Chapter Seven: Primary Hyperparathyroidism

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In my very long and complicated article I detailed primary hyperparathyroidism (PHPT) like a good scientist should. With all my heart I tried to make it plain enough for people in general to get a sense of how things work, but looking back on it, I doubt many will. Anyway, this book structure makes a place for summary and synthesis.

Is this PHPT lite?

Not really.

It is PHPT practical, devoid of all but assets material to evaluation and treatment. Even so, in those areas I go into perhaps greater depth than in the parent article. The two articles complement each other as best I can arrange.

Alabama Grist Mill Dam by Beverly Hammond catches the sense of how PTH works on serum and urine calcium and phosphate. Also, it is beautiful. 

A Disease of Misrule

PHPT arises because the parathyroid glands produce their hormone – parathyroid hormone (PTH) in excess of need and out of harmony with the mineral system within which PTH is the central regulator.

One could say through the actions of PTH the parathyroid glands rule the calcium kingdom, so powerful are its effects. And like the ruler of a well structured nation they are, in turn, held in check as were the ruling kings and queen of England by their royal subjects and their parliament.

But like those rulers of an earlier time might take to rampage that imperils their very kingdom, against which no force prevails to bring them back into the proper order of their world, like that is this disease. And as what only revolution – even regicide – could cure, so comes the surgeon in this case, to do that very deed.

Now, let me tell about the agent of this ruler, the imperial hormone, PTH, principle among peers. I have drawn a simple picture of its rule. See where it stands – above the rest, prime, enacting the will of the crown royal.

Kidney and GUT

Look first at calcitriol, active vitamin D, at the bottom in the kidney rectangle. PTH orders kidney cells to increase calcitriol production – blue lines mean stimulation. Calcitriol in turn signals gut cells to absorb more calcium and phosphate from food. So through calcitriol, PTH raises the amount of both minerals entering the blood which would tend to raise their concentrations.


PTH does the same for bone. It causes bone cells to break down its calcium phosphate mineral phase so that extra calcium and phosphate enter the blood. The red line means bone mineral goes negative – is lost.

Opposing Actions on Ca and Phos


To raise serum calcium more, PTH signals kidneys cells to conserve calcium. Remember, calcium is filtered out of blood in large amounts, but only 1% to perhaps 7% of what is filtered escapes into the urine – the rest is reclaimed back into the blood.


But unlike for calcium, PTH signals kidney cells to lower the fraction of filtered phosphate reclaimed back into blood. So serum phosphate is under opposing influences: More comes in from food and bone, kidneys conserve less. Serum phosphate level falls.

Why should it fall when the flow of phosphate in from food and bone increases? Why don’t the two effects balance out the third?

It is like the milldam. Let the stream run as it will, yet the dam adjusts the height of the pool behind – upstream of it. Lower the dam, and as soon as the pool empties down to the new dam level the flow downstream – urine phosphate losses here – is what it was when the dam was higher. Even if the stream flow is increased – more phosphate in from food and bone, the height of the pool remains low because the dam is set low. No flow can keep the pool above the dam for very long.

A Disordered Kingdom

Think of it. The serum calcium, over favored, so to speak, too high. And serum phosphate, normally calcium’s equal, now too low. All out of balance. Both of them move in excess through the body. Into blood from bone and in from food. And both go out through the kidney narrows, those long thin nephron tubes that on their way through they put in jeopardy. Being both in excess, how can calcium and phosphate fail to crystallize from time to time and block the tubules or form the stones we write about?

Feedback Loops

I said through this hormone, like the monarch of well run kingdom, the parathyroid glands rule within the check and balances of watchful peers and parliaments. Call them feedback loops, if you like.

Of them I illustrate only three.

Serum Calcium on PTH

Foremost, serum calcium controls PTH secretion through the calcium sensing receptor on the surfaces of parathyroid cells. LIke – if I might once again harken back to an earlier time, king and archbishop, the serum calcium controls and is controlled by the parathyroid glands. Calcium acts directly on the gland whereas PTH acts to influence serum calcium indirectly through reordering the actions of kidney, gut, and bone as I showed in my drawing.

Serum PTH, Calcium, and Phosphate on Calcitriol

Serum calcium and serum phosphate both suppress kidney production of calcitriol – red lines from them to calcitriol. So as serum calcium rises it reduces calcitriol production. But fall of serum phosphate further stimulates calcitriol production by taking its foot off the brake. Since PTH and low serum phosphate stimulate calcitriol production and only higher serum calcium offsets them, it is two to one: the net effect is that it rises.

