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. Robert M

    Dr. Coe, I’ve done 24 hr urine test 7 times, my average Ca 24 is 402. Leading up to the most recent test I was on 12.5mg of thiazide once a day along with an effort to reduce sodium and protein. Results from the recent test was 380 vs 480 on the prior test. Urine sodium levels showed improvement. I have a renewed desire to solve this because I’m more concerned about bone disease than I am stones. My first DXA 4 years ago showed osteopenia in one forearm. I have my 2nd scan on Monday. I’ve recently been on 25mg of chlorthalidone along with a renewed effort to lower dietary sodium and protein but a side effect I’m having is ED. I tried to go 12.5mg once a day but same side effect. So my main question: Is it likely that I can get the urine calcium down to reasonable levels with ONLY a very strict low sodium and low protein diet or from your experience will that be very difficult to obtain without a thiazide type drug? I see two options right now — go without medication and go very strict on diet OR go with the chlorthalidone, along with stricter diet, AND adding one more medication for the ED, something I REALLY don’t want to do if I don’t have to. I guess I’m just looking for a reality check in this regard. Could I get your thoughts? Also, is 400+ average Ca 24 typical for idiopathic hypercalcuria or is that off the charts? Seems to me to be very high to me. I’ve had the thyroid checked, etc. and a cause has not been identified. Thank you again. Best to you, Robert

    • Fredric Coe, MD

      Hi Robert, You do indeed have a high urine calcium and unless there is a systemic disease as cause – this is something your physician must determine – it is idiopathic hypercalciuria. As you note, IH can cause bone disease. If you want to avoid thiazide sodium intake needs to be low indeed – there are no trials, so I am just guessing in what I hope is an informed way. About 1000 to 1500 mg would be needed along with high diet calcium. In the one decent study it took this kind of sodium and calcium to bring bone mineral balance to neutral in postmenopausal women with bone disease. Diet protein raises urine calcium but whether it lowers bone mineral is a vexed question; low protein below 0.8 gm/kg/day is not advisable. If bone does not stabilize you may have to consider a bone directed medication. Regards, Fred Coe

  2. Robin

    Hi Dr. Coe,
    New copy without all the autocorrect errors!
    This is a great site and it has been very helpful in trying to figure out my issues. I am curious if idiopathic hypercalcuria causes any symptoms such as polyuria, polydipsia and nocturia? I can’t find these associated with IH in any articles.

    My initial concerns which got me into my endocrinologist was a worsening of nocturia, polyuria and polydipsia. 4.5-6.5 liters per day. I am a 48 yo female and these symptoms have gone on for 10 years but have been increasing the last 2- years, interfering with sleep and daytime routines. And extreme fatigue (I am not overweight and very active, run 3-5 mi, but has become very hard to keep up) I have no history of kidney stones.

    My initial labs:
    Spot urine osmol 158mos/kg (300-900)
    Spot serum osmolality 289mos/kg (280-300)
    Ferritin 16 ng/ml (6-264)
    Vitamin D 32ng/ml (30-80)
    PTH intact 68 pg/ml (8-54)
    Calcium, PTH 9.1 mg/dl (8.4-10.6)
    Arginine vasopressin <1 pg/ml (1-13.3)
    Overnight water fast 14 hrs: Urine osmolality 750 mos/kg (300-900)
    24 hour Urine volume 4600ml
    24 hour Urine calcium 432.3 mg/24hr (100-300)
    Serum calcium 9.4 mg/dl (8.4-10.6)
    24 hour creatinine 1584 mg/24hr (800-1800)
    Serum creatinine .77 mg/dl (.52-1.04)

    I was placed on 2.5mg of indapimide for four weeks and repeat labs:
    Urine calcium, random 7.7 mg/dl (?)
    Serum calcium increased to 10.1 mg/dl (8.4-10.6)
    Urine creatinine, random 29.93 mg/dl (?)
    Serum creatinine, random .7 mg/dl (.52-1.04)

    I have other labs too but thought these most pertinent. It seems like my calcium/creatinine ratio .22 and .18 indicate PHPT and my serum calcium is increasing on the indapamide which does occasionally unmask PHPT from my reading. I am still not convinced I don't have an ADH problem or partial diabetes insipidus, nephrogenic or central, due to the nocturia (2-3 per night with up to 800ml). I also thought it could be hyperaldosteronism. My endocrinologist initial thoughts were IH and I have yet to see him after I started on indapimide and my calcium went up. But perhaps just IH?

    Family hx: dad had kidney stones and parathyroids removed. Also an adrenal tumor.
    Grandma with thyroid issues, HTN- unable to lower with meds and ultimately dialysis.

