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ACUTE RENAL FAILURE

Acute Renal Failure

Whats new ?

Alison J Armitage

There is accumulating evidence that so-called


renal-dose dopamine is of no use in the prevention or
treatment of ARF

Charlie Tomson

Loop diuretics increase urine output in patients with less


severe renal injury, but the resulting increase in urine
output does not improve outcome
If colloids, rather than crystalloids, are used in
resuscitation, gelatin solutions are more likely to prevent
ARF than hydroxyethyl starch

Acute renal failure (ARF) is a common medical emergency with a


significant mortality. In developed countries, at least 50% of cases
of ARF develop in hospital and are therefore potentially preventable. Because ARF can occur in various settings, all doctors must
be aware of the basic principles involved in its management and
know when to seek expert help.

Apart from adequate fluid resuscitation, the only


intervention shown to reduce the risk of renal failure in
critically ill patients is tight glycaemic control

several days after a sudden marked reduction in GFR, even if GFR


starts to improve immediately.

Definitions
ARF is defined as a reduction in glomerular filtration rate (GFR)
occurring over days or weeks. This is an imprecise definition, with
respect to both the change in GFR required and the length of time
over which the change develops. However, it is useful for practical purposes. In routine clinical practice, measurement of serum
creatinine is used to follow changes in GFR. Common working
definitions of ARF are as varied as:
an increase in serum creatinine of > 50 mol/litre
an increase in serum creatinine of > 50% from baseline
a reduction in calculated creatinine clearance of > 50%
need for dialysis.
Considerable caution is required in interpreting measurements of
serum creatinine in ARF, for several reasons as follows.
Creatinine production depends on muscle mass, and though
normally constant can increase in patients with acute muscle injury
(as in rhabdomyolysis).
Creatinine concentration may exhibit a modest decrease as a
result of dilution during rapid fluid resuscitation (e.g. an increase
in extracellular fluid volume from 12 litres to 14 litres reduces
serum creatinine from 300 to 257 mol/litre).
Because of the reciprocal relationship between creatinine concentration and GFR, small changes in GFR close to the normal
range have much less effect on serum creatinine than small changes
when GFR is already significantly reduced (Figure 1).
Changes in serum creatinine concentration lag behind changes
in GFR. Creatinine concentration may continue to increase for

Epidemiology
The incidence of severe ARF (defined as an acute increase in
serum creatinine to > 500 mol/litre) is about 140/million/year.
In Scotland, the incidence of ARF requiring dialysis was recently
estimated at about 130/million/year. Less severe ARF (defined
as an increase in serum creatinine to 177 mol/litre or by 50%

Reciprocal relationship between creatinine concentration


and glomerular filtration rate

Plasma creatinine concentration (mol/litre)

1400

Alison J Armitage is a Specialist Registrar at Southmead Hospital,


Bristol, UK. She qualified from the University of Bristol, and is training
in nephrology and general medicine on the South West Rotation. Her
research interests include renal epidemiology and health services
research.

High muscle mass


Low muscle mass
1000

800

600

400

200

20

40

60

80

100

120

140

Glomerular filtration rate (ml/minute)


Note that plasma creatinine levels vary with muscle mass. In
patients with low muscle mass, serum creatinine remains within
the normal laboratory range despite the fact that glomerular
filtration rate is about 30 ml/minute lower.

Charlie Tomson is Consultant Nephrologist at Southmead Hospital,


Bristol, UK. He trained in Newcastle upon Tyne and Leicester, and was a
consultant at St Bartholomews Hospital, London. His research interests
include the causes of cardiovascular pathology in renal disease.

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ACUTE RENAL FAILURE

from baseline) occurs in about 210/million/year. About 50% of


all episodes of ARF occur in patients in whom renal function was
normal on admission to hospital.

