Let’s talk about secondary hyperparathyroidism.
What does this mean to you?
It means that the parathyroid glands are responding
to decreased calcium.
So, what happened first?
A decrease in calcium.
The decrease in calcium will then trigger
the parathyroid from releasing the parathyroid
The main causes include… well, most common
would be, let’s say your patient has diabetic
nephropathy, may result in chronic renal failure.
So, therefore, you walk into a dialysis clinic
and each one of those patients is experiencing
When renal failure is taking place, each one
of those patients sitting on their thrones,
you know for a fact, is Vitamin D deficient
because the kidneys aren’t working properly,
don’t have 1-alpha hydroxylase activation,
Vitamin D is not properly formed or active
Vitamin D is not formed; the calcitriol not
being present may result in osteomalacia or
That decrease in calcium may then trigger
Our discussion in nephrology took us through
what may then happen when there is renal failure.
Now, because the kidneys aren’t working
properly and you have too much PTH, the PTH
does not work on the kidney whatsoever because
the kidney’s dead.
It’s going to go to the bone and start destroying
it, but we do not call this osteitis fibrosa
cystica, do we?
What do we call this?
Every single patient in a dialysis clinic
is receiving some form of calcium because
for a fact you know that with chronic renal
failure, the patient will be deficient of
Vitamin D or calcium.
Increased serum phosphorus binds with calcium.
Why is phosphate even elevated in a patient
with renal failure?
Important beyond belief, right?
Because the kidneys are dead.
If the kidneys are dead... remember normally,
what does PTH do with the phosphate in the
It flushes it out, it inhibits the reabsorption
If the kidney is not working, understand that
your patient is in a state of hyperphosphataemia.
Now, if there is hyperphosphataemia, it will
then bind to the calcium exacerbating the
effect of decreased calcium activity.
Vitamin D deficiency…
For whatever reason, meaning maybe from the
diet, but that’s rather difficult in developed
country; maybe there’s liver damage.
Remember, what’s a major circulating form
of Vitamin D?
25 hydroxylation of your Vitamin D. What if
you don’t have the liver?
Then you don’t even have the first step
of activation, so you become Vitamin D deficient.
So, think of all the different reasons as
to why a patient might have cirrhosis, right?
NASH, maybe autoimmune disease or alcoholism,
hepatitis, whatever it may be.
Clinical features, if the kidneys aren’t
working properly may result in renal osteodystrophy
and something called metastatic calcification.
Nothing to do with cancer and what that basically
means is that with all these calcium, it is
then depositing upon normal tissue, isn’t
You’ve heard of metastatic calcification,
you’ve heard of dystrophic calcification.
Metastatic calcification, secondary hyperparathyroidism,
may result or deposit a normal tissue and
Nothing to do with cancer; be careful with
Biochemical findings… with secondary hyperparathyroidism,
well, the initial event was the low calcium.
Look for that.
This then causes secondary.
The phosphate levels are variable depending
on the etiology.
What does that mean?
Take a look.
What’s the most common cause of hypocalcemia
It’s the chronic renal failure.
If there’s chronic renal failure, if the
kidneys aren’t working, you can’t flush
out the phosphate, your phosphate levels will
be high… incredibly important.
You need to chelate that phosphate in a renal
If there is Vitamin D deficiency for, by any
other cause, what does that mean?
For example, liver damage or maybe industrialized
I don’t spend a lot of time outside in the
So, if I have lack of UV exposure from the
skin, I don’t release Vitamin D. I may then
become Vitamin D deficient.
It has nothing to do with the kidney.
So, when there is deficiency of Vitamin D
due to other causes, then you trigger secondary
hyperparathyroidism, it turns to the kidney,
waste away the phosphate.
The phosphate will be low.
And understand that the PTH may then turn
to the bone and when you start resorbing your
calcium and such from the bone, you’ll find
an increase in… what are you-what are you
going to use as a marker for bone destruction?
Any time there’s bone issue, alkaline phosphatase.
ALK Phos will be elevated, if you’re thinking
about PTH activity on your bone or any type
of issue with the bone.
But, here, you should understand as to why.
Tertiary hyperparathyroidism, what the heck
is causing tertiary hyperparathyroidism?
Well, step by step.
Who controls your PTH?
When parathyroid activity becomes autonomous
from a pre-existing secondary hyperplasia,
that’s tertiary hyperparathyroidism, has
nothing to do with primary hyperparathyroidism.
Secondary hyperparathyroidism was-was caused
by the inciting event of hypocalcemia whereas
tertiary would be a pre-existing secondary