    Thank for any insight or information especially on the symptoms you have seen in your patients with IH if this could be likely for me.

    You have provided a wealth of knowledge here. Thank you again.

    • Fredric Coe, MD

      Hi Robin, You do seem to have idiopathic hypercalciuria given the high urine calcium, normal serum calcium, and lack of obvious systemic diseases. There are indeed some cases of IH with nocturia, noted especially in children, and ascribed [ without complete data – to activation of the calcium receptor in the renal collecting ducts with reduction of aquaporin insertion. The proper way to treat IH is with marked diet sodium reduction to 1500 mg – the present healthy people ideal – and see how far down the urine calcium comes with just that one measure. It may fall a lot. Indapamide is fine on top of this low sodium intake. Nocturia is a special problem because urine calcium overnight stays up in IH – we published that – and thiazide does not reliably lower it. The low sodium may well do so. Potassium citrate may do better with it. So, first achieve the low sodium diet and see what happens. Use the 24 hour urine sodium as a measure of diet intake – it is very close. Regards, Fred Coe

      • Robin

        Thank you I am going to lower my salt and see what happens. The polyuria/nocturia drives me nuts but has maybe kept me from getting stones. My brother and dad have them.

  3. Elaine

    I am 54 years old with severe osteoporosis ( – 3.9 hips and – 2.9 spine) and long history of kidney stones (since I was 15), mainly calcium oxalate.
    All my tests, including 24 hour urine calcium tests shows normal results. Should I repeat the urine 24 hour test?

    • Fredric Coe, MD

      Hi Elaine, Normal is a metaphor in urine studies. I would suspect you have a higher than not urine calcium and perhaps a low calcium diet, but without information I cannot be sure. Genetic hypercalciuria masked by low calcium diet is a pathway to bone disease like yours. Alternatives abound, so it this is not correct you need more detailed evaluation. It is important to figure out what is wrong and fix it. Regards, Fred Coe

  4. Suzanne

    Hello Dr. Coe –
    I appreciate all of the data you share. I do have 2 quick questions.
    2011 had surgery to remove parathyroid tumor found after 1st kidney stone.
    5 years have passed and symptoms have come back, multiple kidney stones, large weight gain and generally feeling terrible.
    Recent Parathyroid Hormone Intact test result normal at 41 and blood calcium 9.3.
    Dr ordered 24 hour stone formation test, results are as follows:
    Calcium Urine: 339 mg/day
    Oxalate Urine: 46 mg/day
    Uric Acid Urine: 617 mg/day
    Citrate Urine: 544 mg/day
    pH Urine: 6.8
    Total Urine Volume: 1.62 L/day
    Sodium Urine: 131 mEq/day
    Sulfate Urine: 19 mmol/day
    Phosphorus Urine: 744 mg/day
    Magnesium Urine: 148 mg/day
    Ammonium Urine: 26 mEq/day
    Potassium Urine: 69 mEq/day
    Creatinine Urine: 1311 mg/day
    Calcium Oxalate: 3.71
    Brushite: 5.85
    Sodium Urate: 2.54
    Struvite: 9.36
    Uric Acid: 0.30
    Do I need to be concerned about Brushite level
    Can I assume that I am IH?
    Thanks for your time!

    • Fredric Coe, MD

      Hi Suzanne, You have a normal serum calcium and a high urine calcium so it is IH but we have described – so have other groups – hypercalciuria after cure of primary hyperparathyroidism and are not sure if it is IH or something like IH. In either case treatment is the same, and I would advise it – low sodium diet, avoidance of high sugar loads, a normal protein intake, high fluids, and if all else fails, some medication. Here is a recent article that outlines all treatments. You may indeed be forming calcium phosphate stones, but even so treatment is much the same. Regards, Fred Coe

  5. Dr ali

    Thank you very much for this nice information about IH, I have question about children with IH, is there any other treatment or not?

    • Fredric Coe, MD

      Dear Dr Ali, IH in children is like in adults. If stones are forming low sodium high calcium diet is ideal and a low dose of a thiazide like drug if more than diet is required. It is inherited so screening of siblings for hematuria or crystals is wise. Children have low urine volumes so control of diet sodium is very valuable. Regards, Fred Coe