Post-renal ARF: increased pressure within the renal collecting


systems results in reduced GFR, reduced tubular reabsorption
of sodium and water, and acquired renal tubular acidosis, phosphaturia and other abnormalities of tubular function. These abnormalities may persist after relief of bilateral obstruction. In addition, obstruction leads to tubulo-interstitial inflammation, caused
by infiltrating macrophages and T lymphocytes and followed by
fibrosis, resulting in incomplete recovery of renal function if the
obstruction is not rapidly relieved.

Pathophysiology
Pre-renal ARF is an appropriate physiological response to effective
or true hypovolaemia, resulting in intense renal conservation of
sodium and water at the expense of decreased GFR. Urea clearance
decreases more than creatinine clearance as a result of the action of
antidiuretic hormone (ADH). By definition, renal function returns
to normal rapidly once the underlying cause is corrected. Reduction in renal arterial perfusion pressure below the level at which
autoregulation of GFR occurs is an important contributor. However,
in hypovolaemic or septic patients (in whom mean arterial blood
pressure may be maintained at normal levels by intense systemic
vasoconstriction), pre-renal ARF may still occur as a result of intrarenal vasoconstriction from increased sympathetic tone, increased
intra-renal production of angiotensin II, and the contribution of
venous pressure receptors to the afferent limb of the reflexes that
cause pre-renal ARF. The early phase of sepsis causes peripheral
vasodilatation and increased cardiac output, as a consequence of
the production of nitric oxide by inducible nitric oxide synthase.
In the renal circulation, however, this leads to feedback inhibition
of constitutive endothelial nitric oxide synthase, resulting in renal
vasoconstriction.

Aetiology
Pre-renal ARF is defined as a reduction in GFR caused by impaired
renal perfusion as a result of hypotension or hypovolaemia that is
rapidly reversed by correction of the underlying cause.
Intrinsic renal disease: the principal causes of ARF caused by
intrinsic renal disorders are listed in Figure 2. ATN and drug
nephrotoxicity are the most common causes in this group.
Post-renal ARF: obstructive nephropathy is more often subacute
or chronic than acute, but often presents as an emergency and
is treated as a form of ARF because it is at least partially reversible on relief of obstruction. The most common cause is benign
or malignant prostatic bladder outflow obstruction; other causes
include infiltrative bladder cancer (causing bilateral vesicoureteric obstruction), other pelvic malignancies, radiation fibrosis,
bilateral stone disease, and retroperitoneal fibrosis with or without
abdominal aortic aneurysm.
Complete bilateral obstruction causes anuria, but is rare. Partial
chronic bilateral obstruction commonly leads to an increase in
urine flow rate as a result of impaired salt and water reabsorption.
Symptoms are very variable. In patients with high-pressure chronic
retention causing renal failure, presenting symptoms may include
nocturnal enuresis and voiding lower urinary tract symptoms (e.g.
poor stream). Chronic back pain is a feature of retroperitoneal
fibrosis. The initial investigation of choice is renal ultrasonography,
which shows bilateral hydronephrosis and may help to identify
the level of obstruction. In rare cases, however, obstructive renal
damage occurs without significant dilatation of the pelvicalyceal
system; this usually results from encasement by tumour.

Acute tubular necrosis (ATN): acute tubular necrosis is an inaccurate term, because necrosis is seldom seen in renal biopsies
taken from patients with this syndrome. It results from the insults
that cause pre-renal ARF, but lasting long enough to cause ischaemic injury to renal tubules. This leads to a long-lasting reduction
in GFR that sometimes persists for weeks after correction of the
initiating insult. This is caused by a combination of:
persistent, intense intra-renal vasoconstriction caused by
endothelin, other autocrine mediators and increased intracellular calcium
loss of polarity of tubular cells, leading to loss of function
loss of adherence of tubular cells, leading to desquamation into
the tubular lumen
formation of tubular casts, blocking the lumen and preventing
urine flow
tubuloglomerular feedback (reflex reduction of glomerular
perfusion caused by high sodium concentration in the distal
tubule)
back-leak of tubular filtrate as a result of loss of tubular viability
and obstructing casts
reperfusion injury, causing oxidant stress.
These observations have led to many attempts to alter the natural history of ATN using, for example, vasodilators, natriuretic
peptides, diuretics and growth factors, but almost all have been
unsuccessful.

