect the kidney some knowl-
edge of renal physiology is required. The kidneys produce urine, which is
made up of water, waste products of metabolism, hormones and drugs. The
production of urine occurs within 1.2 million (approximately) functional
units called nephrons housed within each kidney (Figure 8.2).

Renal artery
(blood flows in) Collecting duct
Glomerulus
Bowman’s capsule
Copyright © 2016. Macmillan Education UK. All rights reserved.

Urine

Renal vein
(blood flows out) Loop of Henle

Figure 8.2 The nephron

The cellular activity of the kidney requires a huge amount of oxygen.

In fact, while the kidney only occupies 1 per cent of total body weight it
uses 10 per cent of the body’s oxygen requirements (Cohen, 1986). The kid-
ney’s high oxygen consumption is proportionate to the amount of sodium
reabsorption, which is a vitally important function for maintaining fluid
balance. However, the cells in the nephrons function at very low oxygen
saturation levels of 1.3–2.9 kPa (normal is 12–15 kPa) and therefore are
very sensitive to change. The kidney requires 1200 mL of blood per minute,
which is one-fifth of cardiac output, in order to produce 1 mL of urine per
minute (Koeppen and Stanton, 2001). Kidney blood flow causes a filtration
pressure within the glomerulus of about 60 mmHg, which in turn produces
a glomerular filtration rate (GFR) of approximately 125 mL/min/1.73 m2
(Koeppen and Stanton, 2001). The key point here is that given all these fac-
tors the kidney is susceptible to alterations in its blood supply and oxygena-
tion and this is where pre-renal causes affect kidney function.
In order to provide 1200 mL/min of blood to the kidney certain factors
need to be in place. These factors are the need for an effective pump (the
heart), an effective circulating volume (the blood), appropriate volume pres-
sure (blood pressure) and a patent vasculature (blood vessels). Any change
to one or more of these factors may cause a reduction of kidney perfusion
significant enough to cause injury. Major causes of pre-renal AKI cause a
rapid loss of GFR and a reduction in urine output (oliguria). Typical causes
of pre-renal AKI are hypotension of any cause, congestive cardiac failure,
diuretic use and haemorrhage (Table 8.3).
Loss of significant volumes of fluid will lead to a low blood pressure (BP)
and reduced kidney perfusion. Volume depletion is by far the major cause of
pre-renal AKI and can be divided into two groups. One is total intravascular
depletion, where intravascular volume is reduced, and the other is effective
volume depletion due to arterial under-filling, where there is adequate vol-
ume (Faubel et al., 2005) (Table 8.4).
Copyright © 2016. Macmillan Education UK. All rights reserved.

Table 8.3 Examples of causes of pre-renal AKI

Cause Examples of common problems

Cardiac Congestive cardiac failure, cardiac surgery, arrhythmia

Volume Burns, bleeding, vomiting, diarrhoea, diuresis

Vascular resistance Shock, antihypertensive treatment, NSAIDs, ACE

inhibitors, hepatorenal syndrome

Vascular patency Renal artery thrombosis, abdominal aortic aneurysm

(AAA), bilateral renal artery stenosis

Table 8.4 Causes of volume depletion

Total intravascular depletion Effective volume depletion

Haemorrhage Reduced cardiac output: congestive cardiac

failure, pulmonary embolism, cardiogenic
shock

Renal fluid loss: diuretics, osmotic Peripheral vasodilation: sepsis, anaphylaxis,

diuresis (such as glycosuria) cirrhosis, antihypertension medication

Gastrointestinal loss: vomiting,

diarrhoea and nasogastric aspiration

Skin fluid loss: burns, sweating

Third space syndrome: pancreatitis,

peritonitis

Source: Adapted from Faubel et al. (2005)

However, additional factors, including commonly used drugs such as

non-steroidal anti-inflammatory drugs (NSAIDs), are known to cause vaso-
constriction of the arterioles of the kidney, thus reducing GFR. Therefore it
is important that a range of possible causes are considered. In Ralph’s case,
his clinical history reveals a number of clues that may point to pre-renal
AKI as a possible cause. The clinical information indicates Ralph is hypoten-
sive, his fluid intake has been low, he has vomited, though the frequency is
not known, and he is taking medication (Bendrofluazide® and ibuprofen),
which all carry the risk of reducing renal perfusion.

Intrinsic AKI
In contrast to pre-renal AKI, where a physiological insult occurs elsewhere
Copyright © 2016. Macmillan Education UK. All rights reserved.

in the body, intrinsic AKI points to the kidney as the source of the problem.
Intrinsic simply means something specific to the kidney, whereas pre-renal
AKI is extrinsic or from without the kidney. Other words used synonymously
with intrinsic are intrarenal, renal or parenchymal, and each points to prob-
lems with the functional parts (nephrons) of the kidney. The structures of
the kidney that are affected are the microcapillaries (glomeruli, afferent and
efferent arterioles), the tubular cells and the interstitium, which is the tissue
that surrounds the nephrons (Figure 8.3). It is also important to note that if
pre-renal AKI occurs this will have an impact upon the nephron and cause
tubular cell death, also known as acute tubular necrosis (ATN). Examples of
intrinsic AKI can be found in Table 8.5.

Afferent Arteriole Efferent Arteriole

(supplies arterial blood (arterial blood leaves)
under high pressure)

Glomerulus Bowman’s capsule

Glomerular Filtrate

Figure 8.3 The glomerulus

Table 8.5 Examples of causes of intrinsic AKI

Vascular Glomerular Tubular Interstitial

Renal artery Goodpasture’s Ischaemia Drug-induced
thrombosis Syndrome Haemorrhage antibiotics,
Surgical cross Henoch- Nephrotoxins, e.g. NSAIDs, diuretics
clamping Schoenlein vancomycin Infection:
Polyarteritis nodosa Purpura Myoglobin bacterial, viral,
Haemolytic uraemic Infective (muscle damage) tuberculosis
syndrome endocarditis Haemoglobin
Malignant Wegener’s (haemolysis)
hypertension granulomatosis
Copyright © 2016. Macmillan Education UK. All rights reserved.

The glomerulus is where filtering of the blood occurs (Figure 8.3).

iltration is driven by BP and so a fall in BP will cause a decline in the GFR.
F
The filtration barrier is made up of three structures: the endothelial cells
of the blood vessel, the basement membrane and the epithelial cells of the
Bowman’s capsule. The glomerulus has a size restriction (anything over
42 Å is retained) and is also negatively charged to prevent substances such
as proteins from escaping into the urine (Koeppen and Stanton, 2001). Any
pathological process that damages this structure alters its function by inhib-
iting filtration or essentially making it more permeable to larger substances,
such as in protein (albumin) leakage (seen in diabetes mellitus) or red blood

cell leakage (as found in glomerulonephritis). As already noted, the nephron

is made up of highly active cells and it is here where wholesale and fine tun-
ing reabsorption of essential substances such as water, sodium and potas-
sium as well as the secretion of excess and toxic substances occurs. These
cells are responsible for maintaining the chemical balance of extracellular
fluid by manipulating substances such as sodium and potassium. Damage
to these cells will alter the ability to maintain chemical homeostasis and
the removal of toxins.
Intrinsic diseases that affect the kidney can be primary to the kidney or
as part of a systemic disease. Where the disease is part of a systemic disease
such as systemic lupus erythematosus (SLE) kidney function cannot be
affected by manipulating external factors such as maintaining circulating
volume. Diseases that affect the microcapillaries involve the blood vessels
or the capillary bundle known as the glomerulus. There are inflammatory
conditions of blood vessels such as polyarteritis nodosa and Wegener’s
granulomatosis, large vascular disease such as renal artery thrombosis, renal
vein thrombosis and surgical cross-clamping as found in abdominal aortic
aneurysm repair. Conditions that affect small vessels include thrombocyto-
paenic conditions such as pre-eclampsia, scleroderma, malignant hyperten-
sion and haemolytic uraemic syndrome (HUS), which is often caused by
Escherichia coli H0157:H7 contamination of food. In these conditions there
is damage to the endothelial cells of the blood vessels and stimulation of the
clotting cascade (Salama, 2002).

Intrinsic AKI: Glomerular Disease

There are diseases of the glomerulus that alter the structure of the glomeru-
lar filtration barrier, causing haematuria and proteinuria. They are usually
immunologically mediated and cause the condition known as glomerulone-
phritis. Proteinuria can be very severe and in some cases in excess of 3 grams
in 24 hours can be lost, which is known as nephrotic, whereas less than
Copyright © 2016. Macmillan Education UK. All rights reserved.

2 grams in 24 hours is called nephritic. Such conditions include Henoch–

Schönlein purpura, Goodpasture’s syndrome, infective carditis and post-
infectious glomerulonephritis (often streptococcal infection). Patients with
these diseases are usually very ill, with skin lesions and often a rash (Holley,
2001). Ralph has a petechial rash, which may indicate an intrinsic cause to
his AKI. Alternatively his rash could have been caused by local capillary
trauma due to coughing during his chest infection. The blood cells found
in the urine of patients with glomerulonephritis are often misshapen and
lumped together in ‘casts’ as they progress through the tubules. Haematuria
can be non-visible and only found by urine dipstick testing, or visible. This
simple test aids diagnosis of intrinsic disease of the kidney.

Intrinsic AKI: Tubular Disease

Damage to the renal tubules (acute tubular necrosis: ATN) is caused in
50 per cent of cases by a reduction in blood flow (ischaemia) to the kidney
and in 35 per cent of cases by a nephrotoxic substance (Faubel et al., 2005).
Ischaemic causes of ATN have already been identified in pre-renal AKI; how-
ever, nephrotoxins are multiple and in theory any substance is potentially
toxic to the kidney. Due to the rich blood supply to the kidney and the
ability to concentrate toxins in high levels the kidney is particularly vulner-
able to toxic substances (Clarkson et al., 2008). Nephrotoxins can be drugs
such as aminoglycoside antibiotics, including Gentamicin® and Vancomy-
cin®; cancer drugs such as Cisplatin®; anaesthetic drugs such as Enflurane®;
antiviral drugs such as Acyclovir® and immunosuppressive drugs such as
Ciclosporin®. Nephrotoxins can also come from within the body, such as
haemoglobin (from haemolysis), myoglobin (from muscle damage) and uric
acid. Each of these nephrotoxins will damage the tubular cells to varying
degrees, which may be sufficient to prevent function or lead to cell death.
Subsequent tubule blockage leads to cellular casts or debris in the urine.