  6. Dan

    Hi Dr. Coe,
    I am really enjoying your articles on IH as I am a mathematics professor and like to know how things work. You use very helpful analogies and do an excellent job of explaining complicated concepts. I have extreme IH with an initial 24 hr urine calcium excretion level of 597mg in 2011. With dietary modification, chlorthalidone, and potassium citrate I was able to lower my levels to about 250-300mg on subsequent collections. No new stones after initially having 6 just before the first urine test. You are absolutely correct in saying that a stone patient is a bone patient. A bone density scan in 2011 showed I had osteoporosis in the lumbar spine at the age of 47. Fortunately the current interventions appear to have produced a positive calcium balance as my follow up scan in 2014 showed about a 6% increase in bone density. I had earlier stones in my 30’s and a family history of stones but the urologist I saw then never requested a 24 hr urine collection. A more proactive stance then could have avoided this bone loss completely. You discussed that calcium excretion increases with increased filtration. GFR decreases as we age. Does this mean that IH individuals could excrete less calcium as they age possibly improving calcium balance? I see myself as being very fortunate that my current treatment has worked so well, considering how extreme my initial calcium loss was, and wonder if the current interventions will continue to work. If not, are there still additional tools left? I have read that neutral phosphates can also reduce urine calcium even further in conjunction with thiazide type diuretics, but I am under the impression that they are not used very much. Bisphosphonates are not an attractive potential option to me.
    Thank you again for your article!

    • Fredric Coe, MD

      Hi Dan, I am honored that a mathematician would approve. My early career dreams were in mathematical biology but alas I lacked the holy fire for such adventure. Urine calcium does fall with falling filtration and I think that is because calcium reabsorption along the tubule can only fall so much on a percentage basis. In the proximal tubule it is reabsorbed mostly in a passive manner along with sodium and water, and as the kidneys lose filtration fractional reabsorption falls from about 20% to perhaps 40%. But that fall is just enough to balance the loss of filtration. The next segment reabsorbs calcium electrogenically and that cannot be regulated down very much. Phosphate is just the other way. Tubule reabsorption can fall enough that urine phosphate remains constant as filtration falls. As for neutral phosphate, its effects on bone are not well explored in humans. Bisphosphonates do prevent fractures in female osteoporosis but have not much trial data in IH. Warm Regards, Fred Coe

  7. Jeannie k. Hughes

    For 15 years I have been walking around with 6 small passable stones. Now for the last 4 years I am making them so big so quick that by the time my Dr and I realize I have a stone too big it is too late. Every year for 4 years once every summer (always) I need surgery. The basket seems to work best with me.
    The last two times I have become spetic. I stayed in hospital for 4 days 2 in intensive care.
    The first year I tried just not eating high oxalates. Next year I added low protein low fat. Next year I went vegan (I made 3 stone two In one kidney two in the other Dr went and got them all at one time. After that I was upset and ate like I wanted to. Big mistake I had a 2cm in Feb by may it was 7. That is the one that almost killed me.
    So my Dr has me on a low sodium, fat, protein, and oxalates. He wants me to eat a yogurt a day, taking a probontic pill, 3 cranberry pills, drink a gal water.
    So I have a read so much on the internet and like what UC drs. Can you tell me how much protein, and sugar I need. I am doing 1000g of calcium, 3000g of salt and under 30g of fat. I have completely taken sugar out. I am drinking a cup of 1percent milk with every meal.
    It scares me now that I have been sepis now. They say the next time will be 50percent chance of doing it again. Is that right?
    Doing the above for a month when I went to my Dr this week I had a bladder infection. Ugh!!!
    My calcium level is 9.2. The blood work shows cal. in urine was OK.
    I am breaking bones too now.
    Two times last year. Elbow three breaks and my upper arm three breaks. My husband has almost house arrested me.
    Any thing you can tell me will be very appreciated. I am at my last straws.
    Jeannie Big Stone Maker

    • Fredric Coe, MD

      Hi Jeannie, I guess so much is missing I need to ask. What are your stones made of? What are your 24 hour urine chemistries? From the course of things I would guess the stones are calcium phosphate and your urine calcium is high and that is why you have bone trouble, but that is really guessing. Let me know more and I will try to be more useful. Here is a good pattern to work off of. Regards, Fred Coe

  8. Kris

    Hello Dr. Coe, now a blood test from last week shows serum calcium has increased to 10.4. PTH is 32. My doctor wants to schedule a scan for parathyroid. Is there anything else I should consider?
    Thank you.

    • Fredric Coe, MD

      Hi Kris, The diagnosis of primary hyperparathyroidism relies on this: high fasting serum calcium values and PTH values not suppressed and high – or rarely – normal but not low urine calcium levels. Be sure all are present. A parathyroid scan is useful in planning surgery but is not a real test for the disease having too wide a false positive and false negative range. Be cause multiple fasting serum calcium levels are indeed high and that the PTH measurements are in the same serum as those fasting calciums. Regards, Fred Coe

      • Kris

        Hi Dr. Coe,
        My latest fasting blood test has ionized calcium 5.4, PTH 22, and serum calcium 9.8. I don’t know if this is still trending towards parathyroid concerns or too soon to tell. Thank you.

