Perhaps the most common abnormality among calcium stone formers, idiopathic hypercalciuria (IH) causes calcium kidney stones and can lead to bone mineral loss and fracturing bone disease. Proper treatment requires a high calcium intake, a low sodium intake, moderation of very high protein intakes, avoidance of refined sugar loads, and – not rarely – use of diuretic drugs which can lower urine calcium losses, prevent stones, and protect bones.

I have found that patients will change their diets and take medications only if they fully understand why such measures are likely to benefit them. That is why I have written this article.

Why The Bathers?

I placed the bathers here because nothing seems so fit a metaphor as bathing for an explication of IH. To me, bone is like the bather in a bathtub, the flow of in from faucets and out in the drain like the GUT and the kidneys that engage each other in regulating the net balance calcium through the body.

The Large Bathers (1884-87) of Renoir and The Large Bathers (1900-1906) of Paul Cézanne both reside in the Philadelphia Museum of Art (This will not render properly on a pad or cell!), and I had trouble deciding which to choose.

Surrounded by gardens toward the end of summer I chose the beguiling Renoir. In winter, the gray stones of our university might have favored the dark and brooding figures of Cézanne.

What is Idiopathic Hypercalciuria?

As hypertension is defined by pressures that associate with harm – stroke, heart failure, heart attack, urine calcium is ‘high’ when it associates with stones.

What is Hypercalciuria?

I have already shown you Curhan’s results linking urine calcium losses to risk of stone disease. For two cohorts of women – red – and one of men – blue – increasing levels of urine calcium – shown along the horizontal axis in six bins – go with increasing risk of becoming a kidneyPQ RISK VS URINE CALCIUM LOW AND MEAN OVERPLOTTED.jpg stone former (Relative risk, on the vertical axis). A risk of 1 means no higher than among people with urine calcium below 100 mg/day – the reference population.

The average, or mean risk for forming a stone, is at the top of each bar, which is plotted from a base of 1 (the dashed line). The lower 95th percentile of risk is at the end of the solid bars which are also plotted up from one.

When the bottom of the solid bar lies above one, which is the case for all bars from 200-249 mg/d on, increased risk is very likely present. So the threshold of hypercalciuria is 200 mg/d both sexes.

As the urine calcium rises, risk – top of the bar – rises in smooth progression. As higher blood pressures predict more risk of strokes, higher urine calcium predicts more risk of stones.

Since diet was not controlled, we do not need special diets to diagnose hypercalciuria using this criterion.

What Does ‘Idiopathic’ Mean?

Many diseases can raise urine calcium excretion, but among hypercalciuric stone formers the vast and overwhelming majority have none of these diseases. Their urine calcium exceeds 200 mg/d for no obvious reason – idiopathic, arising of itself, without overt cause.

Normal Calcium Excretion

Since 1900 scientists have collected 24 hour urine samples from people in clinical research units, perfect collections, and measured urine calcium. I collected all such values I could from published papers – a tiring exercise. Here is my yield of values from normal from normal adult men (blue) and women (red) published as a collection nowhere else.

normal uca male anf female.pngThe Curhan demarcator – 200 mg/day resides at about the 75th percentile: 25% of normal people are above it. But stone formers are perhaps 7-10% or less of the human population. Like high blood pressure high urine calcium confers risk, but risk does not always culminate in disease.

The 95th percentiles of these distributions, at about 275 and 325 mg/d of calcium for women and men, once defined ‘high’ urine calcium. That is statistically rational.

But like old definitions of ‘high’ blood pressure (160/90), these limits greatly underestimated risk of disease. I renounce criteria not long ago promoted by my colleagues and I: >250 mg/day women, >300 mg/day men, >4 mg/kg body weight either sex, 140 mg of urine calcium/gm urine creatinine.

No doubt they confer risk of stone, given the Curhan demarcator. But they are too high and we should abandon them for clinical use.

Hypercalciuria Raises Supersaturation and May Promote Plaque

Supersaturation produces and enlarges crystals and therefore stones. We now have superb evidence that rising supersaturation associates with rising stone risk. Calcium oxalate and calcium phosphate supersaturations rise smoothly with urine calciumleaving no doubt that urine calcium raises risk of calcium stones via increasing supersaturation.

Many calcium stones from on plaque, tissue deposits of calcium phosphate crystals in human renal papillae. Plaque abundance rises with urine calcium excretion, and a plausible theory, vas washdown, links them.

Idiopathic hypercalciuria is Hereditary

Family Studies

FAMILIAL NATURE OF IHI am not sure if we were the first, but here is our evidence from 1979. 

The arrows point to stone formers, filled symbols are men (square) and women (circles) with IH, * are children, and dashed people are deceased. In the 9 families IH was about 50% prevalent. Many others have found IH heritable.

It is not likely to be a simple trait from one abnormal gene, but some outcome of a number of genes. As this reference mentions, urine calcium is not the only stone forming trait that appears genetic; urine citrate appears to be, as well.


Dr. David Bushinsky, in decades of outstanding research, has proven that rats can be bred for what appears to be a rather close match to human IH. His strategy was to breed rats with the highest calcium excretion, and continue doing this for generations.

What attracts my notice is the progression over the generations. For the first 40 generations, urine calcium rises almost linearly. Thereafter, it is at a near plateau, more or less.