Intrinsic AKI: Interstitial Disease

Interstitial disease of the kidney occurs when an inflammatory process is
initiated in the cells between nephrons. Commonly inflammation occurs
as a consequence of hypersensitivity to drugs but it can also be caused by
infection or systemic disease such as SLE (Baker, 2002). Infectious causes
can be direct, as found in upper urinary tract infection leading to pyelone-
phritis, or they can be systemic, such as streptococcal, staphylococcal, HIV
and hepatitis A. Drugs that induce acute interstitial nephritis (AIN) include
many perceived safe drugs such as antibiotics (ampicillin, erythromycin),
non-steroidal anti-inflammatory drugs, Ranitidine®, diuretics (Furosemide®,
thiazides), paracetamol and aspirin (Baker, 2002). It is likely that any drug
has the potential for initiating hypersensitivity in a person and causing
Copyright © 2016. Macmillan Education UK. All rights reserved.

kidney injury. Patients with AIN frequently present with pyrexia, rash, joint
pain, hypertension, fluid retention and possible signs of systemic disease. It
can occur at any time after exposure to the drug and is not dose dependent.
There are a number of possible causes in Ralph’s case. He may have ATN
due to low BP but he has also had an infection and was treated with an
antibiotic. Further to this Ralph has been taking ibuprofen (a NSAID) and
Bendrofluazide® (a diuretic), which may indicate interstitial nephritis. Ralph
has a rash on his chest, which is a possible sign of a vasculitic disease, and
protein in his urine could indicate glomerular damage. This information
adds to the complexity of assessment of someone with AKI and by no means
can it be assumed that the cause is pre-renal or intrinsic at this point.

Post-renal AKI
Post-renal AKI relates to conditions that interfere with the flow of urine
from the tip of the papillae (renal pyramids) to the tip of the urethra.
Obstruction is the usual cause, with elderly men being most at risk due to
prostatic hypertrophy and/or cancer (Table 8.6).
In these conditions patients usually present with reduced (oliguria) or
loss (anuria) of urine output, urinary retention, loin pain and possibly fever.
Anuria usually suggests urinary tract obstruction; otherwise it is unusual in
AKI (Hilton, 2006). Urinary retention and bilateral kidney obstruction will
eventually cause back pressure into the kidney tubules, which counteracts
the pressure across the filtration barrier of the glomerulus, thus reducing
glomerular filtration rate and renal blood flow. This in turn would even-
tually cause an intrinsic AKI due to ischaemia of the tubular cells. This
additional information adds more possibilities to the cause of Ralph’s AKI.
Ralph has a reduced urine output, which may be symptomatic of obstruc-
tion, especially as he has a history of urinary hesitancy, not uncommon for
a man of his age. Ralph also has diabetes mellitus, which is known to cause
papillary necrosis, which obstructs the ureters with necrotic tissue. Each of
these potential causes requires investigation to differentiate cause and initi-
ate appropriate management.

Risk Factors for AKI

It is important to note what factors increase the risk of AKI. NICE (2013)
recently identified a range of risk factors particularly in relation to different
clinical scenarios; however, a general theme can be seen and is summarised
in Table 8.7.
In relation to Ralph, increased age is a risk factor for AKI. The reason
for this is multifactorial, including multiple co-morbidities, but one major
Copyright © 2016. Macmillan Education UK. All rights reserved.

Table 8.6 Examples of causes of post-renal AKI

Intraureteral obstruction Bladder and urethral Obstruction by external

obstruction pressure

Stones Urethral stricture Malignancy: rectal,

Papillary debris caused by Prostatic hypertrophy/ ovarian, uterine, cervical
drugs, diabetes, stricture cancer Fibroids
Blood clots Tuberculosis Crohn’s disease
Myeloma Spinal cord injury Haemorrhage
Multiple sclerosis Aortic aneurysm
Diabetes mellitus

Table 8.7 Risk factors for AKI

• CKD (eGFR < 60 mL/min/1.73m2)

• Heart failure
• Liver disease
• Diabetes mellitus
• History of AKI
• Oliguria
• Limited access to fluid
• Hypovolaemia
• Use of drugs with nephrotoxic potential
• Use of iodinated contrast
• Symptoms or history of urological obstruction
• Deteriorating early warning score
• Age 65 or over

Source: Adapted from NICE (2013)

reason is that kidney function of older people lacks renal reserve. This
means that the kidney has an age-related reduced GFR which, when put
under stress, such as dehydration, cannot compensate effectively (Pannu
and Halloran, 2002). The elderly kidney is also sensitive to the effects
of drugs, especially NSAIDs, which cause vasoconstriction and a decline
in GFR and may be implicated in Ralph’s AKI (Jefferson et al., 2010).
Underlying chronic kidney disease, often identified by proteinuria or
cardiovascular disease (especially hypertension and renovascular disease),
is also a risk factor in that it will affect the kidney’s ability to respond
to injury. In addition, diabetes mellitus causes long-term vascular dam-
age to the kidneys (see Chapter 10) and sepsis causes renal vasoconstric-
tion (see Chapter 3). These four factors immediately place Ralph at high
risk for AKI. Surgery, especially cardiac surgery, predisposes individuals
to AKI and accounts for 25 per cent of hospital-acquired AKI (Lamiere
Copyright © 2016. Macmillan Education UK. All rights reserved.

et al., 2005, Thakar, 2013) and hypotension is a major risk factor that is
increased with the use of diuretics. The increase in organ transplantation
is contributing to more cases of AKI due to the use of immunosuppressive
therapy (Lamiere et al., 2005).
In summary, an understanding of the underlying causes of AKI can
inform the assessment strategy employed in Ralph’s case. It is apparent
that Ralph has a number of potential causes for his condition. His history
of potential hypovolaemia and hypotension may suggest pre-renal AKI,
whereas possible intrinsic causes such as his medication may have caused
acute tubular necrosis. Finally, Ralph may also have a urinary system
obstruction that may have contributed to his kidney injury.

The Case Scenario: The Immediate Assessment Priorities

Samples of blood and urine taken for analysis from Ralph revealed the following
results:
Capillary blood glucose: 8.5 mmol/L
Venous blood biochemistry – urea and electrolytes (U&Es)
Urea: 40 mmol/L
Creatinine: 200 µmol/L
Na+: 133 mmol/L
K+: 6.5 mmol/L
Cl–: 107 mmol/L
HCO3: 19 mmol/L
Cholesterol: 7.5 mmol/L
CK: 180 iu/L
Calcium: 2.2 mmol/L
Pi: 1.2 mmol/L
Glucose: 10 mmol/L
Venous blood liver function tests (LFTs)
Albumin: 35 g/L
Bilirubin: 10 µmol/L
ALT: 15 iu/L
Alkaline phosphate: 123 u/L
Lactate: 2.0 iu/L
CRP: 72
Venous blood haematology
Hb: 13.2 g/dL
HCT: 0.45 L/L
WCC: 22 ¥ 109/L
Platelets: 10 ¥ 109/L
Immunology
ANA, ANCA, complement, protein electrophoresis, anti-GBM all tested normal
Virology
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No HIV, hepatitis A or B
Urinalysis
Protein +
pH: 6
No other abnormality
Urine output: 150 mL in 8 hours
Sodium: 10 mmol/L
Fractional excretion Na: < 1 per cent
Urine osmolarity: 1250 mOsm/kg H2O

The Case Scenario continued

Immediate Assessment
1. How does the information gleaned so far help with the next step of assessment?
2. Devise a comprehensive acute assessment plan for Ralph and explain the
rationale for each measure.
3. How is AKI differentiated from chronic kidney disease?
4. How is Ralph’s level of kidney function calculated?
5. Re-examine Ralph’s biochemistry results then calculate his eGFR at www.renal.
org/eGFRcalc/GFR.pl and consider what it means with respect to the amount
of kidney function he has.

Assessment and Reaching a Diagnosis

The NCEPOD 2009 report Adding Insult To Injury highlighted some signifi-
cant issues in relation to patient care that should not be ignored. The NCE-
POD report identified that only 50 per cent of patients received good care,
there was poor assessment of AKI risk factors and of patients once they had
developed AKI, there was an unacceptable delay in recognising AKI post
admission in 43 per cent of patients, one-fifth of cases were both predict-
able and preventable, and complications were missed in 13 per cent of cases,
avoidable in 17 per cent of cases and managed badly in 22 per cent. Finlay et
al. (2013) reported the need for continuing improvement when they found
basic elements of care were still being omitted by practitioners. In view of
this poor indictment of clinical practice it is essential that healthcare staff
take note and improve their patient care.
Notwithstanding other aspects of assessment, namely ABCDE identified
in Chapter 1, assessment will focus upon specific issues related to Ralph and
AKI. However, it is important to note that assessment of airway, breathing
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and circulation is essential especially because AKI is potentially a life-threat-

ening condition. There must be appropriate prioritisation in the assessment
of Ralph and assessment of risk because focusing upon the wrong issues may
prove fatal for someone with AKI. All patient management should be linked
to a ‘track and trigger’ system/early warning system such as NEWS (RCP,
2012) for managing change in the patient’s health status.

Airway and Breathing

While conscious, Ralph will be maintaining his own airway; however, his
SpO2 at 92 per cent suggests a degree of hypoxaemia. It is therefore impor-
tant to observe and document his respiratory rate, depth and rhythm and

sounds regularly and to monitor oxygen saturations using pulse oximetry

continuously. Oxygen therapy should be commenced at 40 per cent via face
mask in an effort to increase the SpO2 above 95 per cent.

Circulation
Retention of electrolytes, in particular potassium, due to renal failure can
lead to serious cardiac arrhythmias. Therefore Ralph requires continuous
cardiac monitoring to assess his heart rate, regularity and rhythm. He is
documented as having a sinus tachycardia, which may be a compensatory
response to his low BP. Ralph’s BP should be recorded at least every four
hours as an indication of improvement or deterioration. Central venous
pressure (CVP) measurement may also be useful in assessing Ralph’s circula-
tory fluid status but will require insertion of a wide bore catheter into the
jugular vein attached to a litre infusion of 0.9 per cent sodium chloride to
enable regular measurement (see Chapter 2).