Calcitriol on PTH

In the full article, I point out that calcitriol itself suppresses PTH. Calcitriol increases expression of the calcium receptor gene so the abundance of the receptor increases; this makes any calcium signal stronger by virtue of there being more signallers. That effect lowers PTH secretion by the glands for any given serum calcium level. Calcitriol inhibits the expression of the genes for the precursor molecule of PTH – pre pro PTH. This acts in concert with the signaller effect.

Failure in PHPT

But in PHPT the parathyroid glands produce PTH outside of normal regulation. They make too much hormone whatever the serum calcium or calcitriol. What should be an elaborate conversation turns into a lecture: PTH production rises and drives the system out of the normal bounds causing disease.

What Makes the Glands Rampage

They grow.

Just as learned historians peer into distant times seeking the inner causes of misrule so do scientists into the genes and interior behaviors of the glands. And there they find the many reasons that explain why the glands should throw off their obligations and pursue the expansion of their own powers to the general deterioration of their domain – bone disease, stone disease, damage from high calcium to vessels, to brain function, stomach acid production, pancreatic function.

Main Abnormalities Produced by PHPT

When we come upon it, PHPT has already progressed to that kind of deterioration. Serum and urine are abnormal. But taken one by one, almost all of the abnormalities could have other causes. It is the pattern of those abnormalities that allows us to diagnose PHPT as their cause. And because the cure is surgery, to recognize that pattern and shun false diagnoses is for all physicians an imperial responsibility.


PHPT raises urine calcium, a lot because extra calcium is absorbed from food and liberated from bone. That alone probably accounts for the kidney stones. But as a group, calcium stone formers also excrete more calcium in their urine than would a group of otherwise unselected men and women without stones, and that extra calcium arises from idiopathic hypercalciuria (IH).

So, just a high urine calcium need not mean PHPT – in fact in most cases it is due to IH.

Low Serum Phosphate

We just spoke about the low milldam and the stream. More phosphate flows through from food and bone into the urine but PTH has lowered the dam. So PHPT lowers serum phosphate.

But low serum phosphate occurs in many kidney stone formers. Some have IH and therefore high urine calcium and low serum phosphate.

Low serum phosphate, therefore, even with a high urine calcium need mean nothing more than IH and certainly does not diagnose PHPT.

High Serum (or plasma) PTH

Should one even measure PTH in a routine calcium kidney stone former? I do not.

But say you did, or your physician did, and the value exceeds normal. Low calcium diet can raise PTH, so can low vitamin D. Even the most modest reduction of kidney function, a level common among older people, raises PTH despite adequate calcium intake and vitamin D. Some say IH raises it, sometimes.

High serum PTH by itself, and even with high urine calcium and low serum phosphate do not diagnose PHPT.

Reduced Bone Mineral or Nephrocalcinosis

PHPT reduces bone mineral but so does low calcium diet, especially in IH. Even all of hypercalciuria, and low serum phosphate, and high PTH and low bone mineral density together, even this fourfold complex is not PHPT all by itself.

The same for nephrocalcinosis. An antique term of art suitable for an earlier period in medical history, multiple kidney calcifications in no way adds to the diagnosis of PHPT.

High Serum Calcium

Here – the talisman, the very make and mark of PHPT – this one finding sets PHPT apart from all the rest.

PHPT Raises Serum Calcium Three Ways

When the parathyroid glands themselves produce PTH in excess, not in response to something else but on their own accord, by themselves so to speak, the hormone directly or indirectly raises kidney calcium retention, bone mineral loss, and intestinal calcium absorption – all three together.

Serum calcium rises as the water pool behind a rising dam, and here the stream flows with more abundance – from bone and food. So the urine calcium is high even though calcium retention by the kidney is high: The dam wall is higher and the stream is flowing faster, too.

High Serum Calcium Cannot Force PTH Below Normal

The PTH level itself if in the normal range is too high. That normal range is for a normal serum calcium.

Remember, the primary controller of PTH is serum calcium. If low calcium diet or vitamin D deficiency lowers serum calcium even slightly, PTH will rise to correct it back. If serum calcium should rise from, as an example, very high vitamin D intake or very high calcium intake, serum PTH will fall to correct it. So the high serum calcium, were it primary – something on its own – would suppress PTH to its lowest level.

Therefore, a high serum calcium without suppressed PTH means it is the glands themselves that are raising PTH – that is PHPT.