Distinguishing acute from chronic renal failure


Raised serum creatinine in an acutely unwell patient can be
caused by ARF, acute-on-chronic renal failure or chronic renal
failure (CRF). These presentations have different prognoses and
may require fundamentally different management. The following
are important in distinguishing them.
Telephone the patients general practitioner, other hospitals
where he might have been managed, and the chemical pathology
laboratories serving his current and previous addresses, to obtain
any previous serum creatinine measurements.
Renal ultrasonography determines renal size and echogenicity,
and is imperative to exclude hydronephrosis (see below).
Reduced renal volume, length or cortical thickness, together
with increased echogenicity, is a feature of many types of CRF,
though renal size may remain normal in CRF (e.g. diabetic nephropathy, amyloidosis).

Intrinsic renal disease: the diseases listed in Figure 2 cause ARF


by numerous mechanisms, including:
destruction of glomeruli
renal arteriolar vasoconstriction (e.g. contrast nephropathy)
ischaemic damage, resulting in ATN
direct tubular toxicity, resulting in an ATN-like syndrome.

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Causes of acute renal failure secondary to intrinsic renal disease


Acute tubular necrosis
General surgery
Cardiac surgery
Vascular surgery
Obstetric complications
Sepsis
Acute heart failure
Burns

Renal embolism
Endocarditis, cardiac thrombus

Nephrotoxicity
Including aminoglycosides and amphotericin

Hypercalcaemia
Sarcoidosis, milkalkali syndrome

Contrast nephropathy
A specific form of nephrotoxicity characterized by renal
vasoconstriction and avid sodium retention

Intravenous immunoglobulin
Probably results from osmotic damage to proximal tubular
cells caused by sucrose in some intravenous immunoglobulin
preparations

Urate nephropathy
Complicating chemotherapy of acute leukaemia or lymphoma
Myeloma
Cast nephropathy, light-chain deposition disease, amyloidosis,
sepsis and hypercalcaemia can all cause renal damage

Impaired renal perfusion + drug-induced impairment of


autoregulation
Angiotensin-converting enzyme inhibitors, non-steroidal
anti-inflammatory drugs, plus atherosclerotic renal vascular
disease or hypovolaemia

Renal parenchymal disease


Rapidly progressive glomerulonephritis (systemic vasculitis,
Goodpastures disease, systemic lupus erythematosus, other
forms of glomerulonephritis)
Acute interstitial nephritis
Haemolytic uraemic syndrome
Cryoglobulinaemia

Hepatorenal syndrome
Reversible intense renal vasoconstriction and sodium retention
complicating cirrhosis

Malignant hypertension
Untreated primary (essential) hypertension or complicating
chronic glomerulonephritis

Poisoning
Including paracetamol, often after recovery from liver damage
Rhabdomyolysis
Following crush injury, drug overdose, status epilepticus

Renal vein thrombosis


Complicating malignancy or pre-existing nephrotic syndrome

Atheroembolism (cholesterol embolism)


Spontaneous or complicating angiography, anticoagulation or
thrombolysis

Acute pyelonephritis
Seldom causes acute renal failure, but ?more likely to do so in
the elderly and in those taking non-steroidal
anti-inflammatory drugs
Infection in patients with diabetes and partial obstruction
(e.g. from papillary necrosis) may cause emphysematous
pyelonephritis and acute renal failure

Raised intra-abdominal pressure (abdominal compartment


syndrome)
Caused by intra-abdominal pressure > 25 mm Hg
(e.g. postoperative abdominal exploration, tense ascites)

give clues; for example, the presence of gas in emphysematous


pyelonephritis (Figure 4).

Renal swelling is seen only in ARF.


Renal size is normal in most patients with ARF.
Anaemia is a feature of CRF, but may occur early in the course
of many diseases that cause ARF.
Bone disease evidence of long-standing renal bone disease
(e.g. radiological evidence of hyperparathyroidism, very high parathyroid hormone levels) is diagnostic of CRF, but hypocalcaemia
and hyperphosphataemia may occur in both ARF and CRF.

