VIDEO: About 27 minutes with a break at 15 minutes
Perhaps the most common abnormality among calcium stone formers, idiopathic hypercalciuria (IH) causes calcium kidney stones and can lead to bone mineral loss and fracturing bone disease. Proper treatment requires a high calcium intake, a low sodium intake, moderation of very high protein intakes, avoidance of refined sugar loads, and – not rarely – use of diuretic drugs which can lower urine calcium losses, prevent stones, and protect bones.
Why The Bathers?
Bone seems, to me, a bather in a bathtub. Calcium flows in from faucets – the GI tract – and out down the drain – the kidneys – as they regulate serum calcium – the height of the water in the tub. I realize the bather does not take up or lose water, but if you ponder the image awhile you may see in it what I see.
The Large Bathers (1884-87) of Renoir and The Large Bathers (1900-1906) of
What is Idiopathic Hypercalciuria?
What is Hypercalciuria?
As hypertension is defined by blood pressures that associate with stroke, heart failure, and heart attack, hypercalciuria is defined by urine calcium excretions that associate with stones.
Increasing urine calcium losses associate with increasing risk of stones in two cohorts of women – red – and one of men – blue. Urine calcium is along the horizontal axis in six bins. The average relative risk of forming stones is marked by the tops of the bars. A value of 1 means no higher than among people with urine calcium below 100 mg/day – the reference population.
The lower 95th percentile of risk is at the bottoms of the bars. When the bottom of a solid bar lies above one, which is the case for all bars from 200-249 mg/d on, increased risk is very likely present. So the threshold of hypercalciuria is 200 mg/d both sexes.
Diet was not controlled, so we do not need special diets to diagnose hypercalciuria using this criterion.
As the urine calcium rises, risk – top of the bar – rises in smooth progression.
What Does ‘Idiopathic’ Mean?
The overwhelming majority of hypercalciuric stone formers have none of the many diseases that can raise urine calcium excretion. Their urine calcium exceeds 200 mg/d for no obvious reason – idiopathic, arising of itself, without overt cause.
Normal Calcium Excretion
Since 1900 scientists have collected 24 hour urine samples from people in clinical research units, perfect collections, and measured urine calcium. I collected all such values I could from published papers – a tiring exercise. Here is my yield of values from normal adult men (blue) and women (red).
The threshold of clinical hypercalciuria, 200 mg/day, resides at about the 75th percentile: 25% of normal people are above it. But stone formers are perhaps 7-10% or less of the human population. So hypercalciuria raises stone risk, but not everyone gets the stones.
Likewise, stone disease is familial, but IH alone does not fully explain why. Presumably other inherited factors matter.
Decades ago we used the 95th percentiles of these two distributions, at about 275 and 325 mg/d of calcium for women and men, to define ‘hypercalciuria‘. No doubt such high values confer risk of stone, but they are too high for clinical use. They remain useful in research to define people with extremely high urine calcium values.
Hypercalciuria Raises Supersaturation and May Promote Plaque
Supersaturation produces and enlarges crystals and therefore stones. We now have superb evidence that rising supersaturation associates with rising stone risk. Calcium oxalate and calcium phosphate supersaturations rise smoothly with urine calcium, leaving no doubt that urine calcium raises risk of calcium stones via increasing supersaturation.
Many calcium stones form on plaque, tissue deposits of calcium phosphate crystals in human renal papillae. Plaque abundance rises with urine calcium excretion, and a plausible theory, vas washdown, links them.
Idiopathic hypercalciuria is Hereditary
Family Studies
I am not sure if we were the first, but here is our evidence from 1979.
The arrows point to the stone formers whose families we studied. Filled symbols are men (square) and women (circles) with IH, asterisks mark children, open symbols did not have IH, and dashed people are deceased. About 50% of immediate blood relatives had IH, in successive generations. Others have also found IH heritable.
IH might look like a simple dominant trait from one abnormal gene, but it results from a number of genes. Incidentally, urine calcium is not the only stone forming trait that appears genetic. Urine citrate appears to be, as well.
Animals
Dr. David Bushinsky bred rats with the highest calcium excretions. Urine calcium rose for the first 40 generations, and thereafter seems at a near plateau. So the trait is breedable.
These animals form calcium stones and develop a more severe bone disease than normal rats if diet calcium is not ample. So they well mimic human IH.
We humans did not breed ourselves for IH. Something about the trait must have conferred a benefit during evolutionary time.