  9. Kris

    Thank you!

  10. Kris

    Hello Dr. Coe,
    I’ve been reading your articles since May when I had a 2.6 cm calcium phosphate stone removed (PCNL surgery). Diagnosis is IH. Recommended preventive treatment would have been chlorthalidone, but I have a sulfa allergy. I am 48 yr. old female, 5′ 5″, 120 lbs. and had a hysterectomy last September. No prior stone history, no family history of stones. I think there is a connection with hypercalciuria and low bone density or risk for osteoporosis. What about acidic diet or conditions in the body that would cause calcium to be pulled from the bones to correct and balance the blood calcium level and PH levels? Could this action be one cause of excess calcium in the urine? I am still searching for a plan to prevent future stones and have read several studies about Vitamin K, K2 (mk4 and mk7), potassium (citrate and bicarbonate), and magnesium along with low sodium, low protein diets. What has been your experience if you had an IH patient with a sulfa allergy – can prevention be achieved without thiazide diurectics?
    Thank you.

    • Fredric Coe, MD

      Hi Kris, Your questions are very sophisticated, and the right ones. If you cannot use a thiazide, low sodium diet at about 1500 mg/day is a perfect start. Achieve that, retest to be sure you did it, and see what happened to urine calcium. Diet protein does raise urine calcium – I never finished that article! – but is protective of bone whereas diet sodium raises urine calcium and can deplete bone of mineral. If high fluids and low sodium do not lower SS CaP below 1 and lower urine calcium to below 200 mg or lower then the next step might be a modest intake of potassium citrate – perhaps 10 mEq one daily. Obviously this could raise urine pH and CaP SS if it does not lower urine calcium further, so one needs to check again. But I would do the sodium first with 3 liters of water intake or so to achieve a urine volume around 2.5 liters daily – steady throughout the day. I think you have already read all this- from your questions, but if you have not this is a good summary with links. Regards, Fred Coe

  11. Bryan P

    Dr. Choe,

    My Citric Acid is 26, I’ve taken Urocit-K 15 twice a day for three months but my Citric Acid level is still low at 57. That’s from last week’s 24 hour urine test.

    The Aston Center in Dallas, Texas doesn’t accept HMO BlueCross right now. I have been accepted as a patient. When they enroll I will see them. I living in a small town in North Texas, I’m 38 years old, local Urology/Nephrology is managing my kidney stones but prevention is not going anywhere.

    Is there anything I can do? Am I loosing citric acid somewhere? I’ve read online articles about bowel disorders/renal tubular acidosis.

    Thank You,


    • Fredric Coe, MD

      Hi Bryan, You do indeed have a low urine citrate, but what is the context. Take a look at a way to think about your stone prevention and see where you might fit in. The low urine citrate could be from renal tubular acidosis, bowel disease, potassium deficiency, a host of causes. Regards, Fred Coe

      • Bryan P

        Dr. Coe, sorry for misspelling your name in my previous post.

        Does potassium citrate lower urine PH?
        My Uric Acid was high in my last 24 hour urine.
        Protein was high, that seems to change from time to time.

        Thank You

        • Bryan P

          I found the answer in your links. Pot Cit raises Urine PH.

          Only thing I’m stuck on….if citrate is absorbed by the bowel will taking potassium citrate increase citrate level? Sounds like putting motor oil into a vehicle with a hole in the pan.

          • Fredric Coe, MD

            Hi Bryan, This is in reply to both comments. Citrate is metabolized as citric acid, so a proton is taken up from blood with every molecule used metabolically. For this reason, potassium citrate will produce bicarbonate in the blood as the liver metabolizes it and that bicarbonate will cause the kidneys to raise urine pH and – through the citrate transporter – reduce reabsorption of filtered citrate so urine citrate rises. Regards, Fred Coe

  12. Mac Thompson

    What a wonderful discussion of IH. My wife is 67, has osteopenia, and apparently IH with U Ca at 561.6. U-Ca/U-Cr has been increasing from Feb 2014 at 0.281 to June 2016 at 0.432 – is this cause for alarm? She does not yet seem to have any kidney stone symptoms.