Forty generations!

ghs uca progression-14-07-25 cAmong humans that is 800 years taking 20 years for a generation, and in fact that is a skimpy generation time for us.

Yet, if we think about the matter, 800 years is nothing in evolutionary time. Even his outermost generation, near 100, or 2,000 years, is nothing as against evolution. So I am satisfied that IH is breedable in animals, and could have easily arisen in us as a response to evolutionary pressures. What those pressures might have been is not a topic for here.

I cannot pass by this heroic accomplishment without a pause, and some stirring of admiration and sense of accomplishment. How brave to have started this, and how persevering and accurate to maintain these generations intact and continuing. How productive, too.

Of importance here, these animals form calcium stones and develop a far more severe bone disease than normals if diet calcium is not ample.


Some years ago we had the opportunity to collect 24 hour urine samples on large numbers of boys and girls who were brothers and sisters of children with kidney stones, and from children in families where none of the children, their parents, or other relatives were known to form stones.

Urine calcium excretions of siblings with more than two stones are farthest to the right – highest in the left panel. Next highest – second from the far right – were siblings with 1 – 2 stones. Siblings with no stones were even lower, third from the far right.

Children from families with no kidney stone history were lowest – most leftward – and almost none had above 200 mg/day of urine calcium loss.

The four bars in the right hand graph say the very same thing. Mean values of urine calcium, shown by the top of each bar, rose progressively with stones.

This is expected if idiopathic hypercalciuria is genetic and causes calcium stones.


Hypercalciuria in children not rarely causes hematuria found on routine screening. Loin pain with hematuria is a common syndromic epithet, ascribed to crystals because IH can raise urine supersaturation and higher supersaturations promote crystals. Hematuria can be familial because it is due to IH and crystals or stones. In adults, unlike children, hematuria can be from malignancy so proper evaluation, even in stone formers, requires imaging and considerable care. 

IH Is Not the Only Reason Stones Are Familial

I will not pursue the matter here, but stones themselves are familial, presumably hereditary, and not always because of IH.

Bone Disease

There Is Bone Disease

An outstanding scientist in the kidney stone field, Dr. Khashayar Sakhaee, has authored a superb review of the bone problem of stone formers. This figure, from a prior study of people living in Rochester, Minnesota, shows the cumulative incidence of vertebral fractures among people who had a symptomatic stone (irregular line) and the expected rate ofnihms271156f1 bone fractures in stone formers fractures based on the entire population (the smooth line) between 1950 and 1974. The excess of fractures was not observed for hip or forearm.

The review collates 20 studies that concern bone mineral density mostly in relation to idiopathic hypercalciuria in stone formers. The broad message is a reduced level of bone mineral as a general finding, observed by many independent investigators using a variety of instruments to assess the bone. One cannot escape the conclusion that among stone formers, most of whom are described as having IH, bone mineral is reduced as a rule.

The authors summarize their wide ranging literature review in a little table I find irresistible. Among 2,052 patients reviewed, between 31 and 65% (939 patients) had some reduction of bone mineral density.

Furthermore, the radius, a site not remarkable for fractures in the Rochester study, is most affected with regard to reduced bone mineral density.

Table from Sakhaee paper on boneWe have shown that the magnitude of IH predicts future loss of bone mineral. 

We measured bone mineral density in a number of stone formers with IH, collected 24 hour urine samples, and then re-measured  bone mineral density three years later.

As a group, the net change in bone mineral density of femoral neck (left panel) and spine (right panel) centered around 0. You can see this because the points more or less fall equally above and below the horizontal line at 0 change.

But when change in bone mineral is plotted against the urine calcium loss (horizontal axis), the change over time is negative – the ellipses slope downward. ASPLIN BMD VS UCAPeople with higher urine calcium loss lost bone.

IH Seems A Factor in the Bone Disease of Stone Formers

Risk of stones begins at about 200 mg/day, and risk of bone disease seems to follow having stones. It is interesting that most points below 200 mg/d on the figures show an increase in bone mineral, most at above 200 mg/d show a decrease.

Although Sakhaee is careful to point out that bone disease associates with stone disease, IH is obviously a prominent issue in his review, and many of the studies of bone disease in stone formers have centered on IH as a causal factor. I suspect the association is stronger than it might seem because IH itself has been diagnosed variably over the 20th century, often using urine calcium criteria far above those needed to increase stone risk.

So What?

Every stone clinic is a bone clinic. All stone formers deserve a bone mineral scan.

Dr. Sakhaee points out that US insurance practices exclude bone evaluation in large swathes of stone forming populations. But bone mineral scans are not very expensive compared to the eventual costs of fractures. A useful medical buying guide places the bone mineral density scan cost to uninsured people at about $200.00, and mentions that in May prices can be lower because it is national osteoporosis month. The price usually includes a simple medical interpretation.

How Does IH Raise Urine Calcium?

The Extra Calcium Can Come From Diet

qplot of percent calcium absorption IH and N from balance plots for gibbs lecture control file using balance data file in CKD ca and p balances folder

In the balance studies from which I derived normal calcium excretions, scientists fed subjects a fixed diet and measured all food calcium eaten and all calcium lost in the stool. The difference between calcium eaten and calcium lost in the stool is net calcium absorbed into the blood.

Typically measurements are made in 6 day blocks after a few days to equilibrate with the diet, so subjects participate for perhaps 8 – 10 days. I have aggregated the calcium absorption measurements that match the urine calcium excretions I already showed you.