Children
We had the opportunity to collect 24 hour urine samples from large numbers of boys and girls who were brothers and sisters of children with kidney stones, and also from children in families where none of the children, their parents, or other relatives were known to form stones.
Urine calcium excretions of siblings with more than two stones (left panel of the figure) are highest – farthest to the right. Next highest – second from the right – were siblings with 1 – 2 stones. Siblings with no stones were even 
lower, third from the far right.
Children from families with no kidney stone history were lowest – most leftward – and almost none had above 200 mg/day of urine calcium loss.
The four bars in the right hand graph say the very same thing. Mean values of urine calcium, shown by the top of each bar, rose progressively with stones.
This is expected if IH is genetic and causes calcium stones.
Hypercalciuria with Hematuria
Hypercalciuria in children not rarely causes hematuria found on routine screening. Loin pain with hematuria is a common syndrome ascribed to crystal passage. 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.
Bone Disease
There Is Bone Disease in Stone Formers
Epidemiology of Fractures
This figure, from people living in Rochester, Minnesota, shows the cumulative incidence of vertebral fractures among those who had a symptomatic stone (irregular line) and the expected fracture rate 
based on the entire population (the smooth line) between 1950 and 1974. The excess of fractures was not observed for hip or forearm.
Bone Mineral Density
Reduced bone mineral density is a general finding in stone formers. 
Among 2,052 patients assembled from 20 separate studies, between 31% and 65% had some reduction of bone mineral density (Table). Although not remarkable for fractures in the Rochester study, the radius was most affected.
The authors of this review did not conclude that IH caused the low bone density of stone formers. I infer it played an important role, however, because IH can promote bone mineral loss (detailed in the next section) and thiazide diuretics – well known to lower urine calcium in IH – appear to reduce bone disease.
Prospective Bone Mineral Observations
Another reason I make this inference is that the magnitude of urine calcium loss predicts future loss of bone mineral.
We measured bone mineral density in a number of stone formers with IH, collected 24 hour urine samples, and then re-measured bone mineral density three years later.
When change in bone mineral by three years (vertical axis) is plotted against the urine calcium loss at time 0, (horizontal axis), the trend – highlighted by 68% containment ellipses – points downward: More urine calcium loss at the beginning, more bone loss by three years. A majority of people with urine calcium above 200 mg/d lost bone mineral over three years, whereas those with values below 200 mg/d tended to gain bone mineral.
How Does IH Raise Urine Calcium?
The Extra Calcium Can Come From Diet
In the balance studies from which I derived normal calcium excretions, scientists fed subjects a fixed diet and measured all food calcium eaten and all calcium lost in the stool. The difference between calcium eaten and calcium lost in the stool is net calcium absorbed into the blood.
Typically measurements are made in 6 day blocks after a few days to equilibrate with the diet, so subjects participate for perhaps 8 – 10 days. I have aggregated the calcium absorption measurements that match the urine calcium excretions I already showed you.
Normal men and women (orange) absorb about 18% of diet calcium. I combined the sexes because they have almost identical values. Women and men with IH – the blue curve – absorb much more calcium, about 30%.
You might ask how calcium absorption can be negative – points to the left of the vertical 0 absorption line. It is because salivary glands, pancreas, liver via the bile, and perhaps the ileum secrete calcium from blood back into the bowel lumen. When diet calcium is less than this ‘endogenous secretion’, stool calcium loss exceeds what is eaten.
An early theory held that IH arose from over absorption of diet calcium: High absorption, more calcium comes into the blood, the kidneys lose it – done. This theory led to decades of low calcium diet as a treatment for stones. No one knew such diets might cause fractures.
The Extra Calcium Can Come From Bone
A Glucose Load Causes Bone Mineral Loss
Years ago Dr Jack Lemann did this informative study. He measured urine calcium excretion (vertical axis) then gave glucose or sucrose (table sugar) to normal people, calcium stone formers, and relatives of calcium stone formers.
Compare the control (left of the big arrows) calcium excretions of the normal subjects to the stone formers: 5 of the stone formers have control values above all but the highest normals. The relatives of stone formers are even higher – and this is fasting, before the sugar load!
Each period was 20 minutes, so this experiment went on for 2 hours. The higher urine calcium with sugar must come from bone – there was no calcium in the sugar drink. It came from bone in normal people and in those with IH but the latter lost far more calcium than the former. Though fasting they had higher urine calcium losses.
In a separate experiment, Lemann proved that the kidneys themselves caused calcium loss from sugar by reducing their conservation of the calcium they had filtered out of blood.
