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, and – not rarely – use of diuretic drugs which can lower urine calcium losses, prevent stones, and protect bones.

All this requires effort and belief. 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.

Unlike Supersaturation, what stones are, citrate, IH is not a topic amenable to piecewise narration. It is one single complex departure from normal, and needs one single complex presentation.

Without apologies, here is that presentation.

As I did with salt, I have added summaries in bold italics. 

Why The Bathers?

I placed the bathers here because nothing seems so fit as bathing for an explication and a metaphor for IH. Not these illuminated and immortal bathers, but the simple bather in a bathtub engaging with the flow of water as, in my terms, the kidneys, bone, and gut engage each other in the flow of calcium through the body.

LIkewise, as the images of bathers capture in canvas a far larger sensibility about life, the image of a humble bather and bathtub captures – I believe – a far larger truth about our bodies.

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.

Renoir attempted to reconcile 17th and 18th styles with late 19th century artistic sensibilities, an effort of three years which his peers considered cowardly retreat into classicism and a betrayal of their shared desire for the new and modern.  

Cézanne also painted a modern homage to classicism, but unlike the shiny realism of Renoir his is an antique world, of goddesses perhaps, framed in formal structures and set back from the worldly plane.

Both artists reconciled earlier artistic visions with their own time, itself devoted to immediacy and the capturing on canvas of ephemeral light which is here and gone on the moment. Both present a world of permanence and monumental scale, the one austere the other playful.

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 Hypercalciuria?

High urine calcium ‘clinical hypercalciuria’ is a urine calcium excretion above 200 mg/day in either sex.

Hypercalciuria is the name we give to a high urine calcium excretion, but ‘high’ must mean something more than mere quantity. I agree with Dr. Gary Curhan that urine calcium is ‘high’ when it causes disease, as blood pressure is ‘high’ when it causes disease. And his criteria for ‘high’ are acceptable to me.

Association with Kidney Stones

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 top of the solid bar reaches above one, which is the case for all bars above the 150-199 bin, increased risk is very likely to be present present; that point of increased risk begins, in both sexes, around 200 mg/day. Throughout the range of urine calcium excretions, risk rises smoothly with urine calcium, which reinforces its significance.

Given this, ‘high’ urine calcium – clinical hypercalciuria – is above 200 mg/day in men and women, because above that level begins risk of at least one disease – stones.

What Does ‘Idiopathic’ Mean?

Many diseases can raise urine calcium excretion, but among hypercalciuric stone formers the vast and overwhelming majority have no disease but rather a familial and almost certainly hereditary tendency to excrete, on average, more calcium than people who do not form stones.

It is for this reason, they are said to have ‘idiopathic’ hypercalciuria – ‘idiopathic’ meaning high of itself, or without overt cause.

Do We Need Special Diets During 24 Hour Urine Collections?

I do not believe special conditions of diet are critical for determining if someone has IH. I say this because the Curhan data were assembled as things were. Some people were no doubt eating more, some less calcium or sodium.

That is not to say diet does not matter. It does. But if one wants to determine who has IH in practice, or choose people for experiments, I think it is reasonable to collect 24 hour urines without setting any diet requirements, and that is exactly how we practice here and, incidentally, do research.

Who, Then, Has Idiopathic Hypercalciuria?

Until someone corrects me I say a stone former with urine calcium excretion above 200 mg/day, either sex, is hypercalciuric. If no disease is causing hypercalciuria that stone former has IH. 

For research, I might select for higher values. For example, above 250 or even 300 mg/day is a better choice if one wants to understand how the high urine calcium comes to be and chooses subjects who will give more robust signals in a research protocol.

Calcium Excretion in Normal Women and Men

IH is not a disease; it is simply the label for someone at the high end of the normal distribution – like tallness.

You can see how a urine calcium values from normal adult men (blue) and women (red) sweep from low to high in one unbroken distribution. People normal uca male anf female.pngwhose values are in the higher registers show up among stone forming populations at a higher rate than those with lower urine calcium losses. That is what the Curhan data show us: People who became stone formers during years of observation were those with higher urine calcium excretions.

See where the Curhan demarcator – 200 mg/day – resides; it is at about the 75th percentile: 25% of people are above it. But stone formers are certainly not 25% of adults. Perhaps 7-10% or less is a reasonable estimate of who will form at least one stone in a lifetime. So high urine calcium is indeed like high blood pressure: It confers risk, but risk will not always culminate in disease.

The 95th percentiles of these distributions, conventional cut points for extreme values, are at about 275 and 325 mg/d of calcium, and once were used for the definition of ‘high’ urine calcium. But if disease causation is the criterion, as it should be, they are way too high. It is like older definitions of ‘high’ blood pressure, which greatly underestimated the risk from values within the upper mid range of values from large populations.

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.

