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. Steve Joh

    Dear Dr. Coe,

    First of all, this is an excellent site and has helped me tremendously! I am 28 years old male with 3 small calcium stones (first diagnosed at the age of 20), hypercalciuria (found out 2 years ago which I treat with thiazides and low sodium intake), low25OHd3( 7ng/dl which must be for many years as I rarely was under the sun ,found out 2 years ago which I treated) and in the process of investigation I found out a shocking result which still bothers me: a LS t-score of -2.9, Fem.Neck of -2.6 and full body of -2.5, without any fractures or bone pain. Other than that I am healthy and active.

    All of secondary causes of osteoporosis seem to be excluded. However, I would like you to evaluate some serum values:
    Ca++: 9.9 PTH: 40, Phos: 3.8
    Ca++:10.1 PTH: 21 Phos: 3.4
    Ca++: 9.8 PTH: 34 Phos: 3.2 (under thiazide)
    Ca++:9.6 PTH: 40 Phos: 4.2 (under thiazide)
    Ca++:10.3 PTH: 38 Phos: 3 (under thiazide)
    Ca++: 10 PTH: 28 Phos: 2.9 (under thiazide)
    Ca++ 9.9 PTH: 31 (under thiazide)
    Ca++: 10.3 (pth, p, not drawn) (under thiazide)
    Serum calcium from 2015: 10.5
    4 ionised calcium values I’ve got all are normal except one (over the upper limit)
    1.25OHd3: 62
    Alkaline Phosphate: 72 (normal)

    As far as the urinary calcium: I’ve got many values. The mean value of untreated is around: 360mg/day
    With HCTZ/amiloried (25/2.5) I didn’t see any difference, I jumped to bendrofluazide 2.5 which got me around 260mg/day (with 800mg dietary calcium) and for the last 3 months I am with indapamide at around 200mg/day (with 1200mg dietary calcium).

    I think with high urine volume and thiazides I won’t get any more stones (considering I had very slow disease progression anyway) but bone disease at such age and finding a diagnosis is what worries me. To investigate further I asked my parents to test their urinary calcium. Father’s was 160mg/day (with approximately 500mg/day dietary calcium), my Mothers was 318mg/day (with calcium diet probably more than 1000mg) and 150mg/day (with 2 dairy servings -about 600mg dietary calcium). Their BMD’s are expected for their age. My mother had a small stone years ago which is no longer detectable with u/s and reported having an uncle with calcium stones). My father at my age had a renal colic ( he reports it was “crystals”, but no further colics after that). Brother hasn’t been tested.

    My fist LS t-score was -2.6. I repeated a year later (under bendrofluazide and average urinary calcium 260mg/day and dietary calcium intake 800-900mg/day) and it went down to -2.9 ( it is interesting that BMC didn’t change that much but bone area showed increment which resulted in lower BMD – which makes me question the validity of this loss). Unfortunately I didn’t have Femoral neck the first year to see how if there was loss of mass in neck too.

    All my years I lead a sedentary lifestyle was skinny and small body frame which makes me wonder if I started life adulthood with a low t-score anyway.

    My questions are as followed:

    1) Does this look like a idiopathic hypercalciuria or some other metabolic syndrome (PHPT?) which involves bone resorption? I want to notice that I get high urinary fluctuations according to dietary calcium. For every 300mg dietary calcium change there is about 80mg urinary calcium change too and generally big fluctuations which made me question the lab for very long.

    2) The graph in your article shows that most non-IH people have less than 250mg/day ca losses. But for how much dietary calcium is that? Does that mean that these lose almost the same urinary calcium with 800 and 1200 mg/day diets?

    3) Does the two discordant urinary values of my Mother (318, 150) guarantee more urinary tests to exclude IH? If we accept that none of my parents have IH, is it rare in clinical practice for an offspring to suffer from IH (probably new mutation?)?

    4) From your experience, do you do holiday drug for thiazides when they are taken for too long? (Maybe to refill intracellular potassium storages?) or it is not necessary.

    5) My serum 25ohd3 hovers around 40ng/dl (with 1.25OH at 62). Is it wise to increase serum 25ohd3 in order to increase the serum CaxP and hopefully help bone calcification?

    6) Any other remarks or suggestions on how to help bone metabolism?

    I tried my best to make it clean and short. I know it is not an easy case and I know my doctors should have the last word, however I highly value your words and your dedication. Thank you.