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 
calcium losses.
The diet went well; most people ate what we asked (middle panel). The normals (the 9 people to the left on the plot) 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, all normal points were above 0).
The patients were different. Many lost more calcium in their urine than they ate, and did so most of the time. This was bone mineral lost in the urine.
On such a low intake surely everyone was losing bone mineral because the fraction of diet calcium that is absorbed into the blood is far below 100%. I just showed you that it is about 18% in normal people and 30% for people with IH.
But those with IH were more flagrant than the normals. Because their urine contained more calcium than they ate we could prove bone mineral was lost.
In IH Urine Calcium Usually Exceeds Net Calcium Absorbed
On the horizontal axis of this figure, calcium absorption is the difference between calcium eaten and lost in the stool. Urine calcium is on the vertical axis. People with IH are red large dots, and normal people are blue microdots.
Each point compares calcium absorbed in a day to calcium lost in the urine. If urine calcium is higher than calcium absorbed (points to the left of the diagonal line of identity), bone mineral is being lost in the urine. Those to the right the opposite – bone is gaining mineral.
At a net calcium absorption of 150 mg/d or more, a majority of the normal points lie to the right of the diagonal line – urine calcium is less than calcium absorbed. Bone mineral is stable or increasing.
Idiopathic hypercalciuria points all lie left of the diagonal line, negative bone mineral balance, until net absorption rises over 300 mg/d. It takes a huge amount of calcium absorption to overcome the tendency of IH people to lose bone mineral.
Bone Calcium Retention vs. Diet Calcium
Perhaps a more practical way to envision these balance data is to plot calcium retention – net calcium absorbed minus urine calcium excreted – against diet calcium intake.
At diet calcium intakes above 500 mg/day, the average retention (the jiggly blue line) for normals passes through 0, meaning that their bone mineral stores will, an average, be stable. Higher calcium intakes make the normal average rise so that by 1,000 mg/day 
a majority of normal points are above 0.
Among the IH subjects (red), retention rises with diet calcium intake, but the average – red line – never passes through 0. Some points do 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. But on average, at all reasonable calcium intakes, IH appears to hamper bone mineral retention.
What Have We Learned?
Low calcium diet is not ideal for normal people and a disaster for those with IH. Given IH, even a liberal calcium intake will not achieve stable bone mineral balance for the average person.
These balance data lay latent in papers published from 1900 through until even recent times. Using a different and sophisticated way to assess bone mineral balance, Lieberman and his colleagues showed as early as 1965 that IH reduced bone mineral stability. Yet low calcium diets remained a common treatment for stone disease for more than a decade thereafter.
IH Kidneys Release Excess Calcium
Filtered Calcium
Calcium gets into the nephrons of the kidneys by filtration from blood. If you do not know about filtration, use this link to learn about it.
Each of the 2 million nephron units we possess in our two kidneys has a glomerular filter that filters water, sodium, calcium, phosphate, oxalate, and thousands of other small molecules and ions out of blood into the long tubules that process the filtrate into urine.
Reclaimed Calcium
The process we care about here is reclaiming filtered calcium back into the blood. Normal people excrete about 2% or less of filtered calcium, those with IH excrete 4% to 5% or more.
Here are a few numbers. We filter about 150 liters/d. The filtrate contains about 40 mg/l of calcium: 40×150 = 6,000 mg/d of calcium. Of that 2% is 120 mg/d, 4% is 240 mg/d, 5% is 300 mg/d. So the differences in percent excreted account for the range of calcium between normals and stone formers.
Where Along the Tubule?
Review the Proximal and Distal Tubules
Each kidney tubule resembles a woman’s hair – long as a long hair, and that thin. Down the center of the hair is its lumen through which the filtrate passes to become urine, and where calcium is reclaimed.
Go back to the filtration article and check out the tubule picture. Pay special attention to the proximal tubule. In the proximal tubule calcium is reclaimed in parallel with sodium. In the distal tubule – on the picture in the link – calcium can be reclaimed independent of sodium.
Urine Calcium Follows Urine Sodium
This picture illustrates the basis for recommending a low sodium diet to lower urine calcium in IH.
It shows how urine calcium (vertical axis) rises as urine sodium (horizontal axis) rises. The rise is far steeper among stone formers with IH (blue) than in normal people (red). Circles show experiments – diet sodium was deliberately altered. Triangles show observations – diet sodium and urine calcium varied on their own.