Normal men and women (orange) absorb about 18% of diet calcium – the curve on the adjacent quantile plot combines adult men and women who in fact display identical behavior. People with IH – the blue curve – absorb much more calcium, about 30%.

You might ask how one gets negative absorptions – points to the left of the vertical 0 absorption line. It is because pancreas, duodenum, and perhaps ileum all can secrete calcium from blood back into the bowel lumen. When diet calcium is less than this ‘endogenous’ secretion, stool calcium loss exceeds what is eaten.

An early theory of IH was over absorption: High absorption, more calcium comes into the blood, the kidneys lose it – done. This theory led to decades of low calcium diet as a treatment. No one knew such diets might cause fractures.

The Extra Calcium Can Come From Bone

A Glucose Load Can Raise Urine Calcium

Years ago Dr Jack Lemann did this informative study. He measured urine calcium excretion (vertical axis) then gave glucose or sucrose (table sugar) to normal people, calcium stone formers, and relatives of calcium stone formers.

jack NEJM pictureLook at the control calcium excretions of the two right hand groups: 5 or so of the stone patients have control values above all but the highest normals; the relatives are even higher – and this is fasting, before the sugar load!

Each period was 20 minutes, so this experiment went on for 2 hours. The higher urine calcium with sugar must come from bone – there no calcium in the sugar drink. It came from bone in normal people and in those with IH but the latter lost far more calcium than the former.

In a separate experiment, Lemann proved that the loss of extra calcium from sugar was because kidneys reduced their calcium conservation, they permitted an increase of urine calcium.

Low Calcium Diet Causes Bone Mineral Loss

We persuaded nine normal people and 27 stone formers with IH to eat a very low calcium diet – 2 mg/kg body weight – for 9 days, and on days 7-9 we collected 24 hour urine samples and measured lcd picturecalcium losses.

The diet went well; most people ate what we asked (middle panel). The normals (the 9 sets of points left of the space) lost in their urine less than 2 mg/kg of calcium daily – lower panel, to the left, so the difference each day between what they ate and lost was positive (upper panel, points above 0).

The patients were different. They lost more calcium in their urine than they ate, and did so most of the time. This was bone mineral lost in the urine.

On such a low intake surely everyone was losing bone mineral because the fraction of diet calcium that is absorbed into the blood is far below 100%. I just showed you that it is about 18% in normal people and 30% for people with IH.

But those with IH were more flagrant than the normals. Because their urine contained more calcium than they ate we could prove bone mineral was lost.

In IH Urine Calcium Usually Exceeds Net Calcium Absorbed

I already showed you calcium absorption as determined by the difference between calcium eaten and lost in the stool.

In this plot, IH is in red large dots, and normals in blue microdots. Net calcium absorbed is on the horizontal axis, and urine calcium is plotted against net absorption on the vertical axis. Points to the left of the diagonal line of identity mean urine calcium exceeds what was absorbed – negative calcium absorption.

At a net calcium absorption of 100 mg/d or more, a majority of the normal points are to the right of the diagonal line – urine calcium is less than calcium absorbed. Bone mineral is stable or increasing.

Idiopathic hypercalciuria points are all left of the diagonal line, negative bone mineral balance, until net absorption rises over 300 mg/d. It takes a huge amount of diet calcium to overcome the tendency of IH people to lose bone mineral.

Bone Calcium Retention vs. Diet Calcium

Here, I plot the net calcium retention – net calcium absorbed minus urine calcium excreted against the calcium eaten for all the people with IH (red) and normal people (Blue) who had balance data in my collection.

At diet calcium intakes above 500 mg/day, the average retention (the jiggly blue line) for normals is about 0, meaning that normals in general will have stable bone mineral stores. Higher intakes make the average rise above 0 and at about 1000 mg/day or so, a common nutritional goal, a majority of normal points are above 0.

retention vs calcium intake in mg per day with smoother means red is IH blue is normalsFor the IH subjects (red), retention rises slowly with diet calcium intake, but the average never reaches 0. Some points lie above 0 meaning that not all IH subjects will share the general high risk of bone mineral loss, just as some normal points lie below 0 even at high calcium intakes.

What Have We Learned?

The message is that low calcium diet is not ideal for the normal population and a disaster for people with IH. But even with a liberal calcium diet IH makes it hard to bring bone mineral into balance which is probably why there is a bone disease.

Using sophisticated measurements of bone mineral turnover, Lieberman and his colleagues showed as early as 1965 that patients with IH had something very abnormal about bone. Low calcium diets remained a common treatment for stone disease for more than a decade later.

IH Kidneys Release Excess Calcium 

Filtered Calcium

Calcium gets into the nephrons of the kidneys by filtration from blood. If you do not know about filtration, use this link to learn about it. 

Each of the 2 million nephron units we possess in our two kidneys has a glomerular filter that filters water, sodium, calcium, phosphate, oxalate, and thousands of other small molecules and ions out of blood into the long tubules that process the filtrate into urine.

Reclaimed Calcium

The process we care about here is reclaiming filtered calcium back into the blood. In normal people about 98% or more filtered is reclaimed, in IH it is less, about 95 – 96%. Not a lot, you think. Here are a few numbers. We filter about 150 liters/d. The filtrate contains about 40 mg/l of calcium: 40×150 = 6,000 mg/d of calcium. Of that 2% is 120 mg/d, 4% is 240 mg/d, 5% is 300 mg/d. So that ‘little’ difference accounts for the range of calcium between normals and stone formers.

