Parathyroid hormone

Yes.

The parathyroid glands, which are tiny sensors on your thyroid, detect this drop and instantly release parathyroid hormone, or PTH.

And PTH is the biological bone thief.

Exactly.

PTH travels directly to your skeleton and binds to receptors on osteoblasts, which then activates specialized cells called osteoclasts through the ARNKL pathway.

Osteoclasts, the biological wrecking balls.

That is exactly what they are.

They break down your skeleton to liberate the stored calcium, dumping it back into the bloodstream to keep your heart beating.

Today, we are talking about a condition that's hiding in plain sight in every dialysis unit and every nephrology clinic in Europe.

When we think about bone disease in CKD, we instinctively reach for the classics, you know, PTH, calcium, phosphate.

We just focus on the renal osteodystrophy.

We tweak the numbers, we adjust the binders, and we feel like we're doing a good job.

Because I think this is, most of us will get our first wake up call, at least for me, it was like this.

Because we traditionally, and we've been taught like that during residency, that renal osteodystrophy and osteoporosis are two separate entities.

Almost like we belong to different clinical tribes or religions with nephrologists chasing PTH and bone specialists on the other side doing DEXAs.

So how common is osteoporosis in CKD really? And should we still be drawing that line between osteoporosis and renal osteodystrophy or the field has finally agreed to let them share the same waiting room?

That brings us to the parathyroid glands.

These are small glands that usually sit along the posterior surface of the thyroid and their job is to regulate calcium through parathyroid hormone or PTH.

During a total thyroidectomy, the parathyroids can be inadvertently removed, injured, or simply lose their blood supply.

When PTH falls, serum calcium begins to fall with it.

And calcium is incredibly important for normal neuromuscular function.

As extracellular calcium falls, nerves and muscles become increasingly excitable.

At the same time, I'm examining the neck and thinking about those mechanical causes we just discussed.

Then I want an ionized calcium.

Hi, Dr. Morris, thank you for sharing your knowledge with us.

I am a 58-year-old Canadian woman who has a hyper, hyper, whoa, parathyroidism, and so far high PTH levels.

I bet it'd be hard for you to break a bone just saying.

I've seen some hyperparathyroid cases.

That sounds good.

Is there any specific information for what herbs I can add now to assist the process of detoxing? Well, you want to have your kidney, your lymphatic, your endocrine gland, because you still got to think about you're only 5'3".

That's the pituitary that controls the PTH.

So you want to look at that too.

And then finally, in the distal tubule, which remember was back in the cortex of the kidney after this main loop of Henle, this is going to fine tune the salt reabsorption using this NCC transporter.

And the distal tubule is also the main site for fine tuning the calcium reabsorption, which is a process that's actively regulated by your parathyroid hormone, or PTH, which we covered in the endocrine section.

And the power source that drives all of this reabsorption is a sodium potassium ATPase pump, and that's located in the blood facing side of the cells that make up this tubing.

So this pump actively pumps salt out of the cells into the blood, which creates a low sodium environment inside the cells, and that creates the sodium gradient that's needed for all these transporters in the tubing to work.

So the fine tuning of potassium happens in that collecting duct where its secretion is increased by aldosterone and by high tubular flow.

And then there's also what's called the calcium phosphate axis, which is also involved in kidney regulation.

So this is controlled by parathyroid hormone, or PTH, and this is released when blood calcium is low.

So here PTH is going to act on the kidney, it's going to increase calcium reabsorption, decrease phosphate reabsorption, and it's going to create active form of vitamin D. It's also worth noting here that in chronic kidney disease, this system typically fails, and this results in very high phosphate, low active vitamin D, low blood calcium, and a state of secondary hyperthyroidism, which ultimately ends up damaging the bones.

The next step would be to do further blood tests.

So some of the tests we mentioned earlier like do a PTH to activate a vitamin D levels alkaline phosphatase magnesium and bicarbonate to get a whole picture of what is happening.

The next step would be then looking at the patient's symptoms.

So she -- Uh, she or he presented with, uh, the leg pain and fatigue.