    • Fredric Coe, MD

      Hi Steve, I do believe you have IH. The high urine calcium, high 1,25D and seemingly normal serum calcium levels. Bone disease is certainly well known as is a reason why it should be there. Your treatment seems to lack definitive reduction of diet sodium to 65 mEq (1500 mg/d), which is very valuable for bone mineral retention. Your serum calcium, being crucial seems a bit patchy. I would be certain via three fasting and off medication measurements, although frankly PHPT seems unlikely. What you need is finesse from your physicians – IH is genetic, life long, and the bone disease not of a common sort. There are limits to how much I can be helpful from a distance except to say judgment about when to consider bone active drugs needs some attention. Of course 1/2 of your immediate blood relatives have risk for IH and should be studied. Regards, Fred Coe

  2. Carol Wenmark

    I am a stone former. My kidneys are loaded with tiny stones. I have known about this for two years. I am a women and 69 and had three other larger stones, which I passed in 2015. I have been round and round with nephrology and endocrinologist to get a final diagnosis, to no avail. I have had four PTH tests which were 77, 66, 38,and 83 over the last six months. I have had two 24 hr urine tests. One in August of 2017 and one in November. Urine calcium was 247, and 171. Urine citrate was 645 then 300. SSCaP 1.60 and .52. Ph 6.963 and 6.398. I read your articles on IH and went on a low salt and increased my water diet in the second 24 hr test. Water vol was 2.50 and 3.80 perspectivly. My serium calcium is 9.3 always. I had my iodized cal and vit d done. 4.9 and 43.. my nephrologist and endo believe I have normocalcemic hyperparathyroidism. I visited Dr Norman at the parathyroid center in Tampa, in Sept of 2017 and they said no that my Pth wasn’t high enough. My nephrologist still insists that I have it. Don’t know what to do and am still not being treated in any way except for diet I initiated. This keeps me free from stone pain. I don’t know what kind of stone I make. I just had a bladder and kidney ultrasound but don’t have the results. Appreciate any insight.
    Thank you,

    • Carol Wenmark

      Forgot to tell you that I also have osteoporosis.

      • Fredric Coe, MD

        Hi Carol, your diet calcium may indeed be low, as with idiopathic hypercalciuria such a diet will cause a lot of bone disease. More and more it looks like you need much more diet calcium and perhaps more vitamin D – at least checked. Regards, Fred Coe

    • Fredric Coe, MD

      Hi Carol, I gather your blood calcium is always normal, your serum PTH values are high, and urine calcium variable. This is indeed secondary hyperparathyroidism. That urine calcium went down with reduced sodium is good – a part of stone prevention. Causes of high PTH with normal serum calcium include a low calcium diet, and the modest reduction of kidney function found in older ages. Perhaps your eGFR is a bit reduced. You do not mention your serum 25 vitamin D, perhaps it is not optimal. By no means even consider surgery. If you have reduced your salt intake and your urine calcium fell, and you continue to produce stones, a low dose of chlorthalidone is not inappropriate provided your physicians concur. It will lower your PTH, too. So, I think you have already begun some treatment, and if stone pain returns the CTD would be a next step. Regards, Fred Coe

      • Carol Wenmark

        Yes, my blood calcium is always normal. My serum 25 vit D is 43. Should I be concerned about the urine citrate being low (went from 645 to 300) in the second 24 hr test and my sscap is not high. The endocrinologist wants me to take Actinel for the osteoporosis…is that a good idea? How much calcium and Vitamin D?
        Thank you so much for taking the time to clarify my confusion. It has been a year of ups and downs. I appreciate this sight and your time.


        • Carol Wenmark

          You seem pretty sure that I gave secondary hyperparathyroidism. Is this because my urine calcium is always normal, PTH is high, but why was it 38 in one testing? And my 24 hr urine is variable and affected by low salt and high fluid. Does this mean my prarthyroid glands are most likely enlarged? Will I eventually have kidney failure.

          • Fredric Coe, MD

            Hi Carol, My main point is that you do not have surgically amenable hyperparathyroidism. Any increase in serum PTH will be secondary to: low calcium diet, reduced kidney function with age; low vitamin D; or some combine of these. Low sodium diet regularly reduces urine calcium, and we know how that occurs via the kidneys. High diet calcium and low diet sodium are an ideal way to gradually reduce serum PTH. Likewise they are good steps for stone prevention – not your issue – and for bone mineral preservation – everyone’s concern. Regards, Fred Coe

        • Fredric Coe, MD

          Hi Carol, A bisphosphonate for bone disease is common practice. He/she needs to prescribe the calcium and D needed. Regards, Fred Coe

          • Carol Wenmark

            Thank you, Fred. Appreciate the time you took to help me get a correct diagnosis. I will pass this on to my Endocrinologist.