Urine microscopy and urinalysis: dipstick tests for haematuria


and proteinuria are positive in rapidly progressive glomerulonephritis (RPGN) and should prompt further investigation. Phasecontrast microscopy of carefully centrifuged fresh urine (liquid
renal biopsy) is helpful in identifying casts formed in renal tubules
from intact cells or cell debris, but is seldom undertaken in routine laboratories, which are geared towards the detection of lower
urinary tract infection (UTI). RBC casts are highly suggestive of
glomerular bleeding, as in RPGN; WBC casts are diagnostic of
acute pyelonephritis. Broad, waxy casts are seen in ATN. Positive
urinalysis is always abnormal, is not characteristic of pre-renal ARF,

Investigations
Renal ultrasonography: as discussed above, ultrasonography
assesses renal size and echogenicity and the presence or absence
of hydronephrosis (Figure 3). Occasionally, other appearances may

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Fractional excretion of urea ([urine urea/plasma urea]/[urine


creatinine/plasma creatinine] x 100%) is less affected by diuretic
therapy and may be a more useful discriminant of pre-renal ARF
and ATN; values of less than 35% suggest pre-renal ARF. However,
treatment of both pre-renal ARF and established ATN requires
prompt and continued correction of hypovolaemia, so these measurements are seldom helpful in guiding management.
Blood tests: in a few situations, blood tests give clues to the
underlying disorder (Figure 5).
Renal biopsy should be considered in all patients with normalsized, unobstructed kidneys in whom a diagnosis of ATN causing
ARF is not suspected. Renal biopsy should be performed without
delay when there is a clinical suspicion of RPGN (e.g. positive
antineutrophil cytoplasm antibodies, haematuria and proteinuria,
raised C-reactive protein), though it may be necessary to commence
immunosuppressive treatment while it is arranged.

3 The typical ultrasound appearance of a hydronephrotic kidney


caused by obstruction.

Management
Fluid resuscitation: aggressive, early fluid resuscitation is the
intervention most likely to ameliorate the course of pre-renal ARF
and ARF caused by ATN. It must be guided by regular clinical
assessment of the patients circulating volume, aided if there is
any doubt by measurements of central venous pressure (CVP) or
even pulmonary capillary wedge pressure.
Measurement of input and output strict fluid balance charts
are often demanded in patients with ARF. It is useful to know the

Blood test abnormalities suggesting specific


underlying renal disorders
4 CT scan showing gas in the right kidney in emphysematous
pyelonephritis. The infection was secondary to obstruction caused by a
sloughed papilla.

Abnormality
Eosinophilia
Very high creatine kinase,
phosphate, K+
Elevated lactate
dehydrogenase
Antineutrophil cytoplasm
antibodies

ATN or obstructive nephropathy, and should always be discussed


with a nephrologist after exclusion of UTI.
Urinary electrolytes: measurements of urinary sodium concentration and osmolality are often misleading, particularly in patients
who have taken diuretics or dopamine (both of which increase
urinary sodium excretion).
Very low urinary sodium excretion or fractional excretion
of sodium indicates that the ability of the tubules to reabsorb
sodium is intact, as in pre-renal ARF, rhabdomyolysis and contrast
nephropathy.
Very high urine osmolality indicates that the tubules are able to
reabsorb water under the influence of antidiuretic hormone, and
suggests pre-renal ARF.
Higher urinary sodium levels and lower osmolality are seen in
patients with ATN, but can occur in many other situations, including patients receiving diuretic treatment and normal individuals
without ARF.