We might have to consider X-rays and even a DEXA scan if that is relevant and in managing such patients always have a MDT approach.

So a team that would help us in this situation are the nephrologist endocrinologist and a dietetic team should be there.

If the PTH is very high and refractory despite optimal medical therapy, we should consider possibilities of parathyroidectomy.

Thank you very much.

But which MEN 2 is associated with primary hyperparathyroidism? It's gonna be MEN 2A.

Remember, MEN 2A, they have primary hyperparathyroidism, uh, they have medullary thyroid cancer, right? Um, and they can also have like a few chromocytomas, right? So that's something you wanna keep at the back of your mind for, for exams, right? So, uh, this person has primary hyperparathyroidism, right? So that'll cau- cause hyperkalemia-- I mean hypercalcemia, right? Because remember, PTH, one of its jobs is to cause you to reabsorb more calcium from your kidneys.

That can cause hypercalcemia, right? So hyperparathyroidism, you know, is a very big cause of hypercalcemia, right? Uh, malignancy, right? In fact, those two things alone account for like ninety percent of cases of hypercalcemia, right? And then remember, thiazides can also cause hypercalcemia.

Remember, lithium can also cause hypercalcemia, right? So keep those things at the back of your mind for exams, right? And again, classic signs of hypercalcemia, right? The stones, bones, groans, psychic overtones, right? So the psychic overtones are the psychiatric effects, right? Those are the moans, right? The bone pain because again, if you have like hyperparathyroidism, uh, you're gonna be chewing up your bone with osteoclast.

When you see all these things, I hope you're thinking about hypocalcemia, right? And this person has hypocalcemia because of, uh, iatrogenic cause, right? So remember, hypocalcemia causes, uh, uh, hyperreflexia, right? So, uh, from a, uh, iatrogenic cau- cause, right? In fact, this is probably like the most common cause of primary hyperparathyroidism, uh, in the, in the US, right? Uh, basically a complication of thyroid surgery.

I remember when I was in medical school at Hopkins, actually, um, I did a, um- uh, endocrine surgery or rotation.

And this was something that we always worried about, right? So after the person would-- after we'll finish the thyroid cases, uh, we always basically just kinda waited, twiddling our thumbs while, uh, like a PTH or a calcium level was sent, right? Just to make sure that, hey, while we're taking out your thyroid or while we're doing thyroid surgery, uh, we did not inadvertently, uh, devascularize the, your, your thyroid, your parathyroid glands, right? Uh, because when PTH dips, y-your calcium is gonna dip very quickly, uh, believe it or not, right? So, so, you know, iatrogenic causes, right? Remember, uh, low albumin can also cause a person to have a hypocalcemia, right? If you have liver dysfunction.

Basically, think of causes of vitamin D deficiency, right? Like, so if your liver doesn't work, you're not gonna make calcidiol, right? Calcidiol is, uh, twenty-five hy-hydroxy vitamin D.

In my case, after they performed the second of two surgeries to remove my thyroid, I remained in the hospital for several days after the fact because I was having issues with serum calcium levels.

And the way that hypoparathyroidism works is It occurs when there are simultaneously low levels of serum calcium and low levels of a hormone called parathyroid hormone or PTH in the blood.

And when you have low levels of both, you end up with an array of symptoms.

Those symptoms include tingling, numbness, muscle spasms, in more severe cases, in long-term cases, kidney disease and dysfunction, calcium deposits in various soft tissues in the body, even cataracts.

And there is nothing that replaces a hormonal hormone, quite frankly.

The other method was a Band-Aid for symptoms.

In my case, when I joined this clinical trial, it was for a PTH analog drug.

And I was a double-blind placebo study.

Patients have hyperparathyroidism due to either multiple parathyroid adenomas or just parathyroid hyperplasia.

Because the parathyroid glands make PTH, whose job is to increase blood calcium, this leads to hypercalcemia, which causes constipation, upset stomach, kidney stones, polyuria, and polydipsia.

If calcium levels are very elevated, patients may have confusion, lethargy, and fatigue.

A pancreatic gastroenoma will cause high levels of gastrin.