  3. Scott Macpherson

    Dear Dr Coe,

    I am a 53 year old male who was diagnosed with severe osteoporosis after suffering a lumbar compression fracture in the absence of significant trauma. Follow up blood work could find none of the typical causes associated with male osteoporosis. Twenty four hour urine collection showed somewhat elevated calcium urine levels.
    My serum calcium levels have always been normal. My Vitamin D levels were borderline low normal but have since increased to a more ideal level. Im currently on Prolia for the osteoporosis which so far hasn’t significantly increased my lumber spine bone density. Im concerned about the severity of my bone disease at such a young age. The doctors have concluded that my osteoporosis is likely caused by IH. I did a follow up 24 hour urine collection after a course of Thiazide medication with no improvement in the urine calcium levels. The levels actually went up slightly. I have had no kidney stone formations as of this point in time.
    Im hoping you could shed some light on whether you think my case seems like IH. I was told by one of the physicians that the prolia therapy may fail for me without improvement of the IH. Im a Canadian dentist who wouldn’t be opposed to travelling to the US for a more in-depth assessment of my situation. If you could recommend a specialist or clinic that specializes in male osteoporosis it would be much appreciated. I wonder if there is genetic testing that could definitively give me a diagnosis of IH. I appreciate any insight you may have regarding my case and any suggestions you may have.

    Thanks , Scott

    • Fredric Coe, MD

      Hi Dr Macpherson, Idiopathic hypercalciuria is indeed a cause – in some patients – of early onset and marked bone mineral loss. Genetic testing is not as yet available except for rather rare versions of it – hypophosphatemic and hypomagnesemic forms. I presume you have normal serum PTH and elevated serum 1,25D, typical findings in IH. The bone disease of IH has sometimes been of the low turnover variety, so blocking osteoclasts may not give vibrant outcomes. You do not mention your family – presumably some other members have bone disease or stones, and no doubt about 1/2 of your immediate relatives are hypercalciuria. I can offer to see you myself clinically. As a courtesy I would be willing to just look at your records. Without a lot more detail, I cannot say much more. Regards, Fred Coe

      • Scott Macpherson

        Hi Dr Coe,

        My diagnosis of IH is by exclusion of any other definitive measurable cause. Im trying to determine the cause of my bone disease in the hope that can improve my outcome. My PTH has always been normal . My vitamin D levels were slightly low at initial diagnosis but have since come up to normal levels with supplementation. None of my siblings or parents have been diagnosed with bone disease or stones.
        I’m curious is there any unusual dietary causes that could explain or have been linked to high calcium urine excretion? Diet colas, aspartame etc ?
        I was taking the medication Nexium for acid reflux for a few years prior to diagnosis. Ive discontinued this medication. Ive read that Nexium has been found to affect absorption of minerals and has been linked to bone density issues.
        I may take you up on your offer of assistance. A phone conversation seems like an appropriate first step.
        Im just trying to determine if I fit the typical description of IH since that has been surmised to be the likely cause of my bone disease. Im also concerned about my two daughters if there is a possible genetic connection.
        I believe you have my email so feel free to message me directly that way.

        Thanks Again,
        Scott Macpherson

        • Fredric Coe, MD

          Hi Scott, I understand you have a lot of detailed issues, and they are indeed correct. My institution – U Chicago – does not as yet support formal telemedicine, so I cannot practice via that obvious and important channel. All I can do is offer to read your records and offer comments to your physicians – and you – but not by way of practicing medicine. That latter has special elements that my university needs to supervise. In general idiopathic hypercalciuria bone disease has been strongly familial, and it is often odd as in your case. Nexium is well known as an extra problem. Often we need to moderate the hypercalciuria and also use bone active medications as well. I am sorry I cannot do more at a distance, Regards, Fred Coe

  4. Annette L McNamara

    Hello Dr. Coe,
    I was told that other things can cause kidney stone history beside parathyroid disease, is this true? Could you please give me any feedback on this doctor in wis. on kidney and vitamin D? Thank you.
    Sincerely Annette McNamara

  5. Al

    Hi Dr. Coe,
    Could you possibly help me better understand two particular subtypes of IH: AH type I and AH type II specifically with bone hyperresorption, *not* renal leak? (Possibly rare, but I strongly suspect my Dad, e.g., had the first.)