    • Fredric Coe, MD

      Hi Mac, you are very astute. She may have IH and bone disease is a very common outcome especially if diet calcium has not been optimal. She may be losing bone at a rapid rate because of menopause but it is a bit late in that process for such very high urine calcium levels. The rising rate of urine calcium could reflect new use of calcium supplements or high calcium diet, or rising diet sodium or some combination. Of crucial importance is control of diet sodium, which should be as low as possible; the ideal is 65 mEq or 1500 mg daily along with 1000 mg of calcium. Of course she may want to be on a primary bone directed medication, which is outside the scope of the site as presently constructed. Her physician should want to be sure her serum PTH is in the normal range – not suppressed – and her serum calcium is definitely normal. She might want a kidney stone protocol CT to be sure there are no stones. Regards, Fred Coe

      • Mac Thompson

        Thank you very much! Her endocrinologist has ruled out common causes of hypercalcemia. She is currently on a regimen that I think is questionable – no calcium supplements, no yogurt, no multi-vitamins, no vitamin D supplement (Calciferol is down to 24.6). A few years ago, she was taking Fosamax but her dentist recommended against it due to bone loss in her jaw. Serum calcium is holding steady at 10.1-10.5. My impression is that her condition is probably deteriorating and that her current treatment is not working well.

        • Fredric Coe, MD

          Hi Mac, I do not think her serum calcium levels are normal; the values quoted are elevated. A hypercalcemic state would better account for her very high urine calcium levels than would idiopathic hypercalciuria. Her serum PTH values are very critical here. If they are suppressed below the normal range it is one class of disease, if they are normal or high primary hyperparathyroidism is the likely cause and can be cured by surgery. The key is definite high serum calcium with normal or high serum PTH values and – of course – the very high urine calcium levels, and exclusion of systemic diseases apart from primary hyperparathyroidism that might create this combination. The very low calcium intake is not ideal in any event. Perhaps you might want to mention these possibilities to your physicians for their opinions. To me the key is several fasting bloods for serum calcium, ionized calcium and PTH – all in the same samples – on at least several different days over a few weeks – I think I would personally do at least 3 in my own practice. If indeed primary hyperparathyroidism is present it is best treated by a surgeon with a lot of experience in parathyroid surgery – these people usually reside in medical school hospitals. Of course, all this is merely commenting from a distance, and is simply what your physicians might want to consider – they probably have already done so and have decided otherwise. Regards, Fred Coe

          • Mac Thompson

            Thank you again Her “Intact Parathyroid Hormone” is 17 and has been as low as 10 and as high as 25 since 2013 – so, on the low side of the 12-88 range. Her “PTH Related Protein” is 14-16, on the low side of the 14-17 range. Her thyroid was damaged by radiation treatments as a child, and she takes Levothyroxin 112 mg – so perhaps her parathyroid was also damaged? I agree that “The very low calcium intake is not ideal in any event” – it seems like a particularly bad idea with osteoporosis. Her endocrinologist wants to solve the mystery of the hypercalemia before addressing bone density, but I fear that additional damage is being done meanwhile.

            • fredric coe

              Mac, I understand. High serum calcium with suppressed serum PTH is a very serious problem and needs resolution. Your physician is obviously thoughtful. If an answer is not forthcoming I am sure he would want referral to a university center that specializes in mineral disorders and is geographically convenient to your family. Regards Fred Coe

  13. sharon thomas

    Is it possible that not eating enough calcium in foods could cause an increase in calcium in the urine. i was counting some greens as 135 mg of calcium when in actuality it was only 50mg. of calcium. Therefore I did not get my 1200 mg/day but only 1115mg. for several months.

    • Fredric Coe, MD

      Hi Sharon, No it is not that way. You have high urine calcium despite low calcium diet and just imagine where that calcium is coming from – bone. Please correct this and treat your hypercalciuria properly: High diet calcium, low diet sodium, moderate diet protein (PCR on your lab report about 1) and if needed thiazide. Regards, Fred Coe

  14. Carla

    Hello Dr. Coe,
    I have recently read that the mineral boron can help to facilitate the absorption of calcium and that it may be a good supplement for those who suffer from kidney stones. I was wondering if there has been any research on the effects of boron supplementation for kidney stone patients, especially those with IH. The information I read said that supplementation of 2 mg/day would be sufficient. I would appreciate your thoughts and insight on this topic.
    Thank you,

    • Fredric Coe, MD

      Hi Carla, Boron has some possibilities but no trials. Here is a recent paper on it. So far the best source is food: From the article: ‘Many of
      the foods that contain boron are likely to have beneficial
      effects on bone, therefore it is suggested that foods such as
      fruits, vegetables, and legumes be the source of boron.” Regards, Fred Coe

      • sharon thomas

        Dear Dr.Coe, Would eating less calcium in foods decrease the calcium in the urine??