Urine Calcium and Sodium are Linked in the Proximal Tubule
As you eat more sodium, urine sodium goes up so output balances intake. One way the kidney accomplishes this balance is that filtration rises with higher sodium intake. Another is that reclamation of water and sodium in the proximal tubule (the part nearest the glomerular filter) goes down – more sodium and water flow downstream in the nephron. Calcium goes with it, the two are linked by the way that part of the nephron works.
For this reason, the steeper slope of urine calcium vs. urine sodium in IH must arise from abnormalities further downstream from the proximal tubule. We cannot presently identify where or how this happens.
What Can We Do With What we Know?
We can shut down filtration and increase reclamation of sodium in the proximal tubule. Both will reduce urine calcium by reducing delivery of calcium downstream. Lowering diet sodium does both, reduces filtration and increases proximal tubule sodium reclamation. The latter is usually more prominent than the former.
Thiazide diuretics do the same. They increase reclamation in the proximal tubule.
Once you understand this, you understand why reducing diet sodium and taking thiazide are two ways to do one thing. So the more you limit diet sodium the less you need thiazide, or at least the less dosage you need. On the other hand, if you take thiazide and eat a lot of sodium, the sodium will undo the effect of the drug.
What Happens to Bone?
Diet Calcium Must Be High
All this gives some insight into why IH appears to reduce bone mineral.
When we eat, the kidneys release calcium into the urine, normals and IH alike. But IH patients release a lot more calcium, depending on their sodium intake. If the diet has adequate calcium in it, bone can get its share even if more than normal is lost in the urine. If the diet is not so adequate, less than 1,000 mg/d, bone may not get its share even in normal people. Given IH, diet calcium must be quite high, at least 1,000 to 1,200 mg. But that cannot be sufficient as I have shown you. Even at such high calcium intakes, bone balance in IH is usually negative.
Diet Sodium Must be Low
The only present remedy for renal calcium wasting in IH is to lower delivery out of the proximal tubule. Low diet sodium, thiazide, ot both can do it. We presently have no other means that have proven effective.
The Combination of High Diet Calcium and Low Diet Sodium Can Preserve Bone Mineral
The best proof of this is one study showing that in perimenopausal women the combination of low diet sodium and high diet calcium can promote bone mineral gain.
The women each ate all four of the diets shown along the horizontal axis: high and low calcium (Ca) and sodium (Na). Specifically, the sodium levels were 1600 and 4400 mg/day, and low and high calcium (518 and 1284 mg/day.
On the vertical axis is calcium in mg/d. The colors say if ‘calcium’ on the vertical axis is calcium absorbed (blue), secreted by the GI tract (red), lost in urine (gray), and bone balance (black).
Low calcium diets were hopeless. High calcium diets with high sodium led to high absorbed calcium (blue) but also high urine and GI endogenous secretion losses (‘ENDOFEC’): red and gray bars point downward. Reducing diet sodium lowered the urine loss (gray bar was less down) and also – surprise – less GI calcium secretion (red bar is less down).
The net result is good for bone. This one combination drove bone mineral balance positive (Black bar above 0).
Before we leave this powerful demonstration, look back on urine calcium (gray bars). The high calcium low sodium diet gave the very same urine calcium as the low calcium high sodium diet. In other words, the women could raise their diet calcium from 500 to nearly 1300 mg/day and yet by lowering diet sodium to 1600 mg/day keep urine calcium unchanged.
What Makes Calcium Go In or Out of Bone?
Blood is saturated with respect to the initial phases of bone mineral, so called early hydroxyapatite forms. Likewise bone has considerable circulation, so that the outer layers of bone can be in physicochemical equilibrium with the blood. In isolated bone reduction of calcium phosphate supersaturation leads to physical dissolution of bone mineral.
It seems not unreasonable that tiny reductions in blood calcium phosphate saturation can occur when kidneys release calcium into the urine at a rate that exceeds diet calcium absorption. The loss of bone mineral from simple sugar ingestion may well be an example of this effect. Of course bone is regulated by myriads of hormone signallers, but short term mineral balance could be affected by physical forces. This is an area that deserves research.
I should say that in presenting this conjecture about bone it is just that. Furthermore I doubt it is sufficient as an explanation. But it shows at least one plausible connection that can be demonstrated in isolated bone, and perhaps in humans.
In another article, as yet unwritten, I will take up the larger issues of bone and kidney in IH, and show the deeper science that is now available.
What Should We Do?