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Antiglomerular basement
membrane antibody
Low C4 complement

Antinuclear antibody,
anti-dsDNA
Cryoglobulin
Plasma urate
Serum (and urine)
electrophoresis

Suggested underlying
disorder
Acute interstitial nephritis
Cholesterol embolism
Rhabdomyolysis
Renal infarction/embolism
Systemic vasculitis causing
rapidly progressive
glomerulonephritis
Goodpastures disease
Systemic lupus erythematosus,
cholesterol embolism,
cryoglobulinaemia
Systemic lupus erythematosus
Cryoglobulinaemia
Urate nephropathy
Myeloma

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It is absolutely illogical to give saline and diuretics at the same


time. Administration of diuretics to patients with a low CVP, or to
patients at risk of hypovolaemia in whom no CVP measurement
is available, is poor clinical practice.
Other agents, including thyroxine, epidermal growth factor,
endothelin antagonists, acetylcysteine, insulin-like growth factor
and atrial natriuretic peptides, have been subjected to clinical trials
in ARF, but all with disappointing or negative results. Intensive
insulin treatment in critically ill surgical patients has been shown
to halve the risk of ARF and requires further study in other settings
(van den Berghe et al.).

input and output, but these charts are often inaccurate because of
the difficulties of measuring all sources of fluid loss (e.g. insensible
losses, diarrhoea, vomitus, blood loss) and fluid gain (e.g. oral
intake, water generated from metabolism). Over-reliance on fluid
balance charts also carries the danger that fluid administration
will be adjusted according to recent output rather than the clinical
state of the patient; for example, it would be possible to clamp
a patient in a severely hypovolaemic state simply by matching
input to output. Positive fluid balance is a necessary part of the
resuscitation of patients with effective or true hypovolaemia.
Another reason for measuring urine output is to assess renal
function. Anuria and severe oliguria are diagnostic of severe ARF,
but urine volume is of little help in any other situation. The following is an extreme example.
A GFR of 100 ml/minute (6000 ml/hour) normally gives a urine
flow rate of about 60 ml/hour because of reabsorption of 99%
of the filtrate delivered to the renal tubules. However, a GFR of
1 ml/minute combined with complete failure of tubular reabsorption (resulting from tubular damage, as in ATN, or from high
doses of drugs that inhibit tubular reabsorption, e.g. dopamine,
furosemide) would also give a urine output of 60 ml/hour.
Changes in urine flow rate are therefore a very poor guide to
changes in GFR, and must be interpreted along with all the other
available clinical information.
Urethral catheters are often placed to enable accurate measurement of urine flow rate. For the reasons discussed above,
this is seldom as helpful as it appears. Urethral catheters are the
single most important source of hospital-acquired Gram-negative
septicaemia they should not be placed without good reason, and
should be removed as soon as possible.
Fluid challenges are often given in the hope that they will
stimulate diuresis as if a head of pressure would help to improve
renal perfusion. It is illogical (and dangerous) to give further fluid
to a patient who has already been fully resuscitated; if the patient
remains oliguric, the extra fluid load may cause life-threatening
pulmonary oedema. It is equally illogical to give 500 ml fluid
boluses to a hypovolaemic patient. The only rational use of fluid
boluses is in combination with CVP measurement; administration
of a fluid bolus to a hypovolaemic patient causes only a transient
increase in CVP, compared with a more sustained rise in patients
approaching euvolaemia.
Dopamine and loop diuretics low-dose dopamine is widely
used in the belief that it restores renal blood flow and improves
GFR. There is mounting evidence (including a recent large randomized controlled trial, Bellomo et al.) that this treatment is of
no benefit. The only setting in which dopamine is justified is as an
inotropic agent. Loop diuretics are also widely used. The rationale is that they may lessen tubular hypoxic damage by inhibiting
energy-dependent transport processes and flushing out tubular
casts. However, there is no clinical evidence that loop diuretics
improve outcome in ARF (Lassnigg et al.).
Loop diuretics and dopamine can both increase urine output
by reducing tubular reabsorption of filtrate, and this can fool the
unwary into believing that GFR has improved. The ability to mount
a diuresis in response to either drug probably identifies patients in
whom the prognosis is better, but there is no evidence that either
drug improves prognosis. Unless the patient is significantly volumeoverloaded, the diuresis caused by these drugs can exacerbate ATN
by causing further hypovolaemia.

