The management of
acute renal failure
Andrew Slack
Serene Ho
Lui G Forni
At-risk populations
The two main in-hospital patient groups at increased risk of
ARF are those with pre-existing renal impairment and associated
co-morbidities, and those at risk of iatrogenic ARF. The first group
includes elderly patients and those with underlying chronic renal
impairment of any cause. Co-morbidities such as congestive
cardiac failure and hepatic disease add to the increased risk of
ARF following relatively mild insults. Those at risk of iatrogenic
ARF include patients undergoing major surgery or radiological
procedures involving intravenous contrast agents. Practically, in
the hospital environment there is considerable overlap between
the two groups.
Abstract
Acute renal failure is a commonly encountered condition in the hospital
setting. In many cases accurate history-taking, careful examination of the
patient and meticulous monitoring of volume balance may reverse this
process. However, acute renal failure presents a unique set of metabolic
derangements which, if untreated, will result in death. We outline the
initial management of acute renal failure as well as the specific treatments that may be required. Some consideration is also given to the use
of renal replacement therapies.
Prevention of ARF
Management of ARF
General management
Early recognition and treatment of ARF saves nephrons and
prevents further decline in the GFR. Importantly, the measured
serum creatinine may not actually rise appreciably until GFR
has fallen significantly. This is of particular relevance in individuals of small build, vegetarians and the undernourished
where a value in the normal range can be misleading. The
mainstay of treatment in ARF is aimed at minimizing damage
to surviving nephrons whilst providing support until the kidney
recovers. This includes restoration of the circulating volume,
relief of outflow obstruction if present, removal of tubular toxins
and specific treatment of glomerular disease. Early restoration of renal perfusion in precipitant ARF due to acute tubular
necrosis is essential. Recovery of GFR depends on the number
of remaining functional nephrons, which increase their filtration
to maintain GFR. However, continued hyperfiltration may lead
to progressive glomerular sclerosis and nephron death leading to
end-stage renal failure.
As there is no specific therapy for ARF, management should be
focused on addressing the causes as well as correcting metabolic
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Hyperkalaemia
This life-threatening complication requires immediate treatment
and arises through cellular shifts of potassium or release from
lysed cells together with decreased renal excretion of potassium.
Acidosis, hyponatraemia and hypocalcaemia all potentiate the
deleterious effects of hyperkalaemia on cardiac function and
hence must also be corrected. Presentation is non-specific, muscle weakness may be present, which if severe can lead to flaccid
paralysis, although symptoms rarely manifest until the plasma
potassium concentration exceeds 7.0 mmol/l. The most serious
concern is the effect on cardiac conduction, which classically
presents as a shortened QT interval with a tall peaked T wave
on the electrocardiograph (ECG). Progressive lengthening of the
QRS duration and the PR interval without treatment ultimately
progresses to a sine wave followed by ventricular standstill
or fibrillation. A variety of other conduction disturbances may
occur including bundle-branch block (left or right), bifascicular block and advanced atrioventricular block. All patients with
ARF should have continuous cardiac monitoring and immediate
therapy is warranted if ECG changes or neuromuscular abnormalities occur. Asymptomatic patients with a plasma potassium
concentration of less than 6.5 mmol/l or whose ECG does not
manifest signs of hyperkalemia can be treated with a cation
exchange resin, such as calcium resonium, and a low potassium
diet. Additional sources of potassium intake should be stopped
and any potentiating drugs discontinued.