Disability
Assessment of Ralph’s altered consciousness must be undertaken. Altered
consciousness is a trigger factor for initiating urgent treatment in an
attempt to prevent deterioration (NICE, 2007). Ralph’s conscious level
should prompt a bedside capillary blood glucose measurement, particularly
as he has a history of type 2 diabetes and hasn’t eaten well recently. His
capillary and venous blood glucose are on the upper side of normal but
not sufficiently abnormal to account for his drowsiness. Drowsiness is a
common clinical feature in AKI. If other potential factors such as hyper- or
hypoglycaemia, hypoxia and hypotension are excluded, altered conscious-
ness occurs in AKI due to the accumulation of uraemic toxins. Vanholder
et al. (2003) identified 90 potential uraemic toxins, including urea, cre-
atinine, parathyroid hormone, guanidines, ammonia and peptides. These
substances are poorly understood: for example, urea only has a very minor
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effect and is believed not to be the cause of uraemic symptoms, requiring

accumulation with other substances to have an effect (Meyer and Hostetter,
2007). It is worth noting that uraemia does not mean high urea levels in
the blood but literally means ‘urine in the blood’: that is to say, the products
normally seen in the urine are retained in the blood but at abnormal levels.
Uraemia causes altered neurosensory function, presenting with cognitive
impairment such as defects in memory, attention and concentration. Unre-
lieved uraemia will lead to coma and death. Clinical signs and symptoms
of uraemia can be found in Table 8.8. Ralph’s consciousness level must be
monitored using the Glasgow Coma Scale (or equivalent) for deterioration
(see Chapter 4) and the frequency of assessment will be determined by his
condition, level of consciousness and potential for deterioration. Ralph

Table 8.8 Signs and symptoms of uraemia (some features may be

dependent upon underlying cause)

Uraemic signs and symptoms

Altered consciousness, irritability, reduced concentration and memory numbness,

weakness, tremor, stupor, coma, hearing disturbance
Dyspnoea, orthopnoea, haemoptysis, nose bleed, sinusitis
Palpitations, arrhythmias, pericarditis, cardiac failure, hypotension
Nausea, vomiting, diarrhoea, thirst, abdominal pain, acid reflux, bleeding, hiccup,
stomatitis, fetor, gastritis, gastric/enteral ulceration, bleeding
Haematuria, proteinuria, frequency, dysuria, suprapubic pain, altered urine output,
loin pain, colic
Arthralgia, muscular pain, cramp
Rash, pruritus, bruising, jaundice, hypothermia, dry skin, oedema, uraemic frost
Red eyes, oedema
Fever, malaise, insomnia, weight loss
Anaemia, thrombocytopaenia (bleeding), altered white cell function

currently has a GCS of 14 so every 15 to 30 minutes may initially be suffi-

cient; however, there must be a nursing initiative to increase the frequency
of testing should his condition deteriorate. Drowsiness in uraemia is a sign
of very high accumulation of uraemic toxins. Patients with chronic kidney
disease can usually tolerate high levels of uraemic toxins and are not usually
drowsy in the way Ralph is; therefore his symptoms appear to point towards
AKI, where drowsiness is more likely.
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Specific Investigations
A range of specific investigations are required to reveal the exact cause
of Ralph’s apparent kidney failure and presenting signs and symptoms.
Table 8.9 outlines investigations required for a general approach to the
assessment of causes of AKI.

Estimating the Level of Kidney Function

Creatinine is a substance that is also thought to be of limited toxicity. Normal
kidney function usually excretes all creatinine, unlike urea, of which about
60 per cent is reabsorbed. Creatinine is a by-product of muscle metabolism
and reflects total muscle mass. Because of its complete removal by the kidney

Table 8.9 Investigations for assessment of AKI

Investigation Specific test content Reason for test

Urea and Urea and creatinine Creatinine to estimate kidney function and
electrolytes hydration (Ur:Cr ratio)
Sodium Assess level and hydration
Potassium Assess level and cardiac risk
Calcium Assess level and differentiate CKD, high
levels cause AKI, low in rhabdomyolysis
Phosphate Assess level and differentiate CKD
Chloride Assess level; acidosis/alkalosis
Magnesium Assess level (may be low)
Bicarbonate Acidosis/alkalosis
Urate Assess level pre-eclampsia (high uric acid
levels are implicated in pre-eclampsia and
lead to AKI)
Lactate Tissue ischaemia/under perfusion, assess
lactic acidosis
eGFR Estimate glomerular To assess level of kidney function
filtration rate
Liver function Albumin Assess level; may be low in
test glomerulonephritis
Creatine kinase Assess level for muscle damage (myoglobin)
Amylase Assess level; pancreatitis may cause AKI
Bilirubin, AST, ALT Haemolysis, liver disease may cause AKI
Arterial blood pO2 Assess oxygen level for oxygenation
gases pCO2 Assess acidosis, CO2 retention
Full blood Haemoglobin Assess for anaemia, need for transfusion
count and White cell count Indicator of infection
coagulation Platelets Level and coagulopathy (e.g. DIC)
studies Group and save Transfusion
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Haematocrit Assess anaemia/hydration

INR Clotting screen
Inflammation ESR Indicator of inflammation
and CRP Non-specific marker for inflammation and
immunology infection
ANA, ANCA, Specific glomerular disease tests, e.g. SLE,
Anti-GBM, vasculitis, myeloma
IgA, IgM, IgG,
electrophoresis,
complement,
antistreptolysin
(Continued )

Table 8.9 (Continued )

Infection Blood culture Infection: sepsis may cause or prolong

AKI
Urine culture Infection: may cause interstitial nephritis,
prolong AKI
Virology Hepatitis A B, HIV
Urinalysis Dipstick Assessing for blood, protein, infection
Electrophoresis Specific test for multiple myeloma which
causes AKI
Albumin creatinine Assess glomerular damage
ratio to assess kidney function/damage
Creatinine Assesses urine output/kidney function and
clearance prescribe volume replacement
Volume
Imaging Chest X-ray Evidence of pulmonary oedema, LVF
Renal ultrasound Assess kidney structure, size and signs of
obstruction
X-ray kidney ureter Obstruction, stones, abdominal masses
bladder
CT/MRI Assess kidney structure
Isotopes studies Assess renal perfusion, cortical necrosis,
vascular obstruction
Biopsy Assess ATN, suspected intrinsic AKI
Cardiac ECG Assess cardiac function: LVF, dysrhythmia

it is a useful marker for glomerular function. It is used as a means for esti-

mating kidney function. Current recommendations advise the use of the
estimated glomerular filtration rate method (eGFR), which uses age, race,
creatinine and sex to calculate kidney function (Lewington and Kanasunda-
ram, 2011). Some caution is needed in AKI because eGFR is normally used for
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chronic kidney disease. The eGFR is requested at the same time as obtaining
urea and electrolytes (U&Es) but there are many eGFR calculators available
on the internet. Using the Renal Association (2011) calculator Ralph’s GFR is
30 mL/min/1.73m2 (normal: about 100 mL/min/1.73m2 without signs of kid-
ney disease), which means he has less than 30 per cent of his kidney function
remaining. In addition to eGFR and following the results of the NCEPOD
(2009) Adding Insult to Injury report in England there will be implementation
of an AKI e-alerts system where an elevation of serum creatinine by 26μmol/L
will automatically produce an alert on a patient’s electronic records system.
The aim is to identify patients with AKI and implement prompt treatment
and consistency of practice across health services (NHS England, 2014).

The Case Scenario: Medical Management and Care Issues

Ralph is diagnosed with AKI and he does not appear to be showing any signs
of improvement. A radial artery sample is taken for blood gas analysis and the
following results received:

Arterial blood gases (ABGs)

PO2: 10 kPa
PCO2: 8.1 kPa
Base excess: –1
Anion gap: 18
pH: 7.31

Immediate Medical Management

1. What two urgent priorities of management and care can you identify for
Ralph?
2. How would these two priorities be managed?
3. What fluid replacement regime would best suit Ralph’s needs?
4. What are Ralph’s main care issues?
5. What are Ralph’s additional management priorities?
6. Examine the blood gas results carefully and consider what might be done.

Differentiating between AKI and CKD

It is important to establish whether Ralph has AKI or CKD to ensure that he
gets the appropriate treatment. Not only is Ralph a prime candidate for AKI
but his increased age, diabetes and hypertension made him a prime candi-
date for CKD. Ralph may have underlying kidney disease and be presenting
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with an acute-on-chronic episode (which is a common presentation of AKI)

or with end-stage renal disease (ESRD). Drowsiness is a common symptom
of AKI but can also manifest in ESRD (National Collaboration for Chronic
Conditions, 2008; Hsu et al., 2008). People with CKD usually have an
absence of acute illness, and also present with anaemia, nocturia, long dura-
tion of symptoms, hyperphosphataemia and hypocalcaemia (Hilton, 2006).
Renal ultrasound will identify the size of the kidney, as those with CKD will
typically have small kidneys (<9 cm), though diabetes may preserve kidney
size for some time. Ralph’s clinical features and history indicate his problem
is acute in nature rather than chronic.

Medical Management Strategies

AKI is a life-threatening condition and it is therefore important that priori-
ties for management are promptly identified. Principles of AKI management
can be found in Table 8.10, where some immediate concerns such as hyper-
kalaemia and fluid resuscitation are noted.

Hyperkalaemia
Ralph demonstrates signs that are potentially life threatening and may
override the initial desire to find an underlying cause. The two immediate
concerns are his high potassium level (hyperkalaemia), which is 6.5 mmol/L
(normal range 3.2–5.0 mmol/L), and hypovolaemia. In the first instance
causes of hyperkalaemia should exclude pseudohyperkalaemia caused by
test tube haemolysis, prolonged tourniquet tightness, leucocytosis and infu-
sion arm sampling to avoid inappropriate treatment (Table 8.11).