    I have observed that these two related subtypes seem to be particularly problematic to treat because Chlorthalidone and reduced sodium may only have the effect they would on a normal. And even 1000 mg of Ca from food may not stop bone loss, but due to hyperabsorption, drive stone production more than normal.

    I see Heller H.J., et al. (2007) “Reduced bone formation and relatively increased bone resorption in absorptive hypercalciuria” followed Bushinski’s rat studies featuring Alendronate with a (very) small, short-term human trial for AH-1, with results that seem to invite further study.

    Can you please tell me, have you or your colleagues tried bisphosonates? And what kinds of dietary and other recommendations in general might you have for anyone with these two subtypes when the tried and true measures are insufficient? Thank you and best regards, Al

    • Fredric Coe, MD

      Hi Al, the subtypes do not exist. They were a useful strategy decades ago and no one uses them now. Dr Heller was part of the Dallas group that proposed the AH RH ideas. Dr Bushinsky’s rat studies are known to me as I have been his friend for decades and played a role in his founding of the colony and many of the early papers. Not relevant to AH of RH. You are a thoughtful person, but these are deep waters and you will not be able to fathom them details – not being fancy, just realistic. Many physicians have trouble here. The correct approach to all idiopathic hypercalciuria is low sodium high calcium diet, low refined sugar, and moderate protein. Diuretics are to be used on top of the diet. Regards, Fred

  6. Ken Johnson

    Hi Dr Coe, I have hypercalciuria, along with osteoporosis and NAFLD. A couple years ago I was diagnosed with low T, low vitamin D and low iron. The deficiencies have been corrected and my osteoporosis score has improved tremendously. As for my urine calcium, it has barely budged despite being treated with both HCTZ and amiloride. What do you think? Recently, I read that a vitamin K deficiency can cause hypercalciuria. Have you heard of that possibility? Thank you.

  7. Charles Leblow

    Dear Dr. Coe,
    I am a 63 year old male with Parkinson’s Disease and MCI. My first stone was discovered back in the mid 1990’s and required Lipotripsy and about 9 months to pass. No problems or other evidence of stones until an CT scan discovered three stones in the same kidney on August of 2014. Less than 2 weeks later I received the Parkinson’s Disease diagnosis. In March of 2017, after three visits to ER in less than a week for pain, I had a Cystoscopy with Laser Lithotrypsy performed with Ureter stent installation to remove “a train of stones” that had passed into the ureter. Stones were made of Calcium Oxalate. Two stones still remain in the kidney.

    The PD diagnosis (with mild cognitive impairment) prompted some major lifestyle changes: I retired and began a daily, vigorous, cardio regimen for 30-40 minutes a day on a stationary bicycle as well as hiking local mountains several times per week. I became Keto adapted to control a (pre) diabetic condition and because there was empirical evidence which suggested that a high fat, extremely low carbohydrate diet could be effective in delaying or minimizing the onset of worsening PD symptoms. As a result of this diet I have lost 30 pounds and am still not medicated for the PD or type 2 diabetes. I firmly believe that the diet is, at the very least, partially responsible for these results and recent evidence suggests (although this still needs to be studied in trials) that an increase in Uric Acid levels appears to be Neuroprotective and at least partially responsible for delaying the onset and worsening of symptoms in PD. The primary way I get my calories and necessary fats, while severely restricting carb intake, is by eating a daily diet of mostly green, raw, leafy, veggies with a serving of either chicken, beef or fish…a great combination for producing stones while promoting high Uric acid levels!

    I have had three 24 hour urine tests performed since the surgery and have been forced to make some changes to the diet as a result of these tests including: drinking more water (2 litres) daily, eliminating certain super high Oxalate veggies, and reducing the servings of red meat in favor of chicken and fish. Unfortunately, the changes to diet have not been adequate and my doctor has prescribed Hydrochlorothiazide 25mg daily to help prevent stone formation.

    Although I have no doubt that this med will help reduce the formation of stones by reducing calcium super saturation, I have serious concerns that there may be a backlash from the loss of the salt and other electrolytes that could impact my cardio workouts and promote an increase in muscle cramping, spasms and rigidity. Additionally, I have Orthostatic Hypotension (common with PD) and exercised induced HBP which requires 25mg Atenolol daily for control. Adding another drug (the thiazide) that also lowers BP seems dangerous to me given my circumstances.