The Diagnosis of PHPT

Thus it is, the diagnosis rests on an elevated serum calcium and a PTH level either in or above the normal range – not low.

The Urine Calcium Must Be Not Low.

There is a genetic defect of PTH regulation, not rare, in which serum calcium is high, PTH normal or even high, but urine calcium very low. That defect, familial hypocalciuric hypercalcemia, runs in families and one must pass it by for it needs no treatment. Stones, if present, have some other cause.

It may be that bone mineral is low, or kidneys have many stones or calcifications in them, or serum phosphate is low, or all or none, and still the prime combination of high serum calcium, and not suppressed PTH with adequate – not low – urine calcium is almost enough.

I say almost because there are four more steps.

No Drug or Disease Causes The Abnormalities

Thiazide Diuretics

Because these drugs lower urine calcium and prevent calcium stones, many patients take them. They raise blood calcium levels perhaps because they enhance renal calcium conservation – raise the milldam. A patient with idiopathic hypercalciuria taking a thiazide diuretic and who still excretes even a normal amount of calcium will seem to have PHPT because serum PTH levels will be normal and urine calcium not abnormally low.

Every physician knows this, but every stone patient needs to know it, too. Physicians may not know what their patients took when blood was drawn. Although in almost every case they will discover the drug as culprit, time and money get wasted for no reason. As a safe interval, one should stop the drug a week before drawing blood for the initial evaluation of any patient.

But what about follow up evaluations? Stopping the drug a week before won’t work. We want to know how well treatment has controlled urine calcium. So 24 hour urine and blood testing must coincide with drug use.

PHPT may appear during treatment and manifest as a rising serum calcium level, but thiazide can make it seem as if that has happened. What can we do?

The secret: tolerate slight increase of serum calcium. If seemingly too high too often, or rising over time, then stop the drug for a week and re-measure.


This ion, used for bipolar disorders, reprises the physiology of PHPT: high serum calcium and not suppressed PTH. But urine calcium has generally been low – as in familial hypercalcemia. Case reports document PHPT in some patients long after the drug has been stopped. Though not a likely cause of stones, lithium can cause massive confusion during evaluation of stone formers. 


Whether primary or from excessive thyroid hormone replacement, states of systemic hyperthyroidism can include high serum calcium. PTH levels tend toward the low or even suppressed side. Be sure about thyroid status when evaluating for PHPT.

Low PTH Conditions

High serum calcium with low PTH – suppressed below normal – do not concern us here. Some stone forming states like sarcoidosis, and CYP24 deficiency cause this, as do malignancies and other disorders.

Normocalcemic Primary Hyperparathyroidism

Does It Exist?

Given all I have said and the many factors that can raise PTH levels apart from PHPT, this diagnosis never fails to baffle and almost amuse me. Of course we can see normal serum calcium with increased PTH in low calcium diet or vitamin D intake, and any level of reduced kidney function. Just being older makes exclusion of mild kidney function loss difficult indeed.

Even so, some people do have high PTH for no apparent reason, and every one of us has a few cases that went on to raise their serum calcium levels. The big article links to long reviews of this topic by respected authorities who say more or less what I have just said, but say it better.

What Do We Do?

Who are these people and what do they look like?

They look like IH with elevated serum PTH levels.

I see no approach but to treat them like IH and wait. If they indeed have an early parathyroid disorder they will gradually raise their serum calcium levels and warrant surgery. Surgery in advance seems folly to me. What if the problem were indeed diet or slight kidney function reduction?

Everyone I write for here has calcium stones, so treatment must be done. That leaves surgery or medical treatment directed at IH. I cannot but favor the latter, and watch carefully along the way.

Treatment of PHPT

My job is to establish the diagnosis. After that, the surgeon does the rest.

That means I do not require the surgery to confirm my diagnosis. I need to know beforehand.

In case the surgery finds not abnormal glands, it means the surgery failed – the disease is present still. If abnormal glands are found and their removal cures the abnormalities, well and good, but the original diagnosis should not require such surgical confirmation.

I mean by this, that if you do as I have said, the diagnosis can be made with surety and surgeons sent on their difficult tasks with confidence. They will do scans, and if the scans find abnormal glands or not should make no difference if I have done my work properly. Likewise for their surgery.

The corollary: Much like carpentry – measure twice, cut once.

Parathyroid surgery is a highly technical procedure, and not all neck surgeons choose to perform it. A valuable resource for university based endocrine surgeons is this site listing surgeons who belong to the  American Association of Endocrine Surgeons. This society is noncommercial and I feel free to recommend it as a resource from this university site.