Table 8.10 Principles of management of AKI

• Identify and correct cause

• Optimise cardiac output and renal perfusion
• Restore urine flow
• Accurate fluid balance, daily body weight
• Review drugs: stop nephrotoxic drugs, adjust doses and monitor blood levels
• Identify, avoid and treat complications: e.g. hyperkalaemia, fluid overload,
acidosis, hyper/hyponatraemia, hyperphosphataemia
• Optimise nutritional support: calories, potassium restriction, minimal nitrogen
• Vigilant monitoring for infection and treat aggressively.
• Minimise the use of indwelling lines and catheters: remove if unnecessary
• Avoid, identify and treat bleeding tendency
• Initiate dialysis before uraemic complications occur
• Expert nursing care
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Source: Adapted from Lameire et al. (2005) and Hilton (2006)

Table 8.11 Drugs that can cause hyperkalaemia

Angiotensin converting enzyme inhibitors (ACEI)

Angiotensin II receptor blockers (ARB)
Non-steroidal anti-inflammatory drugs (NSAIDs)
Digoxin
Spironolactone especially in those with underlying renal insufficiency

Table 8.12 ECG changes in hyperkalaemia

• Peaking (‘tenting’) of T waves: K+ > 5.5 mmol/L

• Flattening and disappearance of P waves: K+ > 6.5 mmol/L
• Prolonged PR interval
• Progressive widening of QRS complex: K+ > 6.5 mmol/L
• Deepened S waves and merging with T waves
• Sine wave patterns
• Ventricular fibrillation and asystolic cardiac arrest: K+ > 12.0 mmol/L

Source: Adapted from Steddon et al. (2006)

Additional causes of hyperkalaemia include potassium supplementa-

tion, gastrointestinal bleeding and in Ralph’s case potassium retention
due to loss of kidney function (Renal Association, 2014). Ralph’s medica-
tion must be considered and any drug that may cause hyperkalaemia – for
example, ibuprofen – should be discontinued, if possible, without causing
additional medical problems. Alternative medication may be required. The
effects of hyperkalaemia are neuromuscular and cardiac but demonstrate
few symptoms. Patients may complain of vague abdominal sensations or
skeletal muscular weakness but more importantly they may develop cardiac
arrest. Cardiac arrest occurs because of decreased membrane excitability,
neuromuscular depression and cardiac arrhythmias (Weisberg, 2008). In
view of this, Ralph must be closely monitored by continuous ECG for pro-
gressive hyperkalaemic changes, which occur in sequence with elevating
hyperkalaemia, as seen in Table 8.12. The degree of hyperkalaemia requires
immediate attention. Treatment must be instigated urgently, especially if
the potassium is over 6.5 mmol/L or ECG changes are present. The aim is
to reduce Ralph’s potassium and limit his risk by the following the Five Key
Steps to Treatment of Hyperkalaemia (Renal Association, 2014). The patient
should never be left until all five have been completed.
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1. Protect the heart

• Cardioprotection: medical or advanced nurse practitioner administra-
tion of prescribed 10 mL 10 per cent intravenous calcium gluconate or
calcium chloride, repeat if necessary. This drug does not reduce potas-
sium level but ‘protects’ the heart from excess potassium excitability.
2. Shift potassium into the cells
• Administration of a prescribed slow intravenous infusion of 50 mL of
50 per cent glucose.
• Administer prescribed insulin (15 iu Actrapid®) and dextrose (50 mL
of 50 per cent) infusion. Effects are seen within 15 minutes and last
between two and four hours.

• Nebulised salbutamol (which drives potassium into the cells) 10–20

mg may be used in conjunction with insulin and glucose providing an

additive effect. Effects are seen within 15–30 minutes and last for two
hours. Monitor for tachycardia, headache and palpitations.
•
The process can be repeated after four hours.
3. Remove potassium from the body
•
Oral calcium resonium (which binds with potassium in the gut) 15 g
with lactulose®, though this is slow to work (≥ 2 hours). This is not
recommended for emergency severe hyperkalaemia but for mild to
moderate hyperkalaemia.
•
Renal replacement therapy only when first-line treatments fail to
control potassium level or if severe hyperkalaemia (≥7 mmol/L) is
present.
4. Monitor potassium and glucose
•
Monitor blood potassium 30 minutes after each administration then
hourly.
•
Monitor U&Es for hypokalaemia 30 minutes after each administra-
tion.
•
Monitor blood glucose level with a blood glucose monitor 30 minutes
after administration then hourly and treat hypoglycaemia with
prescribed dose of 10 per cent glucose.
5. Prevent recurrence
•
Review medication and stop any that may cause hyperkalaemia, in
particular ACEi, ARBs, loop diuretics, NSAIDs and trimethoprim.
•
Review dietary intake including salt substitutes.

Insulin and glucose are the most effective means for conservatively keeping
the potassium low and their efficacy is improved with nebulised salbuta-
mol® (Mahoney et al., 2005). Insulin works by increasing cellular uptake
of potassium by increasing intracellular sodium. Intravenous access will
be necessary for infusions and strict fluid balance monitoring of all intake
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and output commenced. All fluid volumes, including intravenous fluids,

nasogastric feeds and oral fluids, must be entered onto the fluid balance
chart. All types of fluid output, including urine, vomit, and wound drain-
age, should be measured and documented accurately. Urine output may
need to be assessed on an hourly basis.

Volume Depletion
The next priority for Ralph is his fluid status. Ralph is displaying evidence
of volume depletion, which if not treated may cause permanent damage
to the kidney as well as more systemic problems such as hypovolaemic

Table 8.13 Assessing circulating volume

• Pulse
• Blood pressure
• JVP or CVP
• Peripheral perfusion
• Lung crackles
• Dyspnoea

shock, leading to inadequate tissue oxygenation and multiple organ failure

(Ragaller et al., 2001). Volume depletion is evident in Ralph in a number of
clinical features (Table 8.13). Most noticeably, Ralph’s jugular venous pres-
sure (JVP) is unrecordable, which means it is low (normal 0 to 3 cm above
the sternal angle).
Ralph is also tachycardic with a heart rate of 110 beats per minute and
his BP is low and falls when he is standing. This effect is known as a pos-
tural drop or orthostatic hypotension and is a classic sign of hypovolaemia.
However, in a systematic review of studies of clinical signs of hypovolae-
mia, hypotension was frequently absent in supine patients. Orthostatic
hypotension is also present in 10 per cent of normovolaemic adults under
65 years old and up to 30 per cent of normovolaemic adults over 65 years
old (McGee et al., 1999). Tachycardia is a normal response to volume deple-
tion in an attempt to ensure vital organs receive blood. A postural increase
of pulse rate by 30 beats/min or more upon standing is an accurate sign of
hypovolaemia (McGee et al., 1999) (Table 8.14). A reduced fluid intake, vom-
iting, continued use of diuretic medication and mild pyrexia all indicate

Table 8.14 Volume depletion: test results

Hypovolaemia
• Blood sodium variable dependent upon loss: low/normal/high sodium level
• Raised urea:creatinine ratio
• Increase urine specific gravity
• Increased urine osmolality
• Haematocrit variable dependent upon cause, e.g. low in blood loss
Dehydration
• High blood sodium level (> 145 mmol/L)
• Raised blood osmolality
• Elevated haematocrit
• Urine specific gravity above 1.030

uncontrolled fluid loss and fluid imbalance, which may be further substan-
tiated when Ralph’s test results are examined. Biochemistry results show
Ralph’s sodium level to be 133 mmol/L (normal range: 135–145 mmol/L),
rendering him hyponatraemic.
There are many causes of hyponatraemia (Table 8.15) that need to be con-
sidered when assessing Ralph’s condition. Hyponatraemia is an important
sign because it indicates volume depletion rather than dehydration. Dehy-
dration means a loss of intracellular water, which would increase plasma
sodium levels. In contrast, volume depletion describes a loss of sodium (and
water) from extracellular space caused by bleeding, excessive vomiting or
diarrhoea. Ralph’s sodium is low and points towards volume depletion, but
there are other clues. Ralph’s urea and creatinine levels are raised due to
retention by the kidney (not urinary retention), but also in comparison to
each other the urea is disproportionally high. This is caused by passive reab-
sorption of urea in the kidney (creatinine is not reabsorbed), which occurs
in hypoperfusion of the kidney but also increased catabolism, steroid ther-
apy, gastrointestinal bleeding and the use of tetracyclines. As a result the
high urea level must be interpreted with caution (Goldberg, 2002). Analysis
of Ralph’s urine also reveals a low sodium content, less than 10 mmol/L
(normal about 100 mmol/L), and a fractional excretion of sodium (FeNa) of
less than 1 per cent (normal 1–2 per cent). This is typical of pre-renal AKI
and demonstrates tubular sodium reabsorption in an effort to retain water
to expand the circulating blood volume.
Conversely, intrinsic AKI has a FeNa of greater than 2 per cent, meaning
the tubules are unable to reabsorb sodium which is lost in what urine there

Table 8.15 Some causes of hyponatraemia

Low plasma osmolality Normal or raised plasma Syndrome of inappropriate

osmolality anti-diuretic hormone (SIADH)
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Vomiting Hyperglycaemia Stress

Diarrhoea Acute uraemia Nausea and vomiting
Diuretic use Alcohol Pain
Excess fluid replacement Mannitol infusion Trauma/surgery
Congestive cardiac Amino acid infusion Infection
failure Sickle cell syndrome Stroke
Cirrhosis and ascites Meningitis
NSAIDs

Osmolality is the measure of osmoles of solutes (e.g. sodium, chloride, glucose) per kg of
solvent (blood)
Source: Adapted from Crook (2006)

Table 8.16 Glossary of terms

Oliguria: a urine output of less than 1 mL/kg/hour or less than 400 mL/24 hours

Anuria: a urine output of less than 100 mL/24 hours

Non-oliguric AKI: high urine volumes but of poor quality

is (MacPhee, 2002). Urine osmolality is also high, indicating concentrated

urine, and in Ralph’s case it is in excess of 500 mOsm/kg H 2O, indicat-
ing pre-renal AKI. Ralph’s urine output (oliguria) is reduced to 150 mL in
eight hours (Table 8.16). Non-oliguric AKI can also occur where normal
amounts of urine are passed but of poor quality, but this type has a better
prognosis. Oliguria occurs when the kidney is attempting to retain water
in the body, thus concentrating the urine, or when little urine is being
made due to kidney damage. Oliguria is often followed by a polyuria
(>3 litres/24 hr) phase due to recovery of kidney function but an initial
inability to concentrate effectively, and usually resolves in a few days. All
these points direct attention to the fact that Ralph is hypovolaemic, which
needs to be addressed. Addressing these problems will require close and
frequent monitoring of Ralph’s fluid balance, which would include daily
weight, hourly urine output, insensitive loss such as sweating and faecal
loss (which is estimated a being ≥ 500 mL/24 hr) measurements and all
fluid input. CVP monitoring provides for a more accurate assessment of
blood volume (see Chapter 2).