Where Along the Tubule?

Review the Proximal and Distal Tubules

Each kidney tubule resembles a single woman’s hair – long hair, that thin. Down the center is its lumen through which the filtrate passes to become urine, and where calcium is reclaimed. Go back to the filtration article and check out the tubule picture. Pay special attention to the proximal tubule. In the proximal tubule calcium is reclaimed in parallel with sodium. In the distal tubule – on the picture in the link – calcium is reclaimed independent of sodium.

Urine Calcium Follows Urine Sodium

This picture is the basis for recommending a low sodium diet to lower urine calcium in IH.

It shows how urine calcium (vertical axis) rises as urine sodium (horizontal axis) rises. The rise is far more obvious among stone formers with IH than in normal people.

Urine Calcium and Sodium are Linked in the Proximal Tubule

As you eat more sodium, urine sodium goes up so output balances intake. One way the kidney accomplishes this balance is that filtration rises with higher sodium intake. Another is that reclamation of water and sodium in the proximal tubule (the part nearest the glomerular filter) goes down – more sodium and water flow downstream in the nephron. Calcium goes with it, the two are linked by the way that part of the nephron works.

Why Does Urine Calcium Rise More in IH than in Normals as Urine Sodium Rises?

It must be downstream of the proximal tubule, because sodium and calcium are reabsorbed together there. Where is not easy say. Calcium and sodium reclamation can differ at multiple places downstream from the proximal tubule, and which ones cause the higher slope in IH is not known.

What Can We Do With What we Know?

We can shut down filtration and increase reclamation, and that is what low diet sodium does. That is what the graph shows us.

Likewise, the thiazide diuretics do the same. We have proven they increase reclamation in the proximal tubuleOnce you understand this, you understand why reducing diet sodium and taking thiazide are two ways to do one thing. So the more you limit diet sodium the less you need thiazide, or at least the less dosage you need. On the other hand, if you take thiazide and eat a lot of sodium, the sodium will undo the effect of the drug.

We can take potassium citrate or increase diet potassium alkali with fruits and veggies. At least the potassium citrate does in fact lower urine calcium at any given sodium intake. 

What Happens to Bone?

I think it is this way. When we eat, the kidneys release calcium into the urine, normals and IH alike. But IH patients release a lot more calcium, depending on their sodium intake. If the diet has adequate calcium in it, bone can get its share even if more than normal is lost in the urine. If the diet is not so adequate, less than 1000 mg/d, bone may not get its share, especially when IH is present.

The best proof of this is the one study showing that in perimenopausal women only the combination of low diet sodium and high diet calcium can promote bone mineral gain. 

What is the Final Word?

Stone formers tend to have IH. For them reduced diet sodium combined with high diet calcium is a reasonable way to live. It reduces urine calcium and protects against bone loss. Thiazide is a fine stone prevention drug, but it is just another – and lesser if more convenient – way to do what reduced diet sodium will do. For a stone former, the diet is best for the whole family, because IH is inherited.


  1. Lisa

    Hi Dr. Coe,
    I had surgery in May for a calcium oxalate stone (my 3rd kidney stone incident but first analyzed). I finally had a 24 hour urine ordered here in Toronto. My results are:
    Calcium per day 12.2 mmol/d
    Citrate per day 7.5 mmol/d
    Creatinine per day 13.3 mmol/d
    Magnesium per day 9.3 mmol/d
    pH 5.5
    Phosphorus per day 29 mmol/d
    Potassium per day 35 mmol/d
    Sodium per day 75 mmol/d
    Urea per day 359 mmol/d
    Uric acid per day 3.5 mmol/d
    volume 5.792 l

    calcium 2.4 mmol/L
    Chloride 104 mmol/L
    Creatinine 49 umol/L
    Ionized Calcium 1.24 mmol/L
    Magnesium 0.79 mmol/L
    Phosphorus 1.19 mmol/L
    K+ 4.0 mmol/L
    PTH intact litho – cancelled
    Sodium 139 mmol/L
    Total CO2 26 mmol/L
    Urea 2.8 mmol/L
    Uric Acid 154 umol/L

    They have not shown any oxalate amount even though I saw it on the requisition and I don’t know why the PTH was cancelled. I am hoping to see a nephrologist after I have completed my 2nd 24 hour urine. I am just wondering what I should be asking him/her once I do get in to see them. It looks to my like I have hypercalciuria but I don’t yet know why. Thanks for any help/suggestions you can give me.

    • Fredric L Coe

      Hi Lisa, You do have a high urine calcium and normal serum calcium, suggesting precisely the condition in the article you post on. The PTH would be unneeded given the normal serum calcium. Omission of oxalate is a mistake as it can be high in any stone former, and should be measured at least once for safety. I know that Canadian health systems function on statistical assessments of cost/benefit, and also prides itself on evidence based decisions. But here the system is wrong. Rare people have very high urine oxalate levels AND incidentally high urine calcium, and the former can cause kidney disease. Given it is rare but dangerous one should always look at least once at 24 hour urine oxalate excretion. Overwhelmingly, it will be unremarkable, but even so. insist on at least one measurement. Idiopathic hypercalciuria is familial, certainly genetic, and strongly improved by low diet sodium and if needed thiazide diuretics. Here is my very favorite article on treatment. Regards, Fred Coe

      • Lisa

        Thank you so much for replying. I re-checked my online results a few days later and the oxalate amount showed up at 556 umol/d which shocked me because I’ve been following your and Jill Harris’ Kidney stone prevention diet for almost 6 months. I will be doing another 24 hour urine next month and then hopefully seeing a nephrologist so I will discuss this with them. Much appreciated.