Other Apex Articles Related to this one:

Primary hyperparathyroidism

Idiopathic hypercalciuria

Five Steps to Stone Prevention


58 Responses to “Chapter Seven: Primary Hyperparathyroidism”

  1. Barbara

    I am a later in life stone former as well and am getting ready to have stone surgery. I keep seeing people posting bloodwork results in regard to PHPT, but not what these tests are actually called. What do I ask my urologist to order? (or is it something I can order from one of those walk-in labs?) I have to have a sepcific request or my urologist is not going to do it – there is no interest in finding out “why” and preventing. (I just finally got her to agree to do 24 hour urine once I am past surgery). Thank you!

    • Fredric L Coe, MD

      Hi Barbara, Fasting serum calcium is above normal with PHPT, serum PTH is not suppressed below normal, and urine calcium is not abnormally low. In later years PHPT is not at all rare in new onset stones, and you are right to ask it be looked for, It is curable with minimally invasive surgery. Regards, Fred Coe

  2. Carol

    Dr. Coe, I was diagnosed with hyperparathyroidism with PTH at 216 and calcium levels consistently over 10. I had two parathyroid glands surgically removed at NIH in 2011; one was the largest hyperparathyroid tumor NIH had ever removed (according to the surgeons present), while the other turned out not to be a tumor but had looked suspiciously large at the time of surgery so was removed.

    Question 1: Do you view the following symptoms as associated with hypoparathyroidism? In the past year I have had movement disorders in the mouth/chin area with lip puckering and chin spasms. I never had this issue before. So I increased my calcium and vitamins D and B12 intake about three months ago mainly via supplements to see if that was related because my calcium had been at 8.5 and had been low like that for years.
    After I increased my intake, the mouth/chin movements quelled substantially (maybe 85%), but not entirely. My calcium reading today is now up to 9.0; ionized calcium serum score is 5.0; Vit D is at 38.5; and PTH at 19. I have recently made appointments with both neurologist and endocrinologist who have ordered CT and MRI and told me to keep my calcium and D up.
    Question 2: Do you have an opinion on whether taking calcium via supplements (rather than natural intake such as via dairy) can cause kidney or heart problems down the line? Back in 2012, post surgery NIH warned me not to take calcium supplements and to get 1200 units of calcium naturally. (They may have changed their views since—don’t know.) Being lactose intolerant, getting my calcium levels up naturally is not easy. I did show a 2 mm kidney stone on an x-ray in 2018 but never felt it. What is your view on supplements for calcium and Vit D over the long term? Thank you.

    • Fredric L Coe, MD

      Hi Carol, I am suspicious you are hypoparathyroid in that your PTH is low and serum calcium at 9 with supplements. The concern is urine calcium. With low PTH renal calcium conservation is reduced so supplements will raise urine calcium and stone risk. I would advise your physicians obtain a kidney stone oriented 24 hour urine test for you while taking sufficient calcium to keep your serum calcium at least at 9 mg/dl. The urine may be high and that is the reason for your stone. Regards, Fred Coe

      • Carol

        Many thanks for your response, Dr. Coe. Since I wrote my message to you and before I saw your reply just now, I have learned more that is consistent with your suspicion about my condition, and it looks like I have found a way forward. First, I got results from a brain MRI that showed a small brain tumor so I contacted Johns Hopkins/Baltimore/Meningioma Center, where I had an EEG and other testing done. The JH neurosurgeon determined the 5mm meningioma was unrelated to the facial movement disorder I was experiencing (which was the same conclusion as that of a neurologist at Georgetown U. Med Center who also reviewed the brain MRI). Second, I went ahead then and snagged an appointment for the end of this month with NIH/Bethesda to review my facial movement disorder as potentially related to my post-parathyroidectomy low-calcium level issues. I also raised my kidney stone history. My status as a former NIH surgical patient for hyperparathyroidism streamlined my acceptance in another NIH parathyroid-related protocol. I will certainly raise the supplements concern and the kidney stone-oriented 24-hour urine test, as you have advised, at my NIH appointment. Am looking forward to getting the facial movement disorder resolved there before it gets worse, and, in the meantime, JH will watch over the meningioma. What dumb luck I have living near these great research centers. Life is good. Again, thank you for your perceptive response and recommendation!