Managing Hypovolaemia
Ralph is hypotensive, hypovolaemic and in need of urgent fluid resuscita-
tion. Fluids are required to return normal circulating volume, elevate his
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BP, increase renal perfusion and reverse pre-renal AKI. The general ‘rule
of thumb’ is to replace lost fluid with its equivalent. Ralph’s BP is not low
enough to warrant the need for colloid (e.g. human albumin solution)
infusion for immediate improvement, and in fact evidence suggests that
colloids appear to offer no survival benefit over crystalloids (e.g. 0.9 per
cent sodium chloride) in critically ill patients (Perel and Roberts, 2007).
Colloids are also thought to cause a hyperoncotic renal failure (Nadeau-
Fredette and Bouchard, 2013) and should be used sparingly. In view of
this Ralph needs a crystalloid infusion and 0.9 per cent sodium chloride is
most appropriate. It is worth noting that 0.9 per cent saline has risks asso-
ciated with it particularly causing hyperchloraemia which in itself reduces

renal blood flow and sodium excretion (Prowle et al., 2010). Dextrose or
dextrose/sodium chloride saline are inappropriate because they would
quickly distribute among total body water with little vascular filling effect.
Mannitol also plays no part in fluid management except when a patient
has rhabdomyolysis, which causes nephrotoxicity from damaged muscle
myoglobin. The amount of 0.9 per cent sodium chloride needed is depend-
ent upon the extent of Ralph’s hypovolaemia, his age and what it takes to
restore his blood pressure. Given Ralph’s advanced age it may be advisable
to infuse 200–300 mL of 0.9 per cent sodium chloride over 10 minutes.
Any improvement in BP, pulse, CVP and oliguria would prompt further
infusions until Ralph is normovolaemic. Great care is needed to avoid
overhydration, which would cause cardiac failure, pulmonary oedema,
respiratory distress, hypertension, peripheral oedema and elevated JVP. In
addition to this, overhydration by as little as 5–10 per cent of the patient’s
body weight is linked to worsening organ function and increased mortal-
ity (Bouchard et al., 2009, Prowle et al., 2010). Medical and nursing staff
should endeavour to maintain urine output with fluid infusions by match-
ing input with urine output plus 30 mL (for insensible loss) or maintaining
a CVP of 8–12 cmH2O. Ralph’s AKI may move into the polyuric phase,
which could increase the risk of further volume depletion as well as potas-
sium depletion. Once again fluid balance becomes an essential monitoring
activity for the AKI patient.
In some instances patients with AKI are commenced on diuretic infu-
sions in an attempt to maintain a urine output. Ralph is prescribed a
diuretic (Bendrofluazide®) but this kind of drug is ineffective when GFR is
below 30 mL/min/1.73m2 and should be discontinued. The diuretic drug of
choice is Furosemide® and may be given as an infusion. This is controversial
treatment with no evidence of its clinical benefit to AKI patients; however,

Table 8.17 Stages of AKI

Initiation: reduction in renal blood flow by 30–50% = oliguria phase

Extension: continued cell hypoxia, inflammatory response, cell death = oliguria/

anuria phase

Maintenance: proximal cortical cell regeneration and proliferation = oliguria/

anuria phase

Recovery: tubular cellular regeneration and proliferation = diuresis phase and

development of concentration gradient and return to normal output

it is thought to promote diuresis but should only be used in patients with

adequate circulating volume (Lamiere et al., 2005; Ho and Sheridan, 2006,
Renal Association, 2014). Dopamine infusion at an alleged ‘renal dose’ has
been shown not to improve patient outcome and has additional risks and
so is not recommended for AKI patients (Kellum and Decker, 2001; Stevens
et al., 2008). In some instances of deterioration such as in septic shock (but
not hypovolaemic shock) it may be necessary to provide blood pressure
support and thus renal perfusion with the use of inotropic drugs such as
Dopexamine® or norepinephrine. However, given Ralph’s health history the
use of inotropic drugs is not necessary.

Managing Acidosis
Ralph’s ABGs show a low oxygen level of 10.0 kPa (normal > 10.6 kPa), a
high carbon dioxide level of 8.1 kPa (normal range 4.7–6 kPa) and a low
but not life-threatening pH of 7.31 (normal range 7.35–7.45). The anion gap
is 18 (normal range 8–16) and base excess is –1 (diagnostic range –3 to +3).
These results indicate that Ralph is hypoxic and in need of oxygen. He is
also retaining acid, which is demonstrated by high carbon dioxide level,
low pH, high anion gap and negative base excess. The kidney is respon-
sible for maintaining long-term acid–base balance by removal of acids
from the body and reconstituting bicarbonate into the blood for buffering
excess acids. Should the kidney fail then it can no longer remove acids
and produce bicarbonate, which leads to metabolic acidosis. Indeed this
is the case for Ralph, though his low oxygen level may be caused by his
chest infection, resulting in respiratory acidosis. Ralph’s acidosis is best
dealt with by treating the underlying cause so fluid resuscitation is essen-
tial. Treatment with bicarbonate is not recommended unless Ralph’s pH
falls below 7.1 because it in fact generates more CO2 when reacting with
hydrogen ions and also delivers a large dose of sodium. Providing oxygen
therapy would be beneficial in order to keep Ralph’s oxygen saturation
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level at 95 per cent or higher with a non-rebreathe mask at 15 litres per

minute until blood gas values stabilise. Then a 24 per cent venturi mask
or nasal cannulae at 2 litres per minute can be used. Naturally this may
change with frequent monitoring, which is determined by the patient’s
condition (O’Driscoll et al., 2008).
One additional point to consider is Ralph’s diabetes medication. Met-
formin® is associated with lactic acidosis production in reduced kidney
function and so would probably be discontinued. Treatment of Ralph’s
diabetes in the short term can be with insulin and glucose (as used in the
treatment for hyperkalaemia) but will require reappraisal for long-term
treatment.

Ongoing Care Issues and the Role of the Nurse

Ralph was found lying on the floor and had been there for an indetermi-
nate period. The reason for this is unclear; however, from an AKI perspec-
tive this may be important. Long-term pressure upon muscle tissue (crush
injury) leads to tissue hypoxia and tissue death. Muscle tissue breakdown
is known as rhabdomyolysis and releases myoglobin, which is nephrotoxic.
A common presentation of this condition in AKI is brown urine (in about
50 per cent of cases) that tests positive for blood upon urine dipstick test,
limb swelling, myalgia, hypocalcaemia and hyperkalaemia. Elevations in
blood levels of amylase and very high levels of creatine phosphokinase (CK)
after 12 hours would indicate rhabdomyolysis. Vigilance is required in the
assessment and monitoring of patients with AKI who have been involved in
this kind of situation.

The Case Scenario: Ongoing Care Issues

Ralph is very ill and requires close observation. He has been commenced on an
IV dextrose and insulin infusion to control his elevated plasma potassium and his
diabetes. He has an intravenous infusion of 0.9 per cent sodium chloride with
10-minute bolus infusions of 200 mL until his blood pressure is within normal
limits. He will then require a continuous infusion set according to hydration and
urine output. He may have been given additional medication such as calcium
resonium, salbutamol® nebuliser and Furosemide®. Ralph’s fluid balance must be
monitored closely to avoid under- or overhydration. He is also receiving oxygen
therapy to treat hypoxia and acidosis. He requires bed rest and continuous cardiac
monitoring for arrhythmia detection. A detailed social, family and risk factor
assessment has been completed.

Nursing Care Issues

1. Consider the appropriate ongoing assessment and monitoring required for

Ralph.
2. Discuss in detail Ralph’s immediate care issues.
3. What is important about Ralph being found on the floor and AKI?
4. Why should the nurse be concerned with infection control in the patient with
AKI?
5. What are Ralph’s nutritional requirements and how can they best be
provided?
6. What are the indications for initiating renal replacement therapy (RRT)?
7. What types of RRT are available to support the treatment of AKI?

The Academy of Royal Medical Colleges (2011) has developed a five-level

competency framework for AKI that identifies the required competencies
of roles ranging from healthcare assistants to specialist nephrology con-
sultants. The nursing role includes that of level 1 recorder, level 2 recogn-
iser and level 3 primary responder (for advanced practitioners). There are
different requirements of knowledge, skills and behaviours for those who
have different responsibilities (these are summarised in Table 8.18) but
the minimum competence for a nurse is that of a recogniser. For detailed
inspection the Acute Kidney Injury Competency Framework (2011) can
be viewed and downloaded from the Academy of Medical Royal Colleges
Guidelines pages.

Table 8.18 AKI competency framework

Knowledge, skills and Competency role

behaviour

Recorder Recogniser Primary responder

e.g. health care e.g. staff nurse e.g. advanced
assistant practitioner

Physiological obs. (BP, � � �

P, T, resps)

Urinalysis � � �

Fluid balance � �

Risk factors � �

U&Es � �

Acute illness � �

Urethral � �
catheterisation

Causes of AKI �

Clinical examination �

Investigations and �
management

Complications of AKI �

Recovery from AKI � �

The knowledge, skills and behaviour competencies build upon each other
and increase in complexity depending upon role. The minimum role for a
qualified nurse is that of a recogniser.

Infection and AKI

Ralph has been treated for a chest infection but it would appear that this
has not been successful. Ralph is pyrexial and has an elevated white cell
count and c-reactive protein (CRP), all indicating infection. Naturally this
will require treatment with an appropriate antibiotic and the collection
of samples of urine, sputum and blood for culture, bacteriology and virol-
ogy. Uraemia renders a person at increased risk of infection because white
cells develop functional abnormalities that reduce the ability to adhere
to and destroy invading organisms (Meyer and Hostetter, 2007). There is
also a reduction in the number of circulating white cells and the response
to microorganisms. This is an important care issue because infection will
account for a mortality rate of 76 per cent in patients with AKI and sepsis
(Steddon et al., 2006). Sepsis is also a major risk factor for AKI and may
delay recovery. The acutely ill patient is at risk of infection from a number
of sources, particularly where invasive procedures are needed. The incidence
of acquired hospital infection has been reported as up to 8.8 per cent, with
lung infection accounting for 26 per cent, abdominal infection at 23 per
cent, vascular access at 16 per cent, urinary tract at 10 per cent and wound
infections at 6 per cent (Hoste et al., 2004). It is vitally important that Ralph
does not develop sepsis and to help monitor this staff should be aware of
the Surviving Sepsis Campaign (Dellinger et al., 2013) and the Sepsis Six risk
factors (Daniels, 2011) (see Chapter 3). Catheterisation to assess urine output
is a common procedure in the AKI patient but frequently causes infection.
Ralph has known urinary retention, which may make urine output assess-
ment difficult, and so an indwelling catheter may be necessary. This will
require increased awareness and caution by the nurse in the prevention of
Copyright © 2016. Macmillan Education UK. All rights reserved.

infection. Invasive procedures should be minimised and catheters removed

when not needed, such as when there is anuria. Constant vigilance is
needed when monitoring the AKI patient, especially around vascular access
sites and urinary catheters.