Hypercalciuria Raises Supersaturation

Urine calcium above 200 mg/day goes with high supersaturation and stones.

Stone crystals cannot know about how much calcium is lost in the urine, they can only respond to supersaturation. High calcium excretion, however, will associate with high supersaturation given the simple logic that for any range of urine volume, and of salt ligands – divalent phosphate and oxalate – more calcium in the urine will raise calcium concentration and therefore the critical product of calcium and oxalate (calcium oxalate crystals in stones) or calcium and divalent phosphate concentrations (calcium phosphate crystals in stones).

This article is a delightful window into stone prevalence in Tennessee that I chose because it illustrates two points and because it is probably not popular and could use some readers. In a study of uranium workers the authors found that 40/208 reported kidney picture from urolithiasis in Tenessee paperstones, much higher than the 7% found in the NHANES 11 survey current at the time. They reported what Curhan has yet to report: Supersaturation, the central issue in crystal formation, was a good predictor of stone formation.

Calcium oxalate supersaturation is shown here in somewhat different units than those we usually present, but as it rises (horizontal axis of the graph) probability of stones (vertical axis) increases. Family history matters: Those with it get stones with less supersaturation.

You might ask by now, what about hypercalciuria in that population?

Those with stones had a calcium excretion of 250 mg/day, those without had a value of 164 mg/day. One was above, the other below the Curhan demarcator. Urine volumes and urine oxalate excretion did not differ.

IH is Hereditary

IH is familial, breedable in animals, and a cause of stones and of hematuria (urinary bleeding) and pain in children.

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.


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. Some of those siblings were stone formers, others were not. As a contrast, we were able to collect samples from children in families that did not harbor the stone forming trait as none of the children, their parents, or other relatives were known to form them.

Urine calcium excretion is shown in the same q plots as I have shown before.

Urine calcium excretions of siblings with more than two stones are farthest to the right – highest. 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.

Even though children are smaller than adults, we can compare amounts of daily urine calcium loss to those of adults because the values are adjusted for body surface area. Such an adjustment is widely used to compare people and even animals of varying sizes.


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. In fact the lovely figure from Tenessee shown above makes clear that a positive family history of stones shifts the probability of stones upward at any given level of supersaturation, and it is mainly supersaturation that IH can influence.

There is more, of course. Possibly, and we have put this idea forward, IH occurs because of altered pathways for calcium movement through the nephrons of the kidneys and it is these altered pathways that might promote crystallization and stones. All that is for a later time, as it is speculative, and a matter of ongoing research.

Bone Disease

IH can cause bone mineral loss and bone disease, so stone formers are at risk for fractures.

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 had occasion to measure bone mineral density in a number of stone formers with IH, collect 24 hour urine samples,
and then make a follow up measurement of bone mineral density three years later. From this, we could ask if changes in bone mineral were at all related to the urine calcium losses.

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 the points are aligned along the initial urine calcium losses (horizontal axis), the change over time is negative: ASPLIN BMD VS UCAPoints above the line at 0 are shifted to the left (lower urine calcium losses) than those below.

The ellipses are designed to fit around 68% of the points without any assumptions about the underlying distribution, if any, that the points reflect (like a normal distribution). For the interested, they are non parametric containment ellipses, and their tilt does
indeed reflect correlation of one axis with the other.

Using statistics not shown here, the slopes of change in bone mineral over time are significant. The higher the urine calcium, the larger the loss of bone mineral.

IH Is A Main Factor in the Bone Disease of Stone Formers

This is a bold statement but defensible.

Stone formers have a general increase of urine calcium excretion, and if risk of stones begins at about 200 mg/day, and risk of bone disease seems to follow having stones, it may well be that urine calcium levels as low as 200 mg/day are enough to promote bone disease.

Although Sakhaee is careful to point out that bone disease associates with stone disease, IH is obviously a prominent issue 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?

I have quoted Dr. David Bushinsky elsewhere, and will repeat myself here:Every stone clinic is a bone clinic, and every stone former should be evaluated for bone disease.’

The stone forming population is rife with bone disease, easily overlooked until a fracture, possibly one that could have been prevented.

Dr. Sakhaee points out that US insurance practices exclude bone evaluation in large swathes of stone forming populations. I say 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 in the urine can come from bone or diet; the lower the diet calcium the more is lost from bone

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

Over the whole of the 20th century it was not rare for laboratories to determine net calcium absorption in normal people and sometimes in stone formers with IH. To do this they fed subjects a fixed diet, usually in a clinical research center, 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.

These studies are laborious. Typically measurements are made in 6 day blocks after a few days to equilibrate with the diet, so subjects remained in the clinical research units for perhaps 8 – 10 days. But the measurements have a kind of immortality rare in science. Howsoever old, they remain usable, and can be aggregated, as I have done here, to show something important about humans.