        • Fredric L Coe, MD

          Hi Carol, It sounds like you have experts enough, and hope things work out well for you. Fred

  3. Jenny

    Dr. Coe, I had my first 12 mm calcium oxalate/phosphate stone removed via ureteroscopy with laser lithotripsy a few months ago at age 48. Initial CT scan without contrast showed 12 mm stone in right kidney and possibly a 5 mm stone or complex cyst in left kidney. I’m postmenopausal and had a hysterectomy at age 44. I had a brief phone consult with Jill Harris and she recommended I read this article. I have done fasting bloodwork in morning twice in past three months:

    February 18, 2021
    Calcium 10.4 mg/dL
    PTH Intake 29 pg/mL
    Vitamin D, 25-Hydroxy 50.4 ng/mL
    Phosphorus not checked

    May 17, 2021
    Calcium 10.1 mg/dL
    PTH Intake 22 pg/mL
    Vitamin D, 25-Hydroxy 64.6 ng/mL
    Phosphorus 3.7 mg/dL

    I have done two 24 hr Litholink collections on March 29 & 30th, 2021:
    Ca24 189, 199
    Ox24 35, 36
    pH 7.533, 7.334
    P24 0.267, 0.386
    PCR 0.6, 0.7
    Ca24/Cr24 279, 269

    I did increase my dietary intake of calcium to ~1000 mg/day about a month prior to May’s blood work and tried to reduce my sodium a bit. I have not had any bone scans done. I would greatly appreciate your thoughts on my situation and whether I need more blood work, urine or other tests to rule out PHPT. Thanks so much!

    • Fredric L Coe, MD

      Hi Jenny, Both serum calcium results are above 10 which is highly suspicious. The PTH levels are low, but still normal. Early primary hyperparathyroidism is a high probability. Given the importance of the diagnosis – surgical cure – I would wait a while and get another pair of morning fasting serums for calcium and PTH. I would ask the PTH sample be in plasma as it is more stable – in serum PTH degrades and perhaps your real values are higher than those reported. Your urine calcium is very high when normalized for your muscle mass – Ca24/cr24 is far about 140. If the next two are like the first two your physicians might want to take the diagnosis seriously indeed and pursue the evaluation accordingly. Regards, Fred Coe

      • Jenny

        Dr. Coe, thank you so much for reply. I greatly appreciate it. Do you recommend any further and specific testing outside of the calcium and plasma PTH? My primary care physician is referring me to an endocrinologist and a another urologist (different than the one who performed the ureteroscopy so I can get a second opinion). I want to be sure I am asking the right questions and getting a more accurate diagnosis when I see these physicians. My goal is to prevent any further kidney stones from forming if all possible.

        • Fredric L Coe, MD

          Hi Jenny, when primary hyperparathyroidism (so long a name!!!) is at issue, the foundation is serum calcium – is it above normal in the fasting state in the morning (when normals were studied to get the ‘normal range’). If it is not the disease is not present. If it is high then the disease may well be present unless the PTH is LOW (suppressed below the normal range). So, if I have the 100 pennies, I spend the first 99 on serum calcium + PTH, fasting, in the morning, and, as for the 100th penny, I spend it, too, in the same way. Once we know this one thing, the rest is routine, if – surgery – highly technical and for experts to do. Regards, Fred Coe

  4. Robert Coates

    Dr Coe; I sent a similar question a week or so ago but it must have not gone thru. Anyway, I am concerned I may have PHPT. A recent serum calcium (not fasting) was 10.0. (was also 10.0 with the same test two years ago). Parathyroid hormone level was 20pg/ml. 24 hour urine calcium was 340. Potassium 46, Phosphorus 663, Citrate 556, Oxylate,U 0.31mmol/24hr, Oxylate, mg/24hr 27.3, Calcium Oxylate crystal 2.42DG. First stone was at age 60, and since then they have formed more frequently. I’ve had three stone removal surgeries in the past 8 years and a recent scan shows four new ones. I had been drinking nearly 2 liters of water but no citrate for the past two years, so of course stones proliferated. A website for The Norman Parathyroid Center in Tampa says if serum calcium is 10 or higher for someone in their 60s, and first onset of kidney stones is in their 60s, with high urine calcium, there is a 90% chance they have Hyperparathyroidism. I realize they are surgeons and surgeons like to do surgery but what is your reaction to this? Is it possible with my numbers that PHPT is a real possibility?