        • Fredric L Coe

          Hi Lisa, So high a urine oxalate usually means diet calcium is not high enough, or calcium is not timed well to meals that contain high oxalate foods, or some very high oxalate foods are being eaten, or there is an underlying issue raising oxalate absorption or even production. Consider these alternatives with your physicians and perhaps you and they can sort out the cause – everything has a cause. Regards, Fred Coe

  2. Vasiliki Anderson

    Hi Dr. Coe,
    I was just diagnosed with IH based on two 24 hour urine tests and the blood test. My level of calcium in urine is 390 and calcium/creatine ratio is 365.
    I am 62 and have never had any stones. Moreover, there is absolutely zero history of stone-forming anywhere in my family. I was tested because my bone scan showed osteoporosis in my hip femurs: 2.5 & 2.7 Z scores.
    The endocrinologist of course prescribed Hydrochlorothiazide 12.5 Mg daily, but I am interested in avoiding this medication if at all possible. For one thing, I have quite low blood pressure to begin with, and also I would be much more inclined to treat the root cause rather than the symptom. So I am wondering about your advice on diet and any other things I can do. (I have always exercised with weights and am very active so I don’t think I can do much more with that). My diet is very healthy, but I may be eating quite a bit of protein.
    I really appreciate any guidance you can provide.
    Thank you so much.

    • Fredric L Coe

      Hi Vasiliki, IH produced bone disease and you can do well with reduced diet sodium and high calcium diet. THe ideal diet sodium would be about 50 – 60 mEq (about 1500 mg/day or less), and diet calcium about 800 to 1000 mg. If the low sodium diet is not enough one can add a very low dose of thiazide to it, low enough to prevent too much side effects. If the disease progresses, standard bone treatments are not unreasonable, including bisphosphonates and newer agents. Regards, Fred Coe

      • Vasiliki Anderson

        Thank you for the speedy and helpful reply! Since you didn’t suggest low protien intake, can I assume that is because I am not at risk for kidney stones, just bone mineral absorption? Thank you!
        Your generosity of time is a true gift to people like me seeking to understand this disease better.

        • Fredric L Coe

          Hi Vasiliki, No; low protein diet is not a good idea. You want about 1 gm/kg/day, a normal intake. Fred

  3. Emily

    Dear Dr Coe,

    I came across your website because you diagnosed my maternal grandmother with hypercalciuria many years ago when she was having kidney stones, and she has described what a difference your work made for her. I have recently passed a calcium oxalate stone myself, and I am currently having further investigations into the cause, which is what led to my recent interest. My mother and other family members have also had kidney stones, and several family members suffer from low bone mineral density/osteoporosis. Therefore, it was really interesting to read about the stone and bone links and the relevance of family history. I am currently feeling quite unwell even though there are no more stones present on ultrasound, and my serum calcium concentrations have been normal on the three occasions they have been checked over the past few months. However, I did have a raised parathyroid hormone level with normal serum calcium, and I have other symptoms of hyperparathyroidism (fatigue, excessive thirst, finding it difficult to concentrate, feeling slightly dizzy). My calcium levels were not checked after fasting, although in one occasion I had had very little to eat beforehand. I am currently waiting for a bone density scan. Can you suggest any other investigations that might be useful for exploring the cause of my stones and other symptoms? I would be happy to send more detailed results if you are willing to look at them. If so, it might be easier to send them via email if there is an email address I can contact you on.

    Many thanks in advance for any advice.

    Best wishes,

    • Fredric L Coe

      Hi Emily, Idiopathic hypercalciuria is genetic and causes stones and a form of bone disease. Obviously I would suggest 24 hour urine testing along with fasting am bloods to be sure about serum calcium. I suspect you have IH, and also perhaps low calcium diet or low vitamin D as a cause of high PTH with normal serum calcium. This kind of normal calcium increased PTH is secondary and without known symptoms of its own. If you wish to write to me personally I can look up my records of your grandmother. If she is still alive ask her permission and also send my regards. Regards to you, as well, Fred Coe

      • Emily

        Dear Dr. Coe,

        Thank you so much for your quick reply and your offer to look into this for me. I will send your regards to me grandma. She speaks very highly of you and I’m sure she’ll be pleased to hear from you. I will also ask for her permission regarding accessing information from her records. Is there an email address that would be okay for me to contact you on? If you would prefer not to share it on here, I could contact your department and ask them if that’s okay?

        Thank you again,

  4. John Scott

    From recent tests my 24 h urine calcium is 338 mg/d and bone density T-score of -1.7 at right total femur(low bone mass). I am allergic to sulfamethoxizole(hives on forearms). Is there an option for my apparent I.H. other than thiazide diuretics ?