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Choice of resuscitation fluid: adequate intravascular volume


replacement is essential in the management of ARF. However,
controversy continues over the optimal fluid for correction of
hypovolaemia.
Crystalloids (e.g. 0.9% saline, Hartmanns solution) are cheap
and safe, but rapidly distribute between the vascular space and
the extracellular space, resulting in oedema, pleural effusions and
ascites if used in high volumes, particularly in the presence of
increased endothelial permeability (as in systemic inflammatory
response syndrome).
Colloids (e.g. human albumin, dextrans, hydroxyethyl starch
HES, modified gelatins) are used in the hope that they will remain in the vascular space for longer and restore microcirculatory
flow more efficiently. This is probably the case in simple hypovolaemia caused by, for example, severe diarrhoea. However, when
plasma protein concentrations may be increased as a result of
haemoconcentration, crystalloids may be very effective. In sicker
patients with sepsis, endothelial permeability to macromolecules
is often increased, with the danger that these molecules will leave
the circulation, elevate interstitial oncotic pressure and exacerbate
the accumulation of fluid in the extracellular space.
A Cochrane meta-analysis of the use of human albumin (the
most physiological colloid available) in hypovolaemia, hypoalbuminaemia and burns patients showed a 6% greater mortality
than with crystalloids. One trial has since shown that 20% human
albumin improves renal outcome in patients with cirrhosis and
spontaneous bacterial peritonitis (Sort et al.), but interpretation
of the results depends critically on whether randomized patients
received adequate correction of hypovolaemia with crystalloids.
Other colloid solutions include gelatin preparations, dextran solutions and HES solutions. None of the available preparations are
free of potentially serious side-effects: in particular, dextrans can
cause anaphylactoid reactions and HES solutions may disrupt
coagulation mechanisms. Gelatin preparations have the shortest
half-life, but in a trial comparing gelatin with HES in critically ill
patients there was twice the incidence of ARF in the HES-treated
group.
A Cochrane meta-analysis comparing synthetic colloids with
crystalloids concluded that there was no proven clinical indication
for use of colloids in resuscitation. Nevertheless, many clinicians
continue to use these plasma expanders on the basis of their
theoretical advantages (e.g. longer plasma half-life, more effective
restoration of microcirculatory flow), despite the lack of evidence
of benefit.
Renal replacement therapy (RRT): many patients with mild-tomoderate ARF can be managed on general medical or surgical

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wards. Patients with multiple organ failure should be managed


in an ICU. Patients with ARF requiring RRT should be managed
on a renal ward. If in doubt, the renal unit should be telephoned
for advice early in the course of the disease, even if transfer of
the patient is not thought to be necessary. Specific reasons for
referral include:
inability to deliver resuscitation measures safely (e.g. absence
of CVP monitoring facilities for a patient with hypovolaemia
or sepsis)
unexplained ARF, particularly with abnormal urinalysis suggesting RPGN or another renal disease needing specific treatment
likely need for RRT (see below), including rapidly increasing
serum creatinine, oliguria (particularly in those with impending
or established pulmonary oedema), hyperkalaemia and severe
metabolic acidosis.
There is currently little evidence to guide decisions on when to
implement RRT in ARF. There is evidence suggesting that early
high-volume haemofiltration may confer benefit in meningococcal
septicaemia, but this may be a consequence of the removal of
inflammatory cytokines rather than of correction of the metabolic
abnormalities caused by ARF.
The options in RRT are usually continuous haemofiltration (more
commonly used in ICUs) and intermittent haemodialysis. Peritoneal
dialysis may be used in ARF, but is often complicated by fluid
leaks, difficulty in achieving satisfactory control of fluid balance,
and infection. A recent randomized trial in Vietnam showed that
continuous haemofiltration was superior to peritoneal dialysis in
terms of both overall outcome and cost-effectiveness (Phu et al.).
Complications of dialysis may prolong the course of ARF. For
example, hypotension caused by excessive fluid removal or by
vasodilatation from heat transfer in haemodialysis may worsen preexisting ATN. Inflammatory responses to the dialysis membrane
and/or pyrogens in the dialysate may also worsen ATN. Evidence
is emerging that haemodialysis using biocompatible membranes
and highly purified water for dialysate preparation gives better
outcomes than conventional haemodialysis. The dose of dialysis
may also be important; several studies have shown that outcome
is better in patients randomized to dialysis or haemofiltration
regimens with improved removal of urea. In patients with severe
lactic acidosis, additional benefit may be gained by performing
haemofiltration with bicarbonate-buffered replacement solution
rather than the usual lactate-based solutions.
Although dialysis is a necessary supportive measure, it is
important to establish the cause of ARF and treat this to speed
recovery.