Kidney Stone Prevention
Without doubt, reduced diet sodium and refined sugar are valuable in all people with IH. Although I did not demonstrate it here, a high diet protein load raises urine calcium and is best brought into the normal range of 0.8 – 1 gm protein/kg body weight/d. Protein intake is calculated from urine urea excretion as the protein catabolic rate (PCR) and best quality kidney stone testing vendors present it on reports.
Bone Disease
Provide Adequate Diet Calcium
Diet calcium must be adequate, 1,000 to 1,200 mg/d. Without concomitant control of diet sodium this alone would raise urine calcium and kidney stone risk. But when combined with low sodium it will not. Multiple proofs of this statement exist. I just showed you one in the lovely four way bone experiment.
Measure Bone Mineral Density
US insurance practices exclude bone evaluation in large swathes of stone forming populations. But bone mineral scans are not very expensive compared to the eventual costs of fractures. A useful medical buying guide places the bone mineral density scan cost to uninsured people at about $200.00, and mentions that in May prices can be lower because it is national osteoporosis month. The price usually includes a simple medical interpretation.
The Kidney Stone Diet
The proper diet for prevention of the common calcium stone arises almost totally from the requirements to treat IH: reduced diet sodium, refined sugar, and protein, and adequate calcium for bone. The last of these, high diet calcium plays another role in stone prevention by lowering urine oxalate. That is fully described in other articles.
As well as stone prevention and the protection of bone, this diet is thought beneficial for reduced risk of hypertension and vascular disease, to which stone formers seem unduly prone.
Because it accords with general diet recommendations for the entire US population, I can recommend its use without hesitancy for stone formers and, incidentally, all the rest of us, too.
221 Responses to “IDIOPATHIC HYPERCALCIURIA (IH)”
Mary P.
Hi Dr. Coe,
I have idiopathic hypercalciuria as the likely cause of osteoporosis of the spine (>3.0). With 12.5 HCTZ, I’ve reduced urine calcium loss from >300 to below 200 (average) but have had poor to marginal response to both oral and IV bisphosphonates – so I am now trying 12.5 HCTZ with 10 potassium citrate BID in the hope of further reducing calcium loss and perhaps improving bone outcomes. My K is doing fine but I’m now being evaluated for possible glucose issues (fasting glucose and A1C) after a slightly high (145) non fasting glucose. After 4+ years on 12.5 HCTZ, my A1C was 5.7 but my glucose has generally been normal for the 5 yrs of 12.5 HCTZj, with a couple of low values. I don’t fit any prediabetic profile otherwise. Do you have any advice or thoughts regarding this issue?
Many thanks for all you share! Your websites are the source of a great deal of helpful information in a field that, for patients, sometimes feels like a “Wild West” of medicine that gets much less attention (and funding?) than the public health impact would justify.
Mary
Fredric Coe, MD
Hi Mary, The drug itself is said to impair glucose tolerance. But the time scale for you – things getting worse over a long time – suggests potassium deficiency. Serum potassium poorly registers systemic potassium stores because most is inside cells. I would add considerable potassium (could be from food to meds) in hopes of improving things. Your physicians however need to approve of this, as they are responsible – not I. Regards, Fred Coe
Diane
Dr. Coe,
If you raised your 24 hour Urine Citrate considerably and made no other changes would that increase or decrease 24 hour Urine Calcium or is there no correlation between the two? Also same question for Calcium Phosphate Supersaturation, does increased Citrate increase or decrease this SS?
Fredric Coe, MD
Hi Diane, Alkali loads that raise urine citrate reduce urine calcium excretion. CaP SS is more complex. If urine pH rises more than calcium falls and citrate rises, risk goes up, and the converse. Of course my use of the word ‘more’ is sans context, so let me offer one. SS CaP is the resultant of calculations that include calcium, pH, citrate and phosphate. The last is usually trivial because its effect depends on pH, so it is the trio of calcium, pH and citrate. Their interactions are very involved so we use a computer program to calculate the SS CaP. Regards, Fred Coe
Michelle Appleby
Hi Dr. Coe.
I could really use some guidance! I am being seen by my nephrologist, who diagnosed me with idiopathic Hypercalciuria. He put me on thiazides, but the were causing me diverticulitis (5 attacks within a 3 mo. period). I went off, the attacks went away. My 24 hr urine is as follows:
PH 6.6
Potassium 32
Total urine volume 2.87
Calcium 485
Oxalate. 48
Uric Acid 545
Sodium 182
Phosphorus 938
Calcium oxalate. 2.68
Brushite. 4.14
PTH 32
Serum phosphorus 3.0
Suspected problem Hypercalciuric nephroliasis, hyperoxaliric nephroliasis.