  5. Carol Wenmark

    Dr Coe,
    I sent you all my test results back in January and you said I had secondary hyperparathyroidism due to vit d deficiency. Saw my endochronologist and she agreed. Since taking 4000 in of vit d and 800 mg calcium my PTH was 31 and calcium was 9.8. Was tested a month later in March 2018 and PTH was 36 and calcium was 9.7. Just saw my endochronologist today after blood work and my PTH was 64 and calcium 9.2. I am on a low salt diet and high water intake. My vit d25 OH was 49 then 61 and now 84. I was told to back off on vit d to 2000 iu and stop taking calcium. My kidneys are full of tiny stones and this situation concerns me the most because things haven’t gotten better for two years. Would appreciate advice on what to do about stones.

    • Fredric Coe, MD

      Hi Carol, I already responded to your labs. I am confused about the sequence = I presume the many tiny stones were there before. If they are new, that is a real worry. I suggested a full evaluation for the cause of stones and think that is essential. What interests me is why your serum calcium fell – had you lowered your calcium intake before the blood draw? Are the bloods all fasting? If not, they can be very misleading as PTH falls with meals and serum calcium rises. Regards, Fred Coe

      • Carol wenmark

        Dr Coe, Are my stones caused by the secondary hyperparathyroidism or are they a completely separate issue and not related to SHPT.

        • Fredric Coe, MD

          Hi Carol, Secondary hyperparathyroidism does not cause stones. It is a response to some drive for more PTH: vitamin D deficiency, low calcium diet, reduced kidney function, intestinal calcium malabsorption. Often stones ’cause’ it because people avoid diet calcium – always a mistake as it will not prevent stones. Regards, Fred Coe

  6. Carol wenmark

    Dr Coe…I emailed you in January and based on my lab results you believed I had secondary hyperparathyroidism. My endochronologist came up with the same due to Vit D deficiency. She raised my Vit D to 4000 in and calcium to 800 mg/day. I am on low salt diet and about 90 oz water/ day. Since implementing these changes, here is my recent blood work.
    D25 OH. CAL. PTH
    2/23/18 49. 9.8. 31
    3/27/18. 61. 9.7. 36
    10/1/18. 84. 9.2. 64
    I am concerned because my kidneys are still loaded with tiny stones. There has been no change in stones for two years. I have never been able to collect a stone. I also don’t know why the PTH has gone up to 64. Should I be seeing a nephrologist for stones?.
    Thank you,

    • Fredric Coe, MD

      Hi Carol, I notice the serum calcium is lower. Have you reduced your calcium intake or changed the kind of calcium foods?? Given multiple stones you should want a full evaluation. Here is my favorite article about the subject. Regards, Fred Coe

      • Carol Wenmark

        I would appreciate if you could look at my current testing. I’m still in limbo as to my diagnosis. Finally passed two kidney stones and they were both calcium oxalate. I took Jill’s course and have been on the low salt, low sugar diet, high water intake since last summer. I am now on the low oxalate diet for the past month. Nephrologist said that he still thinks I have primary HPT. He said a urine calcium over 400 is most definitely PHPT. I can’t figure out why my urine calcium went so high. I’m taking a cal supplement 800 mg/day. I do eat a lot of calcium in my diet. Am I getting too much? Vitamin d is i2000iu/day. My blood tests were non fasting.
        My nephrologist wants to put me on hydrochlorothiazide and do another 24 hr urine in three months. I don’t know if I sent this so you can see my recent test results. If I didn’t send them correctly please tell me how to get them to you.
        Sent from my iPaimage1.JPG

        • Carol Wenmark

          Forgot to tell you that I still have many stones. My nephrologist requested that I contact you about my test results before going on thiazide. Thanks so much.

        • Fredric Coe, MD

          Hi Carol, I am always happy to help but this is a slightly unusual issue – to intervene in a real clinical decision as opposed to simply offering routine technical information about 24 hour urine findings. If your nephrologist would actually want my advice concerning your medical management, S/He would need to contact me and send me the materials deemed pertinent. I would then respond to him/her as well as to you. It is the better way to do this, with a proper relationship. Warm Regards, Fred Coe

      • Carol wenmark

        Here are my last three test results from litholink.

        Vol 24 sscaox. Ca24. Ox24. Cit24. SSCaP. Ph. So UAE. Ua24. Date
        3.38. 3.99. 373. 27. 684. 1.74. 6.944. 0.05. 0.561. 1/7/19
        3.80. 2.37. 171. 26. 300. 0.52. 6.398. 0.17. 0.651. 11/26/17
        250. 3.09. 247. 18. 645. 1.60. 6.963. 0.05. 0.478. 7/27/17

        Here are my last three PTH, calcium and Vit. D,25-OH
        1/15/19. 46. 9.9. 68
        12/31/18. 33. 9.7. 61
        10/1/18. 64. 9.2. 84. Lowered vit d to 2000iu from 4000 after this test.
        Sorry I sent this in three different emails. My nephrologist values your opinion. Thank you.

        • Fredric Coe, MD

          Hi Carol, just looking at numbers, serum calcium levels seem normal so primary hyperparathyroidism is not a realistic idea. It all looks like idiopathic hypercalciuria. Regards, Fred Coe

      • Carol wenmark

        A few more results…sodium is 56, mg24 is 167, cr24 is 1005 on current 24 hour urine. Sorry I sent this in a few emails. Thank you, De Coe

        • Fredric Coe, MD

          Hi Carol, the low sodium should have lowered urine calcium; I do not know what 167 is. Regards, Fred Coe

          • Carol Wenmark

            167 is urine magnesium. All other numbers were good. Ca24/cr24 was 371. Can”t understand why my calcium is so high. I stopped taking calcium pills and get my 1200 mg in food. Appreciate you so much.