        • Fredric Coe, MD

          Hi Sharon, If you have idiopathic hypercalciuria it might but at the expense of risk of bone mineral loss and possible fractures later in life. It is not a very good idea and should be avoided. Regards, Fred Coe

  15. Sheila Conran

    Dear Dr Coe
    Thank you for a very informative article. My children – twins aged 4 – were only recently diagnosed with Hypercalciuria. I deliberately didn’t call it IH because I don’t know what the origins of their conditions are. Their most recent urinary calcium levels as of 14 Feb 16 are 6.66 mmol/L and 5.7mmol/L respectively. This was a one off sample not 24 hr. I was given no dietary advice and while they were initially prescribed Potassium Citrate this was subsequently stopped as one of the boys was having increased abdo pain. He had the abdo pain prior to commencement of PC but this was not addressed or investigated. The dietary advice in your article is wonderful. Both boys but more especially the boy with the higher urinary calcium level & abdo pain was craving salt, sugar meat, and to a lesser extent food items with bicarb(at least that’s why I think he sought out these foodstuffs). Recently cheese was being demanded more frequently. The salt & sugar cravings were alternating every 2 days or so but on occasions every few hours. He also complains of joint pain as well as head neck, back, eyes and thigh The other boy suffers badly with headaches and eye pain and to a much lesser extent knee pain. Can you throw any light on these extra symptoms? Also should they have a bone density scan? Serum calcium was checked and normal and I did point out that my understanding was that this was not adequate in confirming bone health which you have confirmed in your article.
    Thank you

    • Fredric Coe, MD

      Dear Sheila, I think it is very hard to diagnose hypercalciuria from just concentrations. A more common approach is to express the urine calcium concentration as a ratio to the urine creatinine concentration, the latter to allow for water conservation. Do they have crystals in their urine, or blood? A common cutpoint for hypercalciuria is a urine calcium /creatinine concentration ratio of above 140 mg calcium/gm creatinine. Try to determine if a creatinine level was measured and factor the urine calcium by that. Regards, Fred Coe

  16. Stephen Knohl

    Dr. Coe,

    Is it possible to have enhanced bone resorption (say from PTH-mediated processes) or enhanced GI absorption (say from 1,25vitD-mediated processes) as the primary process leading to hypercalciuria without hypercalcemia? I ask because of the hypercalciuria seen in entity known as normocalcemic hyperparathyroidism (which admittedly could be the result of a primary renal leak, but for argument’s sake let’s assume it is not) or the hypercalciuria of sarcoidosis (that is often seen without hypercalcemia…ionized or total). Assuming that no renal leak exists, I can only surmise that the increased load from turning the faucets (from your bathing analogy) can lead to hypercalciuria from either an increase in ultrafilterable calcium or an increase in the GFR. If GFR doesn’t climb and there is no increase in ultrafilterable calcium, then I’d say to my question is “no”…am I wrong?

    • Fredric Coe, MD

      Hi Steve, An outstanding question and I hope I can do it justice. PTH increases renal calcium reabsorption so, in primary HPT as an example, filtered load increase has to overcome increased reabsorption. In sarcoidosis, serum PTH is profoundly reduced, and distal tubule calcium reabsorption depressed. This permits marked hypercalciuria without hypercalcemia. Hyperparathyroidism with normal serum calcium and hypercalciuria is indistinguishable from IH except for the elevated PTH and such cases are odd. We have studied a few patients whose fasting PTH values were high, serum calcium normal, and hypercalciuria was present. What we found was a more marked fall in PTH with food so that increased distal reabsorption from high PTH was no longer present. I do not know for sure but these few cases seemed to me an early stage of primary hyperparathyroidism. We have not noted them in our publications. I think reduced proximal tubule and thick ascending limb reabsorptions are critical for understanding these cases, and it is unfortunate that endogenous lithium clearances are so cumbersome that only our group has made substantial observations in IH. If I had to guess there has always been an association of IH and primary hyperparathyroidism as shown by the common residual and long lasting normocalcemic hypercalciuria we and others have published after curative primary hyperparathyroidism. After surgery such patients look exactly like IH and remain that way. So I think they always were that way and have the tubule abnormalities of IH. As for bone mobilization, we have not studied experimental cases – where bone mobilization is promoted by space flight or bed rest so I cannot tell what happens. Warm Regards, Fred

      • Stephen Knohl

        Thanks for explanation. Regarding sarcoidosis, theoretically, there must be a transient increase in blood calcium to drop the PTH or is it the hypervitaminosis D that drops the PTH?

        Thanks again.

