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VASCULAR CAUSES OF ACUTE KIDNEY FAILURE
Specific causes of acute kidney failure
▪
Prerenal
failure and acute tubular necrosis
▪
Vascular causes of acute
kidney
failure
▪
Nephrotoxic causes of acute
kidney
failure
▪
Glomerulonephritic and vasculitic causes
of
acute kidney failure
▪
Interstitial nephritis as a cause of acute
kidney
failure
▪
'Haematological' causes of acute
kidney
failure
▪
Hepatokidney Syndrome
▪
Tropical
Vascular causes of acute kidney failure
Acute cortical necrosis
Acute cortical necrosis is an uncommon cause of acute
kidney
failure, accounting for around 1 per cent of cases in the
developed world, but more (3.8 per cent) in the experience of
one large centre in the developing world (North India). However,
these figures may be an underestimate, given that investigation
is not pursued in many patients who fail to recover from what
was presumed to be acute tubular necrosis, on the grounds that
test results do not reliably predict prognosis or affect
management, which is supportive.
Acute cortical necrosis presents in the same context as acute
tubular necrosis, which is almost always the diagnosis made
initially on clinical grounds. Suspicion should arise
immediately if a patient without obstruction is anuric, as was
found in 79 per cent of 113 patients in the largest study
reported, but cortical necrosis is often considered only when
renal function fails to improve.
Most cases of acute cortical necrosis are the result of
obstetric disasters, particularly postpartum haemorrhage,
abruptio placentae, eclampsia, or septic abortion. Snake bite,
haemolytic uraemic syndrome, acute gastroenteritis,
pancreatitis, septicaemia (often with disseminated intravascular
coagulation), trauma, and drug-induced intravascular haemolysis
are risk factors in the non-obstetric population.
The
pathological findings are of microvascular thrombosis, mainly
affecting interlobular arteries, arterioles, and glomeruli, with
complete infarction of affected areas of cortex. The medulla and
a rim of juxtamedullary tissue are spared.
The
best investigations to establish the diagnosis of acute cortical
necrosis are
kidney angiography and contrast-enhanced CT
scanning. The former reveals attenuation of interlobular
arteries, an increase in the subcapsular vessels, and a negative
outer cortical nephrogram. The latter shows enhancement of the
kidney medulla, but no enhancement of the
kidney cortex and no
excretion of contrast. Biopsy necessarily samples only a very
small piece of tissue and may mislead because of the patchy
nature of
kidney damage. Radiopharmaceutical investigations that
depend upon
kidney excretion (for example, DMSA
(dimercaptosuccinic acid) scans) are unhelpful in patients with
very poor
kidney function.
In
the months or years after an episode of acute cortical necrosis,
the kidneys tend to contract: cortical calcification, producing
an eggshell or tramline appearance on the abdominal radiograph,
is a characteristic sequel, but this is not useful in making the
diagnosis acutely.
Return of
kidney
function in cases of acute cortical necrosis
occurs very slowly, if at all, and is attributable to the
survival of islands of intact cortical tissue. About 50 per cent
of patients recover sufficiently to come off dialysis, but the
glomerular filtration rate rarely exceeds 10 to 20 ml/min.
Hypertension (including accelerated phase) may be a major
problem, and a subsequent decline in
kidney
function with the
necessity for a return to dialysis/transplantation is not
uncommon.
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