Nutritional Requirements
While Ralph is unwell and may be anorexic and nauseated (a common
uraemic symptom) he will require nutritional support (Table 8.19). Malnu-
trition with AKI will independently increase Ralph’s risk for morbidity and
death (Stevens et al., 2008). Fiaccadori et al. (2009) call the malnutrition

Table 8.19 Goals of nutritional support

• Prevent protein-energy wasting

• Preserve lean-body mass and nutritional status
• Avoid metabolic derangements
• Avoid complications
• Improve wound healing
• Support immune function
• Minimise inflammation
• Improve antioxidant activity
• Reduce mortality

Source: Adapted from Fiaccadori et al. (2009)

process in AKI ‘protein-energy wasting’ (PEW) to explain lean body mass

wasting and fat depletion. This involves a number of contributing factors:
inadequate nutritional support; pre-existing poor nutritional state; acidosis;
blood loss; superimposed catabolic illness (e.g. sepsis, trauma); nutrient loss
in RRT; and derangements in metabolic and hormonal pathways (Fiaccadori
et al. 2009). Fiaccadori et al. (1999) observed severe malnutrition in approxi-
mately 40 per cent of patients with AKI on intensive care units. Ralph is at
risk of protein-energy wasting, characterised by the loss of lean body mass
and fat mass (Fiaccadori et al., 1999). He is also at risk of protein catabolism,
hyperglycaemia due to insulin resistance, and decreases in trace elements,
water-soluble vitamins (except vitamin C) and vitamins A and E. Malnutri-
tion exacerbates the inflammatory state found in patients with AKI.
Nutritional support requires a multidisciplinary approach, including a
dietician to calculate Ralph’s needs, and should commence within 24 hours
of admission. Enteral feeding is preferred in order to avoid complications
associated with parenteral feeding. Enteral feeding has the benefit of
improved outcome should the gastrointestinal tract be functional. Each
person requires individual assessment, which avoids blanket approaches
Copyright © 2016. Macmillan Education UK. All rights reserved.

to nutrition. In some instances protein restriction may be necessary to

prevent nitrogen build-up but is unlikely in most cases due to the fre-
quency of catabolism. Protein intake, often given as amino acids, can vary
between 0.8 and 1.7 g/kg/day. Ralph will also need a high calorific intake to
attenuate catabolism and this can vary, depending upon need, from 25 to
35 non-protein kcal/kg/day (Renal Association, 2014). In Ralph’s case a
minimum of 1,500 kcal/day is necessary and in many instances in excess of
2000 kcal/day may be given (Stevens et al., 2008). Nutritional demand may
increase in hypercatabolism or if Ralph needs renal replacement therapy
and supplementation of trace elements, vitamins and electrolytes, and
fluid restrictions may be necessary and should reflect Ralph’s fluid status

and urine output. Nutritional status is a major prognostic factor in patients

with AKI and significantly and independently influences length of stay,
increased complications and increased mortality (Fiaccadori et al. 2009).

Renal Replacement Therapy

Many of the conservative measures for managing Ralph’s condition may
be inadequate to control metabolic imbalances caused by AKI. To prevent
further deterioration renal replacement therapy (RRT) may be initiated
(Table 8.20). It is generally believed that early initiation of RRT is beneficial
to patient outcome but precise optimal time is unclear and remains a clini-
cal decision (Stevens et al., 2008; Lewington and Kanagasundaram, 2011;
NICE, 2013).
Ralph may require RRT if he does not improve soon. There are three
options: peritoneal dialysis, intermittent haemodialysis or haemofiltration
and continuous haemodialysis or haemofiltration. Each method of RRT has
advantages and disadvantages (Table 8.21). In each instance Ralph would
need some form of access, either a peritoneal dialysis catheter or a central
venous catheter. RRT brings an additional set of challenges for the AKI
patient, such as the additional invasive treatment and anti-coagulation.

Table 8.20 Indications for renal replacement therapy

Clinical indications Biochemical indications

Urine output <0.3 mL/kg/24 hr or Refractory hyperkalaemia > 6.5 mmol/L

absolute anuria for 12 hr

AKI with multiple organ failure Serum urea > 30 mmol/L

End organ damage: encephalopathy, Refractory electrolyte abnormalities:

bleeding

Refractory fluid overload Refractory metabolic acidosis: pH ≤ 7.1

Poisoning and drug overdose Tumour lysis syndrome with

hyperuricaemia and hyperphosphataemia

Severe hypo/hyperthermia Urea cycle defects and organic acidurias:

hyperammonaemia, methylmalonic
acidaemia

Create intravascular space for For additional information consult the

infusions: blood, plasma, nutrition Renal Association Standards (2012) on AKI

Table 8.21 Advantages and disadvantages of renal replacement therapy

Modality Patient Solute clearance Volume control Anti-coagulation

haemodynamic
instability

Peritoneal Yes Moderate Moderate No

dialysis (PD)

Intermittent No High Moderate With/without

haemodialysis
(HD)

Hybrid Possible High Good With/without

techniques

CVVH Yes Moderate/high Good With/without

CVVHD Yes Moderate/high Good With/without

CVVH: continuous haemofiltration, CVVHDF: continuous haemodiafiltration

Source: Adapted from Stevens et al. (2008)

There is insufficient evidence to state which is the best form of treatment

though clinical circumstances will clearly dictate choice (Lewington and
Kanagasundaram, 2011). However, Macedo and Mehta (2013) suggest that
RRT is commenced before there is full-blown failure and the patient is
symptomatic in order to support organ function and prevent complications
which will influence mortality. It is important that the correct treatment
is provided for Ralph at all times and if there is any doubt or concern then
referral for nephrology advice is a necessity. NICE (2013) provides referral
criteria to guide staff in such circumstances (see Table 8.22).
Copyright © 2016. Macmillan Education UK. All rights reserved.

Ralph’s medication must be discontinued for the immediate situation

as the action and metabolism of some drugs may be affected by reduced
kidney function (Table 8.23). Most drugs are eliminated from the body
by the kidney, which makes it essential to consider this in AKI. In many
instances problems of toxicity or accumulation can be overcome by reduc-
ing the dose; however, this requires knowledge of GFR. Many drugs will
require reduced dosage due to margins of safety from toxicity. Some drugs
such as Vancomycin® and Genatmicin® will require careful monitoring of
therapeutic levels with repeated doses altered accordingly. Wherever pos-
sible nephrotoxic drugs should be avoided in order to minimise any further
injury to the kidney.

Table 8.22 Nephrology referral

Discuss AKI management with a nephrologist as soon as possible (and within 24 hours)
if one of the following is present:

Potential diagnosis requiring AKI with no clear Inadequate treatment

specialist treatment (for example, cause response
vasculitis or glomerulonephritis)

Complications associated with AKI Stage 3 AKI eGFR is less than < 30
mL/min/1.73 m2 after
AKI episode

Patients with renal transplant CKD stage 4 or 5

and AKI

Refer adults immediately for Renal replacement therapy if any of the following are not
responding to medical management:

Hyperkalaemia Metabolic Symptoms or Fluid overload

acidosis complications and/or pulmonary
of uraemia such oedema
as pericarditis or
encephalopathy

Table 8.23 Effects of reduced kidney function on drugs

• Increased drug sensitivity

Ralph will need expert nursing care to help him through his illness,
which will include a multidisciplinary approach. Nursing care will include
essential aspects of patient comfort and safety, such as skin care, mouth
care and hydration, because of the multiple effects of uraemia. Examples of
essential nursing skills as applied to AKI patients can be found in Table 8.24.
In addition disease-specific knowledge is needed to minimise risks from
potential complications such as infection, and management of additional
problems such as nausea, vomiting, pain and itching must be assessed
and implemented. Psychological care remains essential, as does accurate
and sensitive communication. The prognosis for AKI over the years has
remained relatively unchanged at around 50 per cent. Critically ill patients

Table 8.24 Essential nursing skills for patients with AKI

Expert nursing focus Example AKI patient problems

Comfort Fatigue, fever, myalgia, pain, insomnia

Infection control Risk of infection in urinary catheters,

vascular access, respiratory,
gastrointestinal, wounds

Mouth care Uraemic ulcers, anorexia, vomiting, thirst,

infection

Skin care Uraemic itching, wound care, fever,

oedema, pressure care, delayed wound
healing, infection, ischaemia

Hydration and fluid balance Under/overhydration, fluid restrictions,

intravenous fluids

Nutrition Anorexia, nausea, vomiting, gastritis,

dietary restrictions, malnutrition,
nasogastric feeding

Medications management Drug dose alteration, side effect

surveillance, prevention of nephrotoxins

Symptoms management Headache, irritability, erratic memory,

confusion, pulmonary oedema

Oxygenation Pulmonary oedema, LVF, infection

Elimination Urinary catheter, urinary obstruction,

infection, diarrhoea, constipation

Health surveillance: safety Hypotension, bleeding, dyspnoea,

hyperkalaemia, fluid overload, infection

Psychological support and education Anxiety, depression, metabolic cognitive

who develop AKI and require RRT generally have a poor prognosis, with
mortality rates exceeding 60 per cent, and unsurprisingly mortality is
higher in older patients (Bagshaw, 2008).
Between 8 and 22 per cent of critically ill patients will not recover renal
function and will require RRT on a permanent basis. The risk of mortality
does not stabilise until after one year following discharge from hospital
(Morgera et al., 2008). In one study only 57 per cent attained complete
recovery of kidney function, with the remaining 43 per cent attaining

partial recovery (Morgera et al., 2008). If kidney function had not recovered
within 6 to 12 months of AKI there was no further recovery of function.
Two per cent of AKI survivors proceed to end-stage kidney disease. There is
a 76 per cent chance of recovery from a single cause but multiple causes of
AKI only have a 30 per cent chance of kidney function recovery (Bagshaw,
2008). More recently a large-scale Danish study of 30,762 patients, of which
4,793 had AKI, reported 30-day mortality between 35.5 per cent (AKI risk)
and 44.2 per cent (renal failure) as compared to 12.8 per cent in non-AKI
patients. Further to this one-year survival ranged between 20.5 per cent
(AKI risk) and 23.8 per cent (renal failure) as compared to 10.7 per cent in
non-AKI patients indicating the high risk for death in patients with AKI and
the need for diligence in care (Gammelager et al., 2012). Therefore, should
Ralph recover he will need long-term follow-up to monitor his kidney func-
tion along with his diabetes, hypertension and arthritis.