        • Fredric Coe, MD

          Hi Steve, Probably the high 1,25 D down regulated PTH gene expression; likewise it will up regulate the PT cell calcium receptor abundance so serum calcium signalling will increase for any serum calcium level resetting the calcium PTH control curve. The opposite – loss of CaSR sensitivity is what I suspect happened in my few cases, and is known to be the beginning stages of PHPT in some patients. Great issues and thank you for bringing them up. Warm Regards, Fred

  17. Bonita

    How can I be sure I am getting – and absorbing – enough calcium on a daily basis if I do not take a suppIement? Cheese is the only dairy product I eat, and I’d prefer not to eat it daily. I get bleary-eyed looking at non-dairy high calcium food lists that include high-oxalate foods or foods that would require large quantities to reach 1,000-1,200 mg. And then there is the added factor of varying percentages of absorbsion. And getting sufficient Vit D. Thank you in advance for your advice.

    (Background: I am 60 and have had two very difficult stone events (2008 and 2011). On my own, I discovered your research, Dr. Coe and even had the pleasure of meeting with you. I was diagnosed with IH – 426 (after some dietary changes but before beginning indapamide). I was also diagnosed with osteopenia and Vit D deficiency (9) in 2011. Since then I have been taking a Vit D supplement and/or Citracal petites off and on and 2.5mg indapamide daily. My diet – most days – is low sodium, low protein, and low oxalate. It is the calcium that has me most concerned and most confused. Annual Litholink labs results for urinary Ca 24 have been 222, 329, 191, and most recently, 248. )

    • Fredric Coe, MD

      Hi Bonita, From your labs you do indeed have hypercalciuria. I presume there are no systemic diseases causing it so it is idiopathic hypercalciuria. Vitamin D OTC 1000 units a day should maintain your vitamin D stores. It is probably reasonable, all else failing, to take a calcium supplement with meals, perhaps 500 mg of calcium as the carbonate or citrate salt; the trick is to time it so it is taken with the food, and with the larger of your two meals daily – that is 1000 mg. If you can get more in from foods, then just add the 500 mg supplement with your largest meal. You did not say how much sodium is in your urine, be sure it is below 100 mEq/day and even better at 65 mEq/day. Since you have been my patient, as you said, you are free to come back once in a while and let us check things out more directly – Warm Regards, Fred Coe

  18. Bryon

    Hello my name is Bryon and am 41 , I start ed having kidney stones about 15 years ago that lasted for about 1.5 year about 4 years ago it started again lithrotripsy every 3to 6 months so 8 times in 4 years on both kidneys. I have developed cancerous tumor on left. We have tried all diets and tested urine with little change. Urinalysis shows high potassium, sodium, uric acid, calcium oxalate,although my blood shows perfect. I have irritable bowl. I have recently been put on potassium citrate, magnesium glyconate, k2, vitamin D because was a little deficient,and a 1000mg. Sodium daily restriction. I have not checked urinalysis since. This has been devastating to my family . I am hoping this diet will work. If someone wants to follow me please let me know

  19. Al R.

    Hello Dr. Coe,
    Thank you very much for your many detailed and helpful articles. The stone and bone connection was especially relevant to me.

    If you are up for the question, would you please share your experience regarding the progression of IH in a given person over time? Specifically, I’m wondering whether I have most likely been excreting huge amounts of calcium since childhood. And, more importantly, as I age, is IH likely to improve, get worse, or remain about the same?

    Here’s a brief history for context: My father formed over 100 CaOx stones throughout his life. They started in his late teens. He also broke many bones, including a vertebra. I passed my first CaOx stone at 35. Increased fluids and supplemented Mg. Then I was fine for 15 years except for a single, small instance of hematuria in the middle. (No imaging was done.) Then hematuria occurred again one day, and imaging found smallish stones in both kidneys, 4 attached, one free. Two supersaturation tests reported UCa ~400 mg/day. A DEXA scan showed low BMD, particularly in a vertebra. I was referred to a good nephrologist and was diagnosed with IH – I’m assuming inherited. We replaced Ca supplements with more dairy, and are testing Chlorthalidone.

    • Fredric Coe, MD

      Hi Al, I suspect you have familial – idiopathic – hypercalciuria yourself and in your family, and it does produce stones and a bone disease of complex nature. Chlorthalidone with very low sodium diet, 1000 mg calcium intake, and a potassium blocking diuretic if serum potassium falls too much sounds just right. IH begins at birth, is a main cause of stones in children, and is highly treatable. It will be in about 1/2 of your first degree relatives. Regards, Fred Coe

      • Al R.

        Hi Dr. Coe,

        Thank you very much for your personal reply. Unfortunately Chlorthalidone & diet haven’t been enough so far. My Ca excretion remained high and I had another stone (thankfully very small) despite clearing 3.5 liters on an average day. So I’d really like to learn more about the specific kind of IH I have, also and how my Ca excretion varies through the day after consuming meals with various amounts of Ca to help me optimize. (I am working with a nephrologist, but also doing a lot of my own research.)