Specific treatment of hyperkalaemia is directed at removing
excess potassium, shifting extracellular potassium into the cells
or antagonizing its membrane effects. Calcium directly antagonizes the actions of hyperkalaemia and, although short-lived, the
effect begins within minutes. Hyperinsulinaemia can be achieved
through giving insulin and glucose intravenously which stimulates Na/K-ATPase activity, causing a shift of potassium into
cells. Effective therapy usually leads to a 0.51.5 mmol/l fall in
Specific problems
Volume resuscitation
In hypovolaemia, volume expansion is recommended. However,
uncontrolled volume substitution may result in clinical deterioration and should be avoided. Isotonic crystalloids remain the
mainstay of volume replacement therapy correcting sodium
depletion as well as restoring solute and water diuresis. Crystalloids expand plasma volume by about 25% of the infused volume however, large-volume saline infusion can be associated
with a hyperchloraemic acidosis which may be associated with
renal vasoconstriction and gut hypoperfusion.8 Colloids, which
include albumin, gelatins and hydroxyethyl starch, result in volume expansion approximate to the infused volume. These should
be used with caution in ARF due to the associated risk of osmotic
nephrosis (osmotic tubular damage) if administered in isolation,
although a recent study comparing the use of 4% albumin compared to saline failed to demonstrate any significant differences
in outcome.9 The hydroxyethyl starches are highly polymerized
sugars characterized by their molecular weight, grade of substitu
tion and concentration. They are degraded through hydrolytic
cleavage, the remnants of which are excreted by the kidney, and
should be avoided in ARF particularly when due to sepsis.
Volume overload
The volume status of a patient with ARF needs to be assessed
carefully. Although somewhat unfashionable, careful bedside
examination including assessment of the venous pressure, capillary refill time, pulse and postural blood pressure changes are
elementary tool for assessing volume status. Hourly urine-output
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Acidosis
Metabolic acidosis in ARF results from increased acid production, increased acid retention and decreased renal reabsorption
of bicarbonate. Acidosis is exacerbated by sepsis, malnutrition and some drugs. Mild acidosis (pH > 7.2) can usually be
reversed with adequate volume resuscitation. Sodium bicarbonate either intravenously or orally may be used if the acidosis is
severe (pH <7.2 or HCO3 1015mmol/l). Although some authors
express caution with regard to the generation of a paradoxical
acidosis on bicarbonate administration, in clinical practice this
is not a problem. The argument stems from the observation that
on addition of sodium bicarbonate to a weakly acidified solution
CO2 is generated. Since there is no significant gradient between
intracellular and extracellular CO2 it is argued that this results in
an increase in intracellular CO2, thus worsening the acidosis. The
evidence for this comes from in vitro work far removed from the
physiological, as well as animal work where predetermined ventilatory restraints were imposed. In effect these studies have used
a closed system whereas in spontaneously breathing patients,
or indeed one being adequately mechanically ventilated, the system is open allowing for CO2 removal.13,14 However, if large
volumes of isotonic sodium bicarbonate in ARF are employed,
they should be used with caution due to observed volume expansion and development of hypernatraemia.
Uraemic pericarditis
Uraemic pericarditis is observed in 610% of patients with
advanced renal failure resulting from inflammation of both the
visceral and parietal membranes of the pericardial sac. Pericarditis in ARF presents with fever and pleuritic chest pain characteristically worse in the recumbent position and a pericardial rub
may be heard on auscultation, although the ECG does not show
the typical diffuse ST and T wave elevations observed with other
causes of acute pericarditis. The development of pericarditis in a
patient with ARF is an indication to institute RRT unless there are
signs of cardiac tamponade due to a pericardial effusion. Under
such conditions, heparin-free hemodialysis or haemofiltration
should be used due to the risk of increased bleeding into the
pericardial sac with anticoagulation.
Uraemic encephalopathy
Uraemic encephalopathy together with uraemic pericarditis tends
to be related to the degree of uraemia. Early clinical features
include rambling speech, disorientation, lethargy, irritability and
hallucinations and, more rarely, coma. Commonly encountered
signs include tremor, myoclonus, and asterixis which tend to
occur with deterioration in mental status. Rarely, transient focal
signs may occur such as hemiparesis or reflex asymmetry but
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Biochemical
Hyperkalaemia resistant to
medical therapy
Acidosis resistant to medical
therapy
Drug overdosage, e.g. lithium
Uraemic pericarditis
Table 1
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