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NERVOUS COMPLICATION
Clinical complications of chronic
kidney
failure
The
clinical complications of chronic
kidney failure are
widespread
such as:
Nervous
System
Obvious
encephalopathy is a very late manifestation of
uraemia, typically leading to confusion, myoclonic
twitching of distal muscle groups, and impaired
consciousness. Seizures are rare unless there is
also accelerated-phase hypertension. Before this
preterminal state is reached, higher mental function
is impaired and patients will complain of difficulty
concentrating and of lethargy. It is important to
exclude synergic sedation from drugs such as
codeine, dextropropoxyphene, carbamazepine, or
benzodiazepines. Electroencephalography (EEG),
although an unnecessary investigation in these
circumstances, shows slowing of the background
rhythm. Brain computed tomography (CT) scans are
unhelpful and magnetic resonance imaging (MRI) can
be frankly misleading. Treatment is with
dialysis—frequent, short, and gentle. The myoclonic
jerks can be suppressed by benzodiazepines such as
clonazepam, 500 to 2500 µg per day.
A
specific encephalopathic ('dialysis disequilibrium')
syndrome can occur during or after the institution
of dialysis in uraemic individuals. From a normal
mental state, the patient develops a headache,
confusion, involuntary movements, and seizures, all
suggesting the development of cerebral oedema. This
is attributed to rapid urea removal leading to
changes in the water content of brain cells. It is
prevented by slow dialysis, avoiding rapid shifts in
urea concentration.
Aluminium-induced encephalopathy—dialysis
dementia—has disappeared as a clinical problem since
dialysis water is properly purified to exclude
aluminium, and aluminium-containing phosphate
binders are not given for very long periods. Such
patients exhibited a gradual deterioration in
intellectual performance, progressing to dementia
with involuntary movements.
Sensorimotor peripheral polyneuropathy is a late
complication of chronic renal failure. This presents
as dysaesthesiae, restless legs, and eventually
weakness with foot drop, also loss of power in the
small muscles of the hand. Nerve conduction studies
do not show specific diagnostic features, there
being a delay in the conduction velocity and a
reduction in the amplitude of the action potential.
The neuropathy is thought to be a result of the
effect of an unidentified toxic 'middle' molecule.
Dialysis results in a slow improvement, but patients
are often left with motor disability. Autonomic
neuropathy manifests largely as abnormal
cardiovascular reflexes, especially during dialysis.
A
specific mononeuropathy of renal failure is the
carpal tunnel entrapment syndrome caused by
b2-microglobulin-derived amyloid deposition. Almost
all dialysis patients develop this by 10 years of
treatment unrelieved by renal transplantation.
One final comment: although renal
failure can lead to many neurological problems, as
detailed above, it is important that such problems
are not automatically attributed to uraemia—drug
accumulation and vascular disorders are common
differential diagnoses.
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