    • Fredric L Coe, MD

      Hi Robert, It is indeed quite plausible, including the hint that your stones began in later life. I would do repeated morning fasting serum calcium measurements and convince myself and physicians the level is actually high – I bet it is, then let the surgeons cure it. This is the message of the article you have posted on. Fasting is crucial, as serum calcium varies with food, and morning, too, as normal values all arise from then. The big problem is to be sure about serum calcium before surgery – surgeons do not do surgery to confirm the diagnosis, but to cure what is surely there. Regards, Fred Coe

      • Robert Coates

        Thank you Dr Coe! I’m trying to convince my urologist to do just as you suggested with the fasting blood tests.

        • Robert Coates

          Well, I had fasting blood serum tests and they came back 9.6 and 9.5 with pth at 29. HPTH was then ruled out by my nephrologist. However, I insisted on a bone density scan, ans sure enough, today I was diagnosed with osteoporosis, following the scan. Doesn’t that make it even more likely I could have HPTH, even with relatively normal numbers?

  5. Stephen Knohl

    Dr. Coe,
    Given that hypercalcemia (or should should I say ionized hypercalcemia as ultimately it’s the unbound, free fraction that binds to the CaSR) should result in a suppressed PTH, isn’t it reasonable to pursue PTH testing in patients on a thiazide who develop hypercalcemia? I’m asking as your writing above would suggest to stop the thiazide and recheck calcium.

    My thought is that if the calcium reasborption increases due to the thiazide, the serum calcium should not elevate unless there is disordered activity of PTH or active vitamin D. Now, perhaps the ionized calcium doesn’t elevate and the total serum calcium simply reflects more calcium relative to water (the latter lost through the action of the thiazide). I guess another possibility is that the often-seen metabolic alkalosis associated with the use of a thiazide could reduce the free calcium concentration and this could provide impetus for a PTH release.

    I’m interested in your perspective on this…thanks.

    • Fredric L Coe, MD

      Hi Stephen, Thiazide lowers FE Ca and PTH. Serum calcium rises bu 0.03 (0.008, 0.052) mmol in the fed state but only 0.02 (-0.03, 0.08) NS, fasting. Serum calcium comes under several influences – higher tubule calcium reabsorption (FE Calcium fasting -1.2 (-2.1, -0.2) and fed -0.7 (-1.2, -0.3)), which raises it, and lower PTH (presumably from the higher serum calcium) which would reduce it via reduced GI absorption via reduced 1,25D activation, and via reduced PTH mediated bone mineral turnover. Indeed PTH falls fasting -5.4 (-10.6, -0.069) and fed -3.5 (-5.6, -1.3). I have to assume higher calcium reabsorption increases serum calcium which then readjusts via suppression of PTH over time – our experiment was 6 months: control then 6 months of CTD. PTH and serum calcium remained in the normal range. Primary HPT is a primary upregulation of PTH so I would presume the rise in serum calcium would be greater with thiazide, but normal ranges are not well established, and would depend on a lot of factors, like diet sodium etc. I am much happier using normal ranges for serum calcium fasting – given all the problems with it – and PTH just being in the normal region or high. Ionized calcium is ideal but I used to run them, and sample handling is a big deal: quality of the blood draw – these are venous with halted circulation during puncture -, for example. It is easy and cheaper to just measure a lot of fasting AM bloods for calcium and PTH, though I have not run any cost benefit experiments. As for alkalosis from thiazide increased PT reabsorption and from potassium depletion, it will certainly lower ionic calcium as a fraction of total calcium, another problem. For all these reasons I avoid sampling on thiazide. Thanks for such a good question! Fred

  6. Cheryl

    Dr. Coe –
    Thank you for this information. I would appreciate your input.
    At my last checkup in Oct, 2019, my Calcium was 10.4, Vit D 19.1 (fasting). I was sent back for a PTH and this was normal (can’t remember the reading) so nothing further was done. I’ve always had a low Vit D but this was the first time my Calcium was elevated. At 53 years of age, I am sitting here waiting for my first ever kidney stone to pass. I feel this all must be related. The ER doctor recommended I follow up with the urologist to have the stone content evaluated.
    What are your thoughts?
    Thank you!

    • Fredric L Coe

      Hi Cheryl, I would suggest your physicians might want to obtain several serums for calcium and PTH fasting, between 7 and 9 am; those are the conditions under which normal serum calcium values were obtained. As well, the low vitamin D needs to be corrected no normal before measurements as low vitamin D levels can mask hyperparathyroidism. If serum calcium values are above normal fasting and PTH is not suppressed and urine calcium is not low, you have the diagnosis – as in the article. You may have it as stones have begun a bit late in life. Regards, Fred Coe


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