REFERENCES
Bellomo R, Chapman M, Finfer S et al. Low-dose Dopamine in Patients
with Early Renal Dysfunction: A Placebo Controlled Randomised Trial.
Australian and New Zealand Intensive Care Society (ANZICS) Clinical
Trials Group. Lancet 2000; 356: 213943.
Lassnigg A, Donner E, Grubhofer G et al. Lack of Renoprotective Effects of
Dopamine and Furosemide during Cardiac Surgery. J Am Soc Nephrol
2000; 11(1): 97104.
Phu N H, Hien T T, Mai N T et al. Haemofiltration and Peritoneal Dialysis
in Infection-associated Acute Renal Failure in Vietnam. N Engl J Med
2002; 347: 895902.
Sort P, Navasa M, Arroyo V et al. Effect of Intravenous Albumin on Renal
Impairment and Mortality in Patients with Cirrhosis and Spontaneous
Bacterial Peritonitis. N Engl J Med 1999; 341: 4039.
van den Berghe G, Wouters P, Weekers F et al. Intensive Insulin Therapy
in the Surgical Intensive Care Unit. N Engl J Med 2001; 345:
135967.
FURTHER READING
Alderson P, Schierhout G, Roberts I et al. Colloids versus Crystalloids for
Fluid Resuscitation in Critically III Patients. Cochrane Database Syst
Rev 2000; 2: CD000567.
Blantz R C. Pathophysiology of Pre-renal Azotemia. Kidney Int 1998;
53(2): 51223.
Esson M L, Schrier R W. Diagnosis and Treatment of Acute Tubular
Necrosis. Ann Intern Med 2002; 137(9): 74452.
Human Albumin Administration in Critically III Patients: Systematic
Review of Randomised Controlled Trials. Cochrane Injuries Group
Albumin Reviewers. BMJ 1998; 317: 23540.
Lameire N, Vanholder R. Pathophysiologic Features and Prevention of
Human and Experimental Acute Tubular Necrosis. J Am Soc Nephrol
2001; 12: (Suppl. 17): S2032.
Metcalfe W, Simpson M, Khan I et al. Acute Renal Failure requiring Renal
Replacement Therapy: Incidence and Outcome. Q J Med 2002; 95:
57983.
Star R A. Treatment of Acute Renal Failure. Kidney Int 1998; 54(6):
181731.

Follow-up: patients with ARF who do not recover normal excretory function, or who had pre-existing renal impairment, should
not be discharged without a long-term plan for management of
CRF (see page 52). Patients who make a full recovery do not
require follow-up unless required for the underlying condition
that caused the ARF.

Practice points
Always discuss the patient with a nephrologist if in doubt
Beware of missing parenchymal renal disease; irreversible
renal damage may occur if appropriate specific treatment is not
initiated rapidly
Central venous catheters are more useful than urethral catheters
in the treatment of sick patients
The choice of resuscitation fluid is less important than the speed
and completeness of correction of hypovolaemia

Prevention
The fact that 50% of cases of ARF occur after admission to hospital
suggests a potential for prevention. This is largely by avoidance,
or early aggressive treatment, of sepsis and hypovolaemia, and
avoidance (when possible) of nephrotoxic drugs.
u

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