            • Fredric Coe, MD

              Hi Carol, Idiopathic hypercalciuria, if that is what you have, raises the urine calcium. If low sodium diet does not bring it down, and your blood calcium is really normal, then meds are in order. Regards, Fred Coe

  7. Lulu

    Hi I am a 50-year-old post menopausal woman postmenopausal since 45 years old I have a high urine calcium read out I’ve had multiple lithotripsy and multiple incidences of kidney stones and my renal doctor wanted me to start thiazides. I however do not want to start any type of water pills because I’ve been reading about the adverse affects of them especially on the heart . I started taking Rice bran in food in the morning and at night but I don’t take any calcium supplements. My calcium level was low but my vitamin D level was extremely low and I don’t know what the differences between those two and I am currently having severe pain in my hips and my shoulders. I don’t know what else to do

    • Fredric Coe, MD

      Hi Lulu, Rice bran and low calcium diet may lead to bone mineral loss. Your best treatment is very low sodium diet to keep your urine calcium down, and a high diet calcium for your bones. Low vitamin D is very bad for bones and I am sure your physician will want to raise it. If your serum calcium is low – as you suggest – the vitamin D deficiency and low diet calcium absorption may be causing serious problems your physician will want to remedy promptly. Regards, Fred Coe

  8. Janet Hanway

    Dr. Coe, I was diagnosed with primary hyperparathyroid disease in August of 2017 and had a parathyroidectomy on 3.5 of my 4 parathyroid glands at Yale New Haven hospital. I have also had very high CA reading in my 24 hour urine tests and am diagnosed with osteoporosis. My 24 hour urine tests have consistently been high and in the neighborhood of 387 or so. While my PTH reading fell to normal after my surgery, it is now a high reading again of 86. My bone density test has deteriorated to the following: The L1-L4 BMD has a T-score of -2.8, the L2-4 BMD has a T-score of -2.8 and the L1 BMD has a T-score of -3.0. The femur BMD T-score is -1.5, the femur neck BMD T-score is -1.9. My doctor has tried decreasing my urine CA through drugs such as chlorthalidone or hydrocholorthiazide but I do not tolerate them. One raised my potassium level and I did not feel well with the other. He is now trying me on a low level of potassium citrate (10MEQ, 3 times daily) to see if I can tolerate it and improve the urine CA level. In addition but unrelated, I have Hashimoto disease of my thyroid. He is asking that I get tested for kidney stones due to the high urine CA level. If the potassium citrate does not work, do you have any other suggestions for approaches to address the high urine CA and osteoporosis issue as my osteoporosis continues to progress even though I am very careful with my diet and do strenuous weight lifting twice a week.

    • Fredric Coe, MD

      Hi Janet, Given that you are at Yale, I hesitate to mention the possibility, but perhaps you have recurrent primary hyperparathyroidism; you seem to have had multi gland disease, and the high PTH and stubborn high urine calcium + failure of bone mineral to increase are most compatible with that possibility. Is your serum calcium perhaps even trivially above normal?? Have they done ionized calcium to check? Hypercalciuria is common after cure of PHPT as we and others have reported, but rising PTH and worsening bone disease are not expected. Perhaps your physicians might consider this idea, if they have not already done so and abandoned it as being unlikely. Regards, Fred Coe

  9. Barb Blue

    Hi Dr. Coe. I am 59 year old post menopause woman. I had my first stone 2/18 with laser lithotripsy. Took Jills wonderful course and follow the diet vigilantly. My last 24 hr urine in May had all good parameters EXCEPT urine calcium was 351. My first 48 hr collection had calcium of 221 and 295–we figured out that my sodium intake was a little too high–and have resolved that issue. 1) Why would my urine calcium jump so much this time?
    Today is my first day of hydroclorothiazinde — 25mg– and I will repeat urine in 2 weeks. Do you recommend increasing potassium intake or should I just wait to see what my urine and blood work looks like. How much of a decrease in urine calcium should I expect? How will I know if it is the medication effect when my urine calcium has been variable (221, 295, 351). My PCP did not believe I needed a bone scan. 3) Do you think I need a bone scan?
    Many thanks !!!

    • Fredric Coe, MD

      Hi Barb Blue, Take a look at the sodium – did it increase. Likewise at the PCR – did your protein increase. Is your urine sodium low enough – below 100 and preferably about 65. Potassium citrate can wait; lower the sodium fully, keep the PCR below 1, and see what the med can do. I suspect part of the increase is you raised diet calcium. Be sure to use foods not supplements if possible. Supplements need to be with meals. A bone scan is a good idea – hypercalciuria causes bone disease. Regards, Fred Coe

  10. Maria Jose

    Hi Dr. Coe. This is Dr. Velasco from Central Vermont.
    I wanted to ask your opinion. I have this 42 y/o woman who has been diagnosed with idiopathic hypercalciuria since 2012 at YNHH. She is on chlortalidone 25 mg a day and k supplements. Her 24 u calcium is 151, electrolytes are WNL.
    She is very frustrated about the disease and her BMD even those she is pre-menopause continues to decline. She is on low dose OCP. I have advised to eat about 0.8-0.9 g of protein a day and to be on a low salt diet. I reviewed some papers and it seems there is not much evidence about using bisphosphonates in pre-menopause woman to improve BMD or worst there is not evidence that that will improve fracture risk. Am I correct? Will you do something differently? Thank you so much.