Normal men and women absorb about 18% of diet calcium – the orange 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% median. 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, so with very low calcium diets this ‘endogenous’ secretion can result in losing more calcium in the stool than is eaten.

One very early theory of IH was simply over absorption: High efficiency 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

Food without calcium causes calcium loss from bone; be careful what you eat if you have IH

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

jack NEJM pictureWe know that calcium stone formers are often people with IH and that relatives of calcium stone formers have IH so this is normals and a population enriched with IH.
Look 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!

Each period was 20 minutes, so this experiment went on for 2 hours. The higher urine calcium with sugar must come from bone. It came from bone in normal people and in those with IH but the latter lost far more calcium than the former.

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 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 with IH were different. They lost more 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 being lost. At that time in the history of this field, such a proof was not so easily accepted as now.

Bone Calcium Balance Is More Negative in IH than in Normals

I already showed you calcium absorption as determined by the difference between calcium eaten and lost in the stool. Balance – or retention – is the difference between the calcium absorbed and calcium lost in the urine during a study period, usually of over 6 days.

Here are the calcium balances – or retentions – of the same people whose absorption data I showed above plotted against calcium intake.

In this plot, IH is in red, and normals in blue. The lines running along the points, are tracking the mean – average – value from left to right, like the common trend line in spreadsheets. At diet calcium intakes above 500 mg/day, the average 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 – blue – 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), the mean rises slowly with diet increase, 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.

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.

What Does All this Mean?

Fractures follow stones like a shadow. No doubt the fractures relate to the excessive bone mineral losses. Stone clinics are bone clinics.

Mineral Metabolism And Bathtubs


A real bathtub has two drains. The one at the bottom is the one you can open or close. The other one, up near the top, is to keep the tub from flooding your bathroom if someone inattentive leaves the faucets open. This second drain is about the level where most people would want their bath water. It has to be. To keep the water line above the open waste overflow drain would require both faucets be wide open.

Fill up a bathtub part way, with the bottom drain and both the hot and cold faucets partly open. Be careful to bring the water level to below the upper drain as we want it to be out of the picture. Wait until the water level is steady.

Call the cold tap inflow from diet, and the hot tap inflow from bone. The drain is the kidneys, the flow through the drain is the urine calcium excretion. The height of the water in the tub is the blood calcium concentration. Because the water level is steady the flow out of the drain equals the sum of water coming in from the hot and cold water taps combined.

A simple and compelling vision of IH is easy to experience. Open the cold tap. This is like diet calcium coming into the blood. As the water rises, the greater weight of water will force more water through the drain so the level will become steady. If you close the tap back to its original position, the water level will fall again.

Called absorptive hypercalciuria, this was for decades a powerful vision that affected treatment. Since calcium absorption is above normal in IH – I just showed you it is, every meal would lead to a larger swing in absorption and urine calcium loss, as in the bathtub. Bone would be unaffected – that there was a bone disease was not known decades ago. Treatment was obvious: Low calcium diet.

A More Realistic View

Plumbing analogues are helpful, but there are many details it cannot capture.

The Flows of Calcium

The gut takes in food calcium, absorbs some, back secretes some, and losOVERALL CALCIUM HANDLINGes the rest in the stool (large tube at the left in this diagram). Bone perpetually take up and gives up calcium as it remodels.

So blood has two supplies: Gut and bone.

The urine calcium is the sum of the two: net gut calcium uptake + the net difference between bone resorbed and mineralized.

The Kidneys

The kidneys take extra words because they are fancy bathtub drains.

They filter water out of the blood at a high and reasonably constant rate. The amount of calcium filtered into the nephrons of the kidneys is the product of that filtration rate and the blood concentration of filterable calcium (UF in the figure). A high percentage of that filtered is reabsorbed back into the blood – about 98%.

So the urine calcium is the amount filtered times (100 – the percent reabsorbed) and that urine calcium has to equal the net gut calcium uptake + the difference between bone resorbed and mineralized.

This system is self balancing in a way. If urine calcium is less than the gut and bone supply into the blood the calcium concentration and filtration will rise, and the reverse. The system is also regulated, because the kidney cells can vary the percent of calcium they reabsorb. They tend to act so as to keep the blood calcium steady.

How More Calcium Gets Into the Urine in IH

Put real people into a clinical research center, feed them exactly the same diets, and measure the things we have just been talking about: Urine calcium, the amount of calcium filtered, and the percent of filtered calcium reabsorbed. How do the kidneys get more calcium out in IH than in normals? Is it more filtration, less reabsorption, both?

In this figure men are on top, women on the bottom, fasting are the two left panels, fed are the right two panels. 4 plot of ucammolhr vs flcammolhr males on top females bottom fast left, solid is n dashed is ihTriangles are IH circles are N. The ellipses of containment are as in the graph of bone mineral density over time. Dashed lines are IH solid lines are N.