    How at risk for further formation of stones am I without adding the Thiazide to my regimen? The most recent 24 hour Calcium Filtration Rate was at 277mg/day (standard range for lab is <250 mg/day). No other values were out of range!

    Last question: What exactly does splitting the Thiazide dosage in 1/2 and taking it twice daily (as opposed to full strength 1xd) accomplish?

    My Urologist seems to be bent on Thiazide to fix this and I have my doubts and concerns which I have expressed to him but I have not been given any alternatives.

    Thanks for your great articles on the interweb!
    Charles Leblow

  8. Susan McIntyre


    Since this infection is known to cause kidney stones and is often undiagnosed/misdiagnosed in immunocompetent people, how often do you think it can be the cause of kidney stones?

    This infection would explain a case of Progressive encephalitis with rigidity and myoclonus after a “cold,” as well as why Takayasu Arteritis, Takotsubo Cardiomyopathy, and some “autoimmune” diseases usually follow other minor infection, like respiratory tract infections and gastroenteritis, which this infection also causes, mimicking colds, flus, pneumonia, and causing GI problems, etc. Do you think Postural orthostatic tachycardia syndrome, which often occurs after a viral infection, could be caused by it?

    My coworkers and I, all immunocompetent, got Disseminated Histoplasmosis in Dallas-Fort Worth from roosting bats, that shed the fungus in their feces. The doctors said we couldn’t possibly have it, since we all had intact immune systems. The doctors were wrong.

    More than 100 outbreaks have occurred in the U.S. since 1938, and those are just the ones that were figured out, since people go to different doctors. One outbreak was over 100,000 victims in Indianapolis.

    This pathogen causes many idiopathic diseases and conditions, including hematological malignancies, autoimmune symptoms, myelitis, myositis, vasculitis. etc. It causes hypervascularization, calcifications, sclerosis, fibrosis, necrosis, leukopenia, anemia, neutrophilia, pancytopenia, thrombocytopenia, hypoglycemia, polyps, stenosis, and perforations, inflammation of various organs, GI problems, hepatitis, etc.

    It at least “mimics” autoimmune diseases, cancer, mental illness, migraines, seizures, etc. It’s known to cause rheumatological conditions, inflammation, and precancerous conditions. It causes hematological malignancies, and some doctors claim their leukemia patients go into remission when given antifungal. My friend in another state who died from lupus lived across the street from a bat colony. An acquaintance with alopecia universalis and whose mother had degenerative brain disorder has bat houses on their property. It’s known to cause delusions, wild mood swings, and hallucinations.

    Just one disease of unknown cause that could be caused by Disseminated Histoplasmposis: I suspect, based on my and my coworker’s symptoms (during our “rare” infectious disease outbreak) and my research, that interstitial cystitis and its comorbid conditions can be caused by disseminated histoplasmosis, which causes inflammation throughout the body, causes “autoimmune” symptoms, and is not as rare as believed. I read that “interstitial cystitis (IC) is a chronic inflammatory condition of the submucosal and muscular layers of the bladder, and the cause is currently unknown. Some people with IC have been diagnosed with other conditions such as irritable bowel syndrome (IBS), fibromyalgia, chronic fatigue syndrome, allergies, Sjogren’s syndrome, which raises the possibility that interstitial cystitis may be caused by mechanisms that cause these other conditions. In addition, men with IC are frequently diagnosed as having chronic nonbacterial prostatitis, and there is an extensive overlap of symptoms and treatment between the two conditions, leading researchers to posit that the conditions may share the same etiology and pathology.”

    I believe the “side effects” of Haldol (leukopenia and MS symptoms) are not side effects but just more symptoms of Disseminated Histoplasmosis, since it causes leukopenia and MS symptoms. What about the unknown reason why beta blockers cause tardive dyskinesia? The tinnitus, photophobia, psychosis “caused” by Cipro? The hypersexuality and leukemia “caused” by Abilify? The fungus is an Oxygenale and therefore consumes collagen. Fungal hyphae carry an electrical charge and align under a current. It’s most potent in female lactating bats, because the fungus likes sugar (lactose) and nitrogen (amino acids, protein). What about female lactating humans…postpartum psychosis? The bats give birth late spring/summer, and I noticed suicide rates spike in late spring/early summer. A map of mental distress and some diseases appear to almost perfectly overlay a map of Histoplasmosis. The bats eat moths, which are attracted to blue and white city lights.