        Question – If possible, please suggest ways we may test these two things.

        So far, I’ve read about a Ca loading test, but checked with a local lab and they didn’t know about that test, and I am concerned that 1g of Ca at once would pose a very high stone risk.

        One other idea I had was to collect measurements similar to those in Table 2 from Dr. Lemann’s study (but for Ca not sugar) which seems to show periodic samples of urine calcium excretion per minute. If creatinine excretion is constant enough, a series of Ca/Creatinine ratio urine tests might work. That’s a standard lab test. There are also “Hypercalciuria test strips” which if their range is appropriate, and if I can actually buy them, might be good enough to be useful.

        Best regards,

        • Fredric Coe, MD

          Hi Al, I re-read your prior note and my reply. There is no extra value from the calcium loading tests in your specific case – marked hypercalciuria and bone disease – and what you would like to do amounts to a research experiment. If you can come to Chicago and are a calcium oxalate stone former we have an active NIH research study ongoing in which we in fact do fasting and meal related mineral physiology and can determine a lot about your physiology. I cannot say this will improve your clinical outcome but can say it would add to your personal understanding of what seems to be a multiple generation bone – stone IH disorder. If you can join us email me directly. Clinically you did not give your urine sodium or calcium excretion on medication, so I cannot say much. Likewise you did not say what happened to your urine supersaturations – did they fall at least by half?? Perhaps you have reduced your stone risk enough. Given the interest in your kind of situation, I would like to know more. Regards, Fred Coe

          • Al R.

            Dear Dr. Coe,
            Thank you for your reply and invitation. I will reply via e-mail regarding studies. However the following follow-up seems to be of general interest. Please allow me to refocus on a very practical question here:

            I recently flew down the East coast and passed a small (~1mm) stone a few days later despite a concerted effort to remain hydrated and to find low salt airport food. That was just a short trip. So I am highly motivated to find practical ways to reduce stone risk while traveling (to supplement the customary medication, hydration, and diet which are all of course extremely important), and would be grateful for suggestions.

            For starters, do you have thoughts about shifting to a low calcium diet for the evening before and day of a flight? In other words, would a low calcium diet on occasional particularly risky days be protective – even though it is completely the wrong strategy long term? Or could that backfire and actually increase risk even in the short term?

            And, would doing an extra 24-hour supersaturation test with a low calcium day as described above, and comparing to a normal test, be a reasonable way of confirming to what degree this would help a given individual with IH?

            Best regards,

            • Fredric Coe, MD

              Hi Al, I doubt the stone you passed after your flight formed during that flight – even small stones take longer to form than a few days. The low calcium diet idea will not work. Any food will increase urine calcium even when that food contains no calcium at all. The best protection from diet is low sodium, with measured urine 24 hour urine sodium values of about 65 mEq/day ideal. This will reduce food induced hypercalciuria and potentiate the thiazide drugs if you are taking them. Regards, Fred Coe

  20. Celia Mac Donald

    A very good choice these women Bathers by Renoir, not only beautiful but joyous, carefree. A much better choice than Cezanne’s version, colder, darker, almost primitive! I can’t help but think of our MSK members who can only dream of enjoying a bath in this way, most of whom also suffer from hypercalciuria, if only their Drs could figure out what is causing their hypercalciuria, stones, calcifications, chronic pain, hematuria and so many other symptoms and suffering. I find the Bathtub example very helpful to understand how the kidneys work and the fact that high urine calcium can only come from the calcium we eat and our bones, that even a daily urine loss of 200 mg/day is a high risk for bone disease, even though I’ve read many times that MSK can cause bone demineralization, I didn’t know to what extent . And that there are other mechanisms in our kidneys that control absorption, excretion and reabsorption that could go wrong, that there is a combination of causes of high urine calcium but the bottom line is, all urine calcium comes from our food and our bones! If only MSK patients’ Drs could figure out what makes their hypercalciuria tick!
    Unfortunately I am still having a hard time with the graphs, as I’m sure our members will too but I’m hoping and will encourage our members to share your article with their Drs who will hopefully understand more than we do.
    As always, thank you for listening and sharing.

    • Fredric Coe, MD

      Dear Celia, Physicians can certainly and happily provide reduced sodium intake, high fluids, thiazide diuretics and potassium citrate, perhaps in combinations to lower supersaturation drastically; this will prevent new stones and crystal attacks. We have treated thousands of patients with IH at the university of chicago and have often published at least our experience. There are formal trials which I plan to review and which support the benefits of treatment. We know enough right now to prevent new stones in a majority of patients. Regards, Fred


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