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·
Under the microscope, you can also see the accumulation
of plasma and fluid (edema) around the cells. The cells
are also more disorganized and can become disjunctional
and become “unstuck.” As the urine flows, it pushes
these clumps of cells into the distal parts of the
tubule that are not ischemic, causing intra-renal
obstruction. The tubule proximal to this region
will become dilated. So, if you get a biopsy sample and
you see a region of dilation in the proximal tubule area
though no signs of necrosis, nonetheless, it is probably
acute renal tubular necrosis (because the necrotic
region is not in the sample that is biopsied).
·
In
patients with hepatitis, you can get biliary
nephrosis.
o
Basically, there is a lot of bilirubin in the blood.
Bile, being green in color, turns the gross appearance
of the kidneys green as well. These patients can go
into shock, decreasing the blood flow to the kidneys,
leading to ischemia and acute renal tubular necrosis.
This is also called hepatobiliary syndrome.
·
There are two types of glomeruli and the pattern of
necrosis varies between them. However, in both cases,
the proximal tubule and some portions of the distal
tubule are most affected (as previously explained)
because they are more sensitive and at greater risk of
injury and necrosis. There are two types of glomeruli:
o
Juxtamedullary
– these glomeruli are larger and are found next to the
medulla. They have very long tubules that go deep into
the medulla. These cells are supplied directly by the
arcuate artery, so they have a much better blood supply
as compared to the cortical nephrons. Because of this,
focal segmental glomerulosclerosis basically starts
within these glomeruli.
o
Cortical
– the tubules remain in the cortex.
-
Toxic Renal Tubular Necrosis
·
This
can occur from a large number of things:
o
Heavy metals – like arsenic and phosphorus. Many years
ago, arsenic ingestion (either poisoning or by suicide)
was a major cause of renal tubular necrosis.
o
Organic solvents – CCl4, ethylene glycol
·
A
histological sample was taken from a woman who had
ethylene glycol renal toxicity. There was extensive
necrosis, and you can see crystals of calcium oxalate
(because it is the end product of ethylene glycol
metabolism). Under polarized light, you can see these
crystals easier because they’re blue and pink colored.
The crystals can cause intratubular obstruction
and lead to renal shutdown.
o
Antibiotics and other drugs – cephalosporins, polymycins,
gentamycin
o
NSAID
o
Fluorinated anesthetics
o
Radiographic contrast material – if a patient requires
taking some radiographic contrast material, make sure
they are very well hydrated, otherwise, they may
experience some renal problems. The renal problems are
usually due to dehydration, which concentrates the toxin
(radiocontrast material).
o
Mushroom poisoning
·
The
pattern of necrosis in toxic injury is different
from that of ischemia.
o
In
ischemic injury, tubular necrosis is patchy, relatively
short lengths of tubules are affected, and straight
segments of the proximal tubules and ascending loop of
Henle are most vulnerable.
o
In
toxic injury, there is extensive necrosis along the
proximal tubule, but also necrosis of the distal tubule,
particularly the ascending loop of Henle. There is a
more even pattern of necrosis in toxic as compared to
ischemic injury. Also, in contrast to ischemic injury in
which all tissue layers are affected, in toxic injury,
the basement membrane is spared and only the
tubular epithelium is affected.
·
As
mentioned earlier, tubular epithelial cell necrosis is
restricted to specific parts of the nephron, depending
on the toxin – that is, each toxin has its own unique
pattern of damage. Usually, the tubular basement
membrane is preserved.
·
Dr.
Khan mentioned the S1, S2, and S3 segments of the
proximal tubule as being examples of different areas
that toxins may selectively affect but don’t
worry too much about that. Just know that different
toxins do affect different parts of the nephron.
·
Tubular epithelial cell regeneration
o
If
you know what the toxic cause is, once you remove the
insult, the tubules will regenerate after 3 or 4
months. These patients don’t need extensive treatment
(just management - dialysis) and eventually renal
function will return to normal.
o
This
is a MAJOR difference (aside from the different
patterns of necrosis) between ischemic and toxic injury
and this is due to the preservation or destruction of
the basement membrane. Regeneration occurs after
toxic injury and not so much in ischemic injury.
Clinically, we need to differentiate between the two
main causes of acute renal failure (acute RTN and RPGN)
quickly because if the cause is acute RTN, prompt
treatment (like dialysis) will allow for greater
regeneration. This does not occur with RPGN.
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