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0:04
Having understood the mechanisms
behind why glucose can
cause these changes,
it's really important
to understand what
the changes are
within the kidney.
Then these can be
seen relatively
simply on biopsy or in
experimental studies.
As I mentioned earlier,
one of the earliest
changes that you see in
the diabetic kidney
is an increase in
the size of the kidney with
increasing not only of
the size of tubules,
but also the
glomerular get larger.
There's an expansion
in the amount
of material within
the mesangium,
possibly in response
to podocyte injury as
a way to hold the
glomerulus together.
There's also characteristically
a thickening
of the glomerular
basement membrane.
Again, possibly to
protect the podocytes
from the extra pressure that
they find themselves under,
and thickening of
the Bowman's capsule
surrounding the glomerulus.
Progressively, these changes
can expand and lead
to ultimately,
glomerulus scarring known
as glomerulosclerosis.
The blood vessels adjacent
to the glomeruli become
hyalinized or thickened with
amorphous pink material,
and ultimately, the scarring
involves the
tubulointerstitial as well.
1:21
This slide conceptualizes
the differences in
histology between
a healthy kidney
on the bottom and
an abnormal kidney with
diabetes on the top.
Characteristically, you can see
that in the diabetic kidney,
there is an increased amount of
material within the mesangium,
more cells and more
material within there.
Mesangium essentially
means between
the angium or between
the blood vessels.
The mesangium job
is really to hold
the filtering blood
vessels in their place.
But this mesangium
becomes markedly
expanded in individuals
with diabetes.
Equally, the podocytes
that sit beautifully along
the urinary surface of the
glomerulus become fewer,
and they also become
further spread
out and the tubules become
abnormal and hypertrophied.