    • Fredric Coe, MD

      Dear Dr Velasco, The bone disease of idiopathic hypercalciuria is indeed evolving and we do not know enough. However we do know this much: Bone mineral balance will rise with low sodium/high calcium diet, and with low dose chlorthalidone. That she is on chlorthalidone and got no response suggests a problem with diet sodium, or calcium, or both. Unfortunately the data here are incomplete. My own balance study used only chlorthalidone and showed positive bone balance, but I was fortunate that calcium intake was ample. To achieve positive bone balance in IH takes a lot of diet calcium, but none of the studies also added low sodium (65 mEq/d or better). In one trial – the only one remotely related to your case – high calcium + low sodium increased bone mineral in peri-menopausal subjects. So, I would use the combine of low sodium and high calcium and CTD and also consider if she can safely continue estrogen after menopause. As for bisphosphonates, I share your concerns because IH bone disease has some low turnover features. If needed she may benefit from some of the newer MC antibody treatments if needed to ward off fractures. Regards, Fred

      • The Patient In Question

        Hello, folks. I’m the patient in question. I was dx’d at U-C in ’06, actually, by Dr. Favus, while doing my residency. I have never formed a stone, and an U/S at U-C found no stones at that time, either. (Isn’t that strange?!) I generally keep Na<1000 mg/day, and Ca intake I obtain from 3 servings of yogurt daily, plus or minus a pile of kale or other high-Ca greens, or a couple of sardines. I experienced bone density improvement one year only, and that was a year when I was living in Indonesia, using Tums for most of my Ca, and eating an extremely low-Na diet with nearly all protein from tempeh, a fermented soy cake. After that, my spinal bone density improved. It worsened after I returned to the States, and I've wondered why ever since.

        Here's my question, Dr. Coe: would it be helpful to add Ca supplements atop my yogurt intake? Perhaps Ca citrate, recheck bone density in a year? From past experience, I know my urinary Ca rises when I use supplements, but I'm unsure whether that would negatively affect bone density. I'm not worried about stones. I'm extremely worried about my spine.

        • The Patient In Question

          IN other words, might my poor spine vacuum up extra Ca if I provide it, given that I don’t seem to form stones (knock on wood)? Could I safely bump Ca to, say, 1500 mg/day and see what happens?

          • The Patient In Question

            I would also welcome insights as to why my hip bone density improved, 2018 vs 2012, but spine worsened. Why would these two types of bone be going in different directions?

            • Fredric Coe, MD

              Hi Again, The bone disease of IH can be focal, and I do not know why. Sorry, Fred

              • Lily

                Hi there, I’m 19 and have had kidney stones since the age of 11. Currently I have one 9 mm stone in the lower pole of my left kidney as well as a 4 mm stone in the middle. Although both are non obstructing I’ve been getting a lot of pain in my left kidney..what can I do to alleviate this? Also, my nephrologist put me on potassium citrate and said my diet was fine. My blood calcium levels fluctuate from 9-10.1. Is there a chance this could be due to my parathyroid? My 9 mm stone grew from 2 mms in January to 9 mm in late April. The 4 mm stone was not there on the last scan I had in March. Why am I producing stones so fast?

              • Fredric L Coe

                Hi Lily, your variable blood calcium does suggest primary hyperparathyroidism, and you should be sure and get proper testing for it. Pain from non obstructing stones is not uncommon, and we do not as yet know if more surgery will improve it. Regards, Fred Coe

          • Fredric Coe, MD

            Hi, I suspect you might settle at about 1200 – that was the trial. Those women were peri-menopausal, so not like your condition, but it is all we have. If you keep the sodium low enough, try 1500 mg calcium but check the urines. Consider a very low dose of chlorthalidone 12.5 mg daily as an extra – it can raise bone mineral balance. Regards, Fred

        • Fredric Coe, MD

          Hi Patient in Question, I gather you have idiopathic hypercalciuria and its associated reduced bone mineral density. Your experiment in Indonesia with very low sodium diet and extra calcium resembles the one – yes only one – actual trial concerning effects of sodium and calcium intake on bone balance – in this article. I believe the very low sodium was important and perhaps the Tums. Here, with some bone loss, I would consider using supplements – the best way is with larger meals – that was how the trial went – along with the lowest possible diet sodium. I would use 24 hour urine testing to be sure of the sodium, hard to gauge. Your urine calcium rise with diet calcium is entirely a function of the corresponding sodium intake and consequent fractional excretion of sodium, so the lower the better. Regards, Fred

          • The Patient In Question

            Thank you for your reply , Dr. Coe. I will try these ideas. I’ve been on chlorthalidone for 12 years now, and it has not really helped–hence my and Dr. V’s frustration and search for new approaches. (Would you mind removing my name from your reply?)

            • Fredric Coe, MD

              Hi Patient in Question, perhaps your diet sodium is high enough to offset the effects of the medication. If bone mineral retention cannot be otherwise maintained bone directed meds may ultimately become your best alternative – I think you know that. Fred

              • The Patient in Question

                Please remove my name from your previous reply. My diagnosis is now linked to my real name on search engines.

              • Fredric Coe, MD

                OK, I think I did that. Fred

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