Look at the left panels. This is before eating. The urine calcium – on the vertical axes – does bear some relationship to how much calcium is filtered – horizontal axis, especially in men and IH women. We would expect that – filter more into the nephron tubes, more comes out.

But, urine calcium is higher in IH than normal – the dashed ellipses ride higher than the solid ones, and the triangles than the circles, even though the amounts filtered overlap entirely. It is as if one balloon rose above the other over a single plot of ground.

Look at the tops of the graphs, on the borders. The pretty curves overlap – they mark out the filtered loads, IH and normal, showing how they do not differ. Look to the right sides of the graphs. The notched bars mark out the amount of calcium in the urine. They do not overlay.

No food has been eaten yet. Of course, some may be still trickling into the blood from last night’s meal, so we cannot be sure. But the IH kidney cells are not reabsorbing the same percent of filtered calcium as are the normals, that is the message. And therefore more calcium is being lost in the urine. One could say the drain is open more in IH and, of course, one or both faucets: Diet remnants or bone.


The right panels are dramatic, are they not? The normal balloons lift up in women and men: No change in filtration, but much more in the urine – lower percent reabsorbed. For IH, the same but a lot bigger. The balloons are like rockets, shaped like rockets. The tubule cells are letting what has been filtered out. The drains open wide. See where the curves on top of the graphs overlap showing how filtered loads are identical, while the bars at the right borders diverge, that for IH high above normals.

And the faucets? Of course it is partly the diet. IH raises absorption. But, with open drains, how can we know?

Proof That Bone Loses Calcium

jl glucose storyIn 1970, Jacob Lemann did this experiment. He gave glucose (no calcium, just sugar) to normal people but reduced filtration and calcium filtered load by asking them to stand quietly. If you stand that way blood pools in the legs, and filtration falls.

On the left side at the top you can see the filtered calcium fell a little. At the bottom you can see that urine calcium loss (UCaV) fell a lot.

When he did the exact same thing but gave glucose (right panels) the filtered calcium actually fell more with standing but the urine calcium rose. This is reduced tubule calcium reabsorption – opening of the drain.

The higher urine calcium could not be from diet – there was no calcium. The filterable calcium stayed steady (1.42 vs. 1.40 mmol/l) between the control and glucose periods – the water level in the bathtub was constant. The bone was giving up the extra calcium.

This was in normal people. I see no basis for arguing that the same would not occur in IH.

How IH Works

The kidneys behave like open bathtub drains, so to keep blood calcium up bone or diet or both must provide more calcium – like open faucets: Bone is at risk.

In normal people and in IH it is as if faucets open and the drain open in such perfect synchrony and quantitative coordination that blood calcium can stay remarkably constant even as calcium reabsorption falls and urine calcium rises.

In a real bathtub, coordination of faucets and drains is not a problem. You want, for example, more flow – perhaps to keep the soap flowing away, or maintain a specific warmth in a cold bathroom – but you also want the water level to stay where it is.

You open the faucets and also open the drain a bit.

But who is you in IH?

This is where we are.

I mean, we who do this kind of research.

What coordinates the faucets to the drain. Which faucet? We know bone can be lost, we know calcium is absorbed more rapidly than normal. So both play a role, but how much of one or the other we are not sure.

Why Would Patients and Physicians Care?

That should be obvious.

The drain is open in IH, more fed than fasting, but open. The serum calcium is maintained by open faucets. There are no alternatives to these statements.

If there is no calcium in the diet bone gives up some of its mineral.

I would like to think that when diet calcium is ample bone is safe, although I have no proof of that and I do not know what I mean by ample. Even at high calcium intakes people with IH can be in negative bone calcium balance.

Therefore: Low calcium diet is never a good idea in IH. Bone can suffer. Perhaps not always, perhaps not in everyone, but often enough it is not a good idea.

This is why patients and physicians should care. It is why it has been useful for you to follow along the tortuous narrow dusty road.

Even if plagued by calcium stones, do not believe that reducing diet calcium is a safe option. It might be under some circumstances but cannot be relied upon as safe. Bone is in jeopardy. Eat calcium and use other measures to control the stones: Water, reduced sodium, avoidance of excessive sugar and protein loads, and use of potassium citrate and thiazide type drugs in combinations as needed.

Stone patients are potential bone patients and we want that potential to remain a potential not a realized and completed disease.

All of these treatment measures are of importance, and I will try to discuss them in subsequent articles.

What Should Scientists Care About?

How do the faucets and drain coordinate.

They seem to do so beautifully, and mysteriously. It is almost too good – their matching, the constancy of serum calcium. If I were young and out to do new science I might ask about this linkage of the faucets and drain.

But I am not.

Is It Clear About the Picture of the Bathers?

Cheers, Fred Coe


  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

Leave a Reply