Summary

A patient presenting with AKI requires a comprehensive assessment and

management strategy that utilises both general and specific knowledge.
Developing knowledge of specific medical conditions can enhance a nurse’s
ability to care for and manage a patient. While it is acknowledged that some
conditions appear more complex than others this should not prevent nurses
from learning to care for such patients. Integration of nursing care and
medical knowledge enables the development of nursing expertise that can
only benefit the patient and enhance the nurse’s confidence.

Suggested reading:
National Confidential Enquiry into Patient Outcomes and Death (NCEPOD).
Adding Insult to Injury: A Review of the Care of Patients who Died in Hospital with a
Primary Diagnosis of Acute Kidney Injury (Acute Renal Failure) (London: NCEPOD,
Copyright © 2016. Macmillan Education UK. All rights reserved.

2009) [Online]. Available from: www.ncepod.org.uk/2009report1/Downloads/

AKI_report.pdf
National Health Service (NHS). ‘Think Kidneys’ www.thinkkidneys.nhs.uk/
National Institute for Health and Care Excellence (NICE). Acute Kidney Injury
Prevention, Detection and Management of Acute Kidney Injury up to the Point of Renal
Replacement Therapy. NICE Clinical Guideline CG:169 (2013) [Online]. Available
from: www.nice.org.uk/Guidance/CG169 (accessed 30 May 2015).

References
Ali, T., I. Khan, N. Simpson, G. Prescott, J. Townend, W. Smith and A. McLeod.
‘Incidence and Outcomes in Acute Kidney Injury: A Comprehensive Population-
based Study’, Journal of the American Society of Nephrology, 18 (2007), 1292–8.

The Academy of Royal Medical Colleges. ‘Acute Kidney Injury: A Competency

Framework Defining the Role of the Expert Clinician (London: The Academy of
Royal Medical Colleges, 2011) [Online]. Available from: www.aomrc.org.uk/doc_
view/9503-acute-kidney-injury-a-competency-framework (accessed 30 May 2015).
Bagshaw, S. M. ‘Short and Long-term Survival after Acute Kidney Injury’, Nephrology,
Dialysis and Transplantation, 23 (2008), 2126–8.
Baker, R. ‘Acute Interstitial Nephritis’, in P. Glynne, A. Allen and C. Pusey (eds), Acute
Renal Failure in Practice (London: Imperial College Press, 2002).
Bouchard, J., S. B. Soroko, G. M. Chertow et al.. ‘Fluid Accumulation, Survival, and
Recovery of Kidney Function in Critically Ill Patients with Acute Kidney Injury’,
Kidney International, 76 (2009), 422–7.
Caddeo, G., S. T. Williams, C. W. McIntyre and N. M. Selby. ‘Acute Kidney Injury in
Urology Patients: Incidence, Causes and Outcomes’, Nephrology Urology Monthly
5(5), (2013), 955–61.
Case, J., S. Khan, R. Khalid and A. Khan (2013) ‘Epidemiology of Acute Kidney Injury
in the Intensive Care Unit’, Critical Care Research and Practice (2013), Article ID
479730, http://dx.doi.org/10.1155/2013/479730
Challiner, R., J. P. Ritchie, C. Fullwood, P. Loughan and A. Hutchinson. ‘Incidence
and Consequence of Acute Kidney Injury in Unselected Emergency Admissions
to a Large Acute UK Hospital Trust, BMC Nephrology, 15(84) (2014). doi:
10.1186/1471-2369-15-84.
Chertow, G. M., E. Burdick, M. Honour, J. V. Bonventre and D. W. Bates. ‘Acute
Kidney Injury, Mortality, Length of Stay, and Costs in Hospitalized Patients’,
Journal of the American Society of Nephrology, 16 (2005), 3365–70. doi: 10.1681/
ASN.2004090740.
Clarkson, M. R., J. J. Friedewald, J. A. Eustace and H. Rabb. ‘Acute Kidney Injury’, in
Brenner and Rector’s The Kidney, 8th edn (Philadelphia: Saunders Elsevier, 2008).
Cohen, J. J. ‘Relationships between Energy Requirements and Na+ Reabsorption and
Other Renal Functions’, Kidney International, 29 (1986), 32–40.
Crook, M. A. Clinical Chemistry and Metabolic Medicine, 7th edn (London: Hodder
Arnold, 2006).
Daniels, R. ‘Surviving the First Hours in Sepsis: Getting the Basics Right (An
Intensivist’s Perspective)’, Journal of Antimicrobial Chemotherapy, 66 (Suppl 2)
(2011), ii11–ii23, doi:10.1093/jac/dkq515.
Copyright © 2016. Macmillan Education UK. All rights reserved.

Dellinger, R. P., M. Levy, A. Rhodes et al.. ‘Surviving Sepsis Campaign: International

Guidelines for Management of Severe Sepsis and Septic Shock 2012’, Critical Care
Medicine Journal, 41(2) (2013), 580–637, doi: 10.1097/CCM.0b013e31827e83af.
Faubel, S., C. L. Edelstein and R. E. Cronin. ‘The Patient with Acute Renal Failure’,
in R. W. Schrier (ed.), Manual of Nephrology, 6th edn (Philadelphia: Lippincott
Williams and Wilkins, 2005).
Feest, T. G., A. Round and S. Hamad. ‘Incidence of Severe ARF in Adults: Results of a
Community Based Study’, British Journal of Medicine, 306 (1993), 481–3.
Fiaccadori, E., M. Lombardi, S. Leonardi, C. F. Rotelli, G. Tortorella and A. Borghetti.
‘Prevalence and Clinical Outcome Associated with Pre-existing Malnutrition in
Acute Renal Failure: A Prospective Cohort Study’, Journal of American Society of
Nephrology, 10 (1999), 581–93.

Fiaccadori, E., G. Regolisti and A. Cabassi. ‘Specific Nutritional Problems in Acute

Kidney Injury, Treated with Non-dialysis and Dialytic Modalities’, Nephrology
Dialysis Transplantation Plus (2009), 1–7. doi:10.1093/ndtplus/sfp017.
Finlay, S., B. Bray, A. J. Lewington, C. T. Hunter-Rowe, A. Banerjee, J. M. Atkinson and
M. C. Jones. ‘Identification of Risk Factors Associated with Acute Kidney Injury in
Patients Admitted to Acute Medical Units, Clinical Medicine, 13(8) (2013), 233–8.
Gammelager, H., C. F. Christiansen, M. B. Johansen et al.. ‘One-year Mortality among
Danish Intensive Care Patients with Acute Kidney Injury: A Cohort Study’, Critical
Care, 16 (2012), R124. doi: 10.1186/cc11420.
Goldberg, L. ‘Biochemical Investigations’, in P. Glynne, A. Allen and C. Pusey (eds),
Acute Renal Failure in Practice (London: Imperial College Press, 2002).
Hegarty, J., R. Middleton, M. Krebs, H. Hussain, C. Cheung, T. Ledson, A. Hutchison,
P. A. Kalra, H. Rayner, P. Stevens and D. O’Donoghue. ‘Severe Acute Renal Failure
in Adults: Place of Care, Incidence and Outcomes’, Quarterly Journal of Medicine,
98(8) (2005), 661–6.
Hilton, R. ‘Acute Renal Failure’, British Medical Journal, 333 (2006), 786–90.
Ho, K. M. and D. J. Sheridan. ‘Meta-analysis of Frusemide to Prevent or Treat Acute
Renal Failure’, British Medical Journal, 430 (2006), 330.
Holley, J. ‘Clinical Approach to the Diagnosis of Acute Renal Failure’, in A. Greenberg
(ed.), Primer on Kidney Disease, 3rd edn (San Diego: Academic Press, 2001).
Hoste, E. A., S. I. Blot, N. H. Lameire, R. C. Vanholder, D. de Bacquer and F. A.
Colardyn. ‘Effect of Nonsocomial Bloodstream Infection on the Outcome of
Critically Ill Patients with Acute Renal Failure Treated with Renal Replacement
Therapy’, Journal of American Society of Nephrology, 15 (2004), 454–62.
Hsu, C. Y., J. D. Ordonez, G. M. Chertow, D. Fan, C. E. McCuloch and A. S. Go.
‘The Risk of Acute Renal Failure in Patients with Chronic Kidney Disease’, Kidney
International, 74 (2008), 101–7.
Jefferson, J. A., J. M. Thurman and R. W. Schrier (eds). ‘Pathophysiology and Aetiology
of Acute Kidney Injury, in J. Floege, R. J. Johnson and J. Feehally, Comprehensive
Nephrology, 797–812 (St Louis: Saunders, 2010).
Kellum, J. A. and J. Decker. ‘Use of Dopamine in Acute Renal Failure: A Meta-analysis’,
Critical Care Medicine, 29(8) (2001), 1526–31.
Khan I. H., G. R. Catto, N. Edward, and A. M. MacLeod. ‘Acute Renal Failure: Factors
Influencing Nephrology Referral and Outcome’, Quarterly Journal of Medicine, 90
Copyright © 2016. Macmillan Education UK. All rights reserved.

(1997), 781–5.
Koeppen, B. M. and B. A. Stanton. Renal Physiology, 3rd edn (St Louis: Mosby, 2001).
Lamiere, N., W. van Biesen and R. Vanholder. ‘Acute Renal Failure’, Lancet, 365
(2005), 417–30.
Lewington, A. and N. S. Kanagasundaram. Clinical Practice Guidelines: Acute Kidney
Injury (London: Renal Association, 2011) [Online]. Available from: www.renal.
org/guidelines/modules/acute-kidney-injury#sthash.LEeva74i.dpbs (accessed 30
May 2015).
McGee, S., W. B. Abernathy and D. L. Simel. ‘Is This Patient Hypovolaemic?’, Journal
of the American Medical Association, 281(11) (1999), 1022–9.
MacPhee, I. ‘Urine Output and Urinalysis’, in P. Glynne, A. Allen and C. Pusey (eds),
Acute Renal Failure (London: Imperial College Press, 2002).