    Apparently, even the CDC didn’t know bats CARRY it and shed it in their feces, although they knew it could grow in bird and bat feces. Researchers claim the subacute type is more common than believed. It is known to at least mimic autoimmune diseases and cancer, and known to give false-positives in PET scans. But no one diagnosed with an autoimmune disease or cancer is screened for it. In fact, at least one NIH paper states explicitly that all patients diagnosed with sarcoidosis be tested for it, but most, if not all, are not. 80-90+% of people in some areas have been infected. It can lay dormant for up to 40 years in the lungs and/or adrenals. It causes RNA/DNA damage. Other doctors are claiming things like sarcoidosis IS disseminated histoplasmosis.

    My coworkers and I had GI problems, liver problems, weird rashes, plantar fasciitis, etc., and I had swollen lymph nodes, hives, lesions, and started getting migraines and plantar fasciitis in the building, and haven’t had them since I left. It gave me temporary fecal incontinence, seizures, dark blood from my intestines, and benign paroxysmal positional vertigo. I had symptoms of several autoimmune diseases, including Fibromyalgia, Sarcoidosis, ALS, MS, etc. that have disappeared since leaving the area and taking Itraconazole antifungal.

    No one, including doctors, could figure out what was wrong with us, and I was being killed by my doctor, who mistakenly refused to believe I had it and gave me Prednisone (at least 2 years after I already had Disseminated Histoplasmosis) after a positive ANA titer, until I miraculously remembered that a visiting man once told my elementary school class that bats CARRY histoplasmosis….so much of it that they evolved to deal with the photophobia and tinnitus it causes by hunting at night by echolocation. There’s a lot more. I wrote a book about my experience with Disseminated Histoplasmosis called “Batsh#t Crazy,” because bats shed the fungus in their feces and it causes delusions and hallucinations, I suspect by the sclerotia it can form emitting hallucinogens, along with inflammation in the CNS.

    • Fredric Coe, MD

      Hi SUsan, I have no knowledge about this fungus as a cause of stones. But I have left your detailed comment on the site in case others know more than I do about the matter. I do want to make clear to others who read your work that your comments are meant to promote debate and do not represent established medical science to date. I am not trained in or expert concerning fungal diseases. Fred Coe

  9. Fredric Coe, MD

    Hi Al, If sodium in the urine is about 1500 mg or less and urine calcium remains high then the hypercalciuria needs additional treatment. Protein intakes about 1 gm/kg/day could raise it. There might be other reasons, too. Idiopathic hypercalciuria is genetic but not one thing – there are various versions, some seem less sodium responsive although we have yet to study this matter properly. Regards, Fred Coe

  10. Anika Kostencheva

    Dear Dr. Coe,

    Greetings from Macedonia!

    During my research on the internet about my daughters condition, I came across your name and your article about IH and decided to contact you.

    My 9 years old daughter has been struggling with urinary tract infections with E. Coli since she was 2 years old.
    Not long ago, after a really bad infection during a routine screening, the doctors discovered that she has hypercalciuria (calcium deposits around her kidneys) and very high level of calcium in her 24h urine – 4.65 mgr, but could not discover any underlying cause of the condition. Her parathyroid hormone was in a normal level (28.2) as well as the vitamin D.

    Around her kidneys there are calcifications. Besides taking pottasium citrate of 90 mmol per day and reduction of natrium and protein, the doctors here in Macedonia did not give her any other therapy.
    As im very concerned about her health, I would like to consult with you about her condition.
    I would be very thankful if you give me your thoughts on how to prevent stone formations, any diet plans or maybe recommendations for medications.

    Thank you very much in advance.

    • Fredric Coe, MD

      Hi Anika, Her high urine calcium is probably hereditary – that is the usual reason, and I gather there are calcium deposits in her kidneys. Protein intake does not need to be below normal just in the range of 0.8-1 gm/kg/day. Very low diet sodium, 50 – 60 mEq (around 1400 mg) will lower urine calcium. High fluids are crucial. Given many stones, perhaps after low sodium diet is in place a very low dose of thiazide drug would be helpful – chlorthalidone 12.5 mg or indapamide 1.25 mg. The dose of potassium citrate seems too high, 40 mEq/day should be enough. You do not mention the stone analysis – that should be done. Regards, Fred Coe


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