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DIAGNOSIS OF ACUTE KIDNEY FAILURE
Diagnosis
A
high index of clinical suspicion is required to diagnose acute
renal failure at an early stage of its development. This is
because symptoms and signs attributable to the accumulation of
fluid, electrolytes, acid or uraemic wastes within the body may
not be apparent until the condition is far advanced.
Furthermore, the symptoms and signs that may arise are not
specific: unsuspected hyperkalaemia is the greatest danger,
since this may produce no symptoms whatsoever before causing
cardiac arrest.
All
patients admitted to hospital with acute illness should be
considered at risk of developing acute renal failure. Those who
have some pre-existing chronic impairment of renal function are
particularly susceptible to acute exacerbations. This group
includes all elderly patients, in whom a combination of low
muscle mass and low dietary meat consumption may conspire to
maintain an apparently 'normal' plasma creatinine level, despite
a reduction in glomerular filtration rate to as little as 25 per
cent of that expected in a healthy young adult.
To
recognize impairment of renal function early, the basic care of
all acutely ill patients should include careful monitoring of
fluid input and output, daily weighing, lying and standing (or
sitting) blood pressure, and regular estimation of plasma
creatinine, urea, and electrolytes.
Although it might seem to the physician to be a simple matter to
monitor fluid input and output, this simplicity is often only
present in theory, excepting in patients who are restricted to
parenteral fluids and who have a urethral catheter. Drinks may
be spilt, extra drinks may be acquired from a variety of
sources, urine may be spilt, and vomit and diarrhoea are often
found in places where they are difficult to quantitate. These
considerations mean that the most likely explanation for fluid
balance charts being difficult to interpret is the erroneous
recording of input or output.
Daily weighing on accurate scales provides a much more reliable
picture of net overall fluid balance. Patients who are acutely
ill invariably lose flesh weight, commonly at a rate of up to a
few hundred grams per day. If weight appears to fall at a rate
faster than this, then negative fluid balance is likely: the
occurrence of greatly increased 'insensible' losses through the
skin and lungs during fever being a common explanation.
Aside from weight loss, the development of a postural drop in
blood pressure is a reliable sign that a patient has become
significantly volume-depleted. If weight rises at any time, then
this must be due to positive fluid balance, whatever the
input/output charts may suggest. It may not be obvious from
clinical examination where the fluid has gone: the possibilities
of sequestration in the peritoneal cavity or in the tissue
interstitium should be recognized.
Plasma urea, creatinine, and electrolytes should be measured on
admission in all acutely ill patients, and repeated daily or on
alternate days in those who remain so. These measurements will
ensure that advanced acute renal failure does not seem to have
occurred 'suddenly' in patients already in hospital. However,
many patients will be found to have significant renal impairment
on admission, and many more will develop some degree of renal
impairment whilst on the ward. In all cases the physician must
try to make a precise diagnosis of the cause.
The
diagnosis of acute tubular necrosis is based on the clinical
context, which often involves circulatory compromise, and the
exclusion of obstruction or renal inflammatory conditions,
usually by ultrasound examination of the kidneys and testing of
the urine for blood and protein, respectively.
In
prerenal failure the biochemical composition of the urine
reflects the response of normal tubules to impaired renal
perfusion. There is avid retention of sodium and water, leading
to low urinary sodium and high urinary urea and creatinine
concentrations, together with a high urinary osmolarity.
Restoration of renal perfusion leads to rapid improvement in
renal function. By contrast, conventional wisdom holds that in
acute tubular necrosis the urinary sodium concentration is
elevated and the urinary urea and creatinine concentrations and
urinary osmolarity are relatively low, but this is not always
so. Biochemical analysis of the urine is rarely useful in
clinical practice. From a practical point of view, treatment is
begun on exactly the same lines whether the expected diagnosis
is of prerenal failure or of acute tubular necrosis. The
response to resuscitation retrospectively defines the diagnosis
and determines further management.
Circumstances predisposing to prerenal failure are almost
invariably associated with raised plasma levels of ADH. This
acts on the collecting duct to increase the tubular reabsorption
of both water and urea, hence the plasma concentration of urea
rises out of proportion to that of creatinine in prerenal
failure. Plasma urea may also appear to be disproportionately
raised in the presence of sepsis, steroids, tetracycline
(catabolic effect), and gastrointestinal haemorrhage (protein
meal).
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