Macedo, E. and R. L. Mehta. ‘Timing of Dialysis Initiation in Acute Kidney Injury and
Acute-on-chronic Kidney Injury’, Seminars in Dialysis, 26(6) (2013), 675–81, doi:
10.1111/sdi.12128.
Mahoney, B. A., W. A. D. Smith, D. S. Lo, K. Tsoi, M. Tonelli and C. M. Clase.
‘Emergency Interventions for Hyperkalaemia’, Cochrane Database of Systematic
Reviews, 2 (2005), art. no. CD003235. doi: 10.1002/14651858.CD003235.pub2.
Mehta, R. L., J. A. Kellum, S. V. Shah, B. A. Molitoris, C. Ronco, D. G. Warnock, A.
Levin and the Acute Kidney Injury Network. ‘Acute Kidney Injury Network: Report
of an Initiative to Improve Outcomes in Acute Kidney Injury’, Critical Care, 11(2)
(2007) [Online]. Available from: http://ccforum.com/content/11/2/R31.
Meyer, T. W. and T. H. Hostetter. ‘Pathophysiology of Uraemia’, in Brenner and
Rector’s The Kidney, 8th edn (Philadelphia: Saunders Elsevier, 2007).
Morgera, S., M. Schneider and H. H. Neumeyer. ‘Long-term Outcomes after Acute
Kidney Injury’, Critical Care Medicine, 36 (2008), S193–7.
Nadeau-Fredette, A-C and J. Bouchard. Fluid Management and Use of Diuretics in
Acute Kidney Injury@, Advances in Chronic Kidney Disease, 20(1) (2013), 45–55.
National Collaboration for Chronic Conditions. Chronic Kidney Disease: National
Clinical Guideline for Early Identification and Management in Adults in Primary and
Secondary Care (London: Royal College of Physicians, 2008).
National Confidential Enquiry into Patient Outcomes and Death (NCEPOD).
Adding Insult to Injury: A Review of the Care of Patients who Died in Hospital with a
Primary Diagnosis of Acute Kidney Injury (Acute Renal Failure) (London: NCEPOD,
2009) [Online]. Available from: www.ncepod.org.uk/2009report1/Downloads/
AKI_report.pdf (accessed 30 May 2015).
National Health Service (NHS) England. ‘Patient Safety Alert on Standardising the
Early Identification of Acute Kidney Injury’ (2014) [Online]. Available from: www.
england.nhs.uk/2014/06/09/psa-aki/ (accessed 1 June 2015).
National Institute for Health and Care Excellence (NICE). Acutely Ill Patients in
Hospital: Recognition of and Response to Acute Illness in Adults in Hospital (London:
National Institute for Clinical Excellence, 2007).
National Institute for Health and Care Excellence (NICE). Acute Kidney Injury:
Prevention, Detection and Management up to the Point of Renal Replacement Therapy,
NICE Clinical Guideline CG:169 (2013) [Online]. Available from: www.nice.org.uk/
Guidance/CG169 (accessed 30 May 2015).
Copyright © 2016. Macmillan Education UK. All rights reserved.

O’Driscoll, B. R., L. S. Howard and A. G. Davison. ‘BTS Guidelines for Emergency

Oxygen Use in Adults’, Thorax, 63(suppl. VI) (2008), vi1–vi10.
Pannu, N. and P. F. Halloran. ‘The Aging Kidney’, in A. Greenberg (ed.), Primer on
Kidney Disease, 3rd edn (San Diego: Academic Press, 2002).
Perel, P. and I. G. Roberts. ‘Colloids versus Crystalloids for Fluid Resuscitation in
Critically Ill Patients’, Cochrane Database of Systematic Reviews, 4 (2007), art. no.
CD000567. doi: 10.1002/14651858.CD000567.pub3.
Provan, D. and A. Krentz. Oxford Handbook of Clinical Laboratory Investigations
(Oxford: Oxford University Press, 2002).
Prowle, J. R., J. E. Echeverri, V. Ligabo, C. Ronco and R. Bellomo ‘Fluid Balance and
Kidney Injury’, Nature Reviews Nephrology, 6 (2010), 107–15.

Ragaller, M. J. R., H. Theilen and T. Koch. ‘Volume Replacement in Critically Ill

Patients with Acute Renal Failure’, Journal of the American Association of Nephrology,
12 (2001), S33–S39.
Renal Association. eGFR Calculator (2011) [Online]. Available from: http://egfrcalc.
renal.org/ (accessed 01 June 2015).
Renal Association. ‘Treatment of Acute Hyperkalaemia in Adults, Clinical Guidelines’
(London, UK: Renal Association, 2014) [Online]. Available from: www.renal.
org/docs/default-source/guidelines-resources/joint-guidelines/treatment-of-acute-
hyperkalaemia-in-adults/hyperkalaemia-guideline-march2014pdf (accessed 26
January 2016).
Royal College of Physicians (RCP). ‘National Early Warning Score (NEWS) –
Standardising the Assessment of Acute-illness Severity in the NHS’ (2012). www.
rcplondon.ac.uk/resources/national-early-warning-score-news (accessed 9 April
2015).
Salama, A. ‘Haemolytic Uraemic Syndrome and Thrombocytopaenic Purpura’, in
P. Glynne, A. Allen and C. Pusey (eds), Acute Renal Failure in Practice (London:
Imperial College Press, 2002).
Steddon, S., N. Ashman, A. Chesser and J. Cunningham. ‘Acute Renal Failure’, in
S. Steddon, N. Ashman, A. Chesser and J. Cunningham (eds), Oxford Handbook of
Nephrology and Hypertension (Oxford: Oxford University Press, 2006).
Stevens, P., A. Davenport, S. Kanagasundaram and A. Lewington. Acute Renal Failure
(Acute Kidney Injury), Clinical Practice Guidelines (London: The Renal Association,
2008).
Thakar, C. V. ‘Perioperative Acute Kidney Injury’, Advances in Chronic Kidney Disease,
20(1) (2013), 67–75.
Vanholder, R., R. de Smet, G. Glorieux et al.. for the European Uremic Toxin Work
Group (EUTOX). ‘Review on Uremic Toxins: Classification, Concentration, and
Interindividual Variability’, Kidney International, 63 (2003), 1934–43.
Weisberg, L. S. ‘Management of Severe Hyperkalaemia’, Critical Care Medicine, 36(12)
(2008), 3246–51.
Copyright © 2016. Macmillan Education UK. All rights reserved.

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Acute Kidney Injury: Mark Bevan

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Acute Kidney Injury: Mark Bevan

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8

Acute Kidney Injury

a rise in serum creatinine of 26 micromol/l or greater within 48 hours; a 50%

For full AKI staging criteria see Table 8.1.

ingful information is forthcoming, providing a more accurate picture. Case

Table 8.1 Criteria for diagnosis of acute kidney injury

AKI stage Serum creatinine criteria Urine output criteria

1 Increase in serum creatinine of 26 Less than 0.5 mL/kg/hour for

2 Increase in serum creatinine to more Less than 0.5 mL/kg/hour for

3 Increase in serum creatinine to more Less than 0.3 mL/kg/hour

Source: Adapted from Mehta et al. (2007)

use of ICU and risk of mortality (Challiner et al., 2014).

Aim and Learning Outcomes

1. Define AKI and distinguish between the differing manifestations of AKI.

The Case Scenario: The Presenting Complaint

Ralph is an 80-year-old man who lives in an elderly care home. He is usually

The Case Scenario continued

His vital signs were recorded as:

Consider the following:

1. With reference to the underlying pathophysiology describe what is meant

Acute Kidney Injury

Table 8.2 Summary of the assessment of the AKI patient

History Presenting condition, symptoms, past medical history,

Clinical examination Vital signs (BP, P, resps)

Urine Output, volume

Blood Estimated GFR: creatinine

ECG LVF, dysrhythmia, MI

Imaging Ultrasound, X-ray, CT scan, MRI, urography, nuclear

medicine, angiography, cystoscopy

Acute Kidney Injury

Pre-Renal AKI Intrinsic AKI Post-Renal AKI

Glomerular injury Tubular Injury Interstitial Injury Vascular Injury

Figure 8.1 Causes of acute kidney injury

Figure 8.2 The nephron

The cellular activity of the kidney requires a huge amount of oxygen.

Table 8.3 Examples of causes of pre-renal AKI

Cause Examples of common problems

Cardiac Congestive cardiac failure, cardiac surgery, arrhythmia

Volume Burns, bleeding, vomiting, diarrhoea, diuresis

Vascular resistance Shock, antihypertensive treatment, NSAIDs, ACE

Vascular patency Renal artery thrombosis, abdominal aortic aneurysm

Table 8.4 Causes of volume depletion

Total intravascular depletion Effective volume depletion

Haemorrhage Reduced cardiac output: congestive cardiac

Renal fluid loss: diuretics, osmotic Peripheral vasodilation: sepsis, anaphylaxis,

Gastrointestinal loss: vomiting,

Skin fluid loss: burns, sweating

Third space syndrome: pancreatitis,

Source: Adapted from Faubel et al. (2005)

However, additional factors, including commonly used drugs such as

Afferent Arteriole Efferent Arteriole

Glomerulus Bowman’s capsule

Figure 8.3 The glomerulus

Table 8.5 Examples of causes of intrinsic AKI

Vascular Glomerular Tubular Interstitial

The glomerulus is where filtering of the blood occurs (Figure 8.3).

cell leakage (as found in glomerulonephritis). As already noted, the nephron

Intrinsic AKI: Glomerular Disease

2 grams in 24 hours is called nephritic. Such conditions include Henoch–

Intrinsic AKI: Tubular Disease

Intrinsic AKI: Interstitial Disease

Risk Factors for AKI

Table 8.6 Examples of causes of post-renal AKI

Intraureteral obstruction Bladder and urethral Obstruction by external

Stones Urethral stricture Malignancy: rectal,

Table 8.7 Risk factors for AKI

• CKD (eGFR < 60 mL/min/1.73m2)

Source: Adapted from NICE (2013)

The Case Scenario: The Immediate Assessment Priorities

The Case Scenario continued

Assessment and Reaching a Diagnosis

and circulation is essential especially because AKI is potentially a life-threat-

Airway and Breathing

sounds regularly and to monitor oxygen saturations using pulse oximetry

effect and is believed not to be the cause of uraemic symptoms, requiring

Table 8.8 Signs and symptoms of uraemia (some features may be

1. With reference to the underlying pathophysiology describe what is meant

Table 8.8 Signs and symptoms of uraemia (some features may be

1. Consider the appropriate ongoing assessment and monitoring required for