My sister has the same issue of high calcium urinary output. 4 of 5 siblings get cal ox stones, often. I lowered my sodium and now drinking 96+ Oz water daily. My diet is very good. No meat for 3 months and urine calcium is still thru the roof. Is there any wat to lower this besides thiazides? As I understand it, I must increase dietary calcium?
Fredric Coe, MD
Hi Michelle, That is a lot of urine calcium, and I suspect your sister may be similar – as well as the other 3 sibs. All this points to possible gene defects that may have more specific treatments. This is an emerging area in stone disease and as yet not very widely spoken about. Possibly you have a defect in your renal sodium phosphate cotransporter (Npi 2c) which your physicians might want to consider, and it may run through your whole family. That is pure guesswork. If this were true oral phosphate supplements of fluconazole both are not unreasonable. Warm regards, Fred Coe
Michelle Appleby
Thank you so much for you response. I did have a gene test, and all came back normal. Including CPY24A1 and SLC34A1. I’m at a loss. Any other suggestions? Again, thank you so much for your time. Yes, 4 of 5 siblings are affected by this.
Michelle Appleby
Thank you so much for you response. I did have a gene test, and all came back normal. Including CPY24A1 and SLC34A1. I’m at a loss. Any other suggestions? Again, thank you so much for your time.
Fredric Coe, MD
Hi Michelle, Was SLC34A3 also considered? Were there possibly ‘variations of unknown significance’ in that gene. Some variants are in flux as to their significance. I am afraid at this distance I cannot do more. That would require I work as a consultant for your physicians and I cannot be sure if that would or would not materially add. Regards, Fred Coe
Sara B.
I was recently diagnosed with nephrocalcinosis of both kidneys after experiencing ongoing flank pain. I have since had 2 ultrasounds and a CT scan all of which confirm the nephrocalcinosis, but didn’t show any stones. I am a 42 year old female who has never had kidney stones and who doesn’t have any other health conditions.
I’ve completed two Litholink tests and will include the relevant number:
8/14/2022: Vol-2.71; Ca-252; Ox-25; Cit-547; SSCaP-1; Na-109; PCR-1.2; ph-6.211
12/09/2022: Vol-3.61; Ca-293; Ox-599; Cit-599; SSCAP-1.17; Na-95; PCR-1.1; pH-6.607
I’m confused as to why my sodium levels dropped, but my calcium increased. I am also confused as to why I continue to have flank pain without stones. My last kidney bloodwork was really good (creatinine.73 and GFR 106) so it appears that my kidney function isn’t affected, yet, but the calcifications worry me. I have seen a nephrologist, but they just wanted me to take thiazide despite my having really low blood pressure and didn’t offer other suggestions besides drinking lemon water.
I have read most of your articles and they are excellent. I would just like to hear your suggestions about my situation.
Thank you very much!
Fredric Coe, MD
Hi Sara, I saw this today and believe I answered – there were perhaps two entries of the same question? – but the software does not let me see all my answers in good order. Your urine calcium is high, and a probable cause of the kidney crystals. Your urine pH is on the high side. So everything points to calcium phosphate deposits arising from the calcium and pH. The high citrate is against renal tubular acidosis. I think your physicians might want to have your entire situation reviewed at a convenient stone center where perhaps something more might be found for you. If there is nothing available in your region, we can visit via telehealth. Regards, Fred Coe
Will Y.
Hi Dr. Coe
Thank you so much for your sharing the knowledge and tremendous help here – so grateful!
I’d like to gain your perspective on my recent kidney stone and urologist’s Chlorithalidone prescription:
– I’m a 40 male, no other underlying medical conditions.
– I had observed stone crytals since 2011 and finally a 5mm kidney stone got surgerically removed by Ureteroscopy in June 2022.
– Following that, my urologist did a 24-hr urine test and found out that my urine calcium is high at 10.2 mmol/d (normal range 2.5-7.5). Other than this, all other blood and urine markers are within the normal range, although sodium is borderline high at 146 mmol/L (normal range 136-146).
– A few other key markers: PTH 3.0 pmol/L (normal range: 1.6-6.9); Calcium Ionized 1.29 mmol/L (normal range 1.15-1.35); Oxalate 388 umol/d (normal range: 135-460); Cretinine 14.4 mmol/d (normal range 6.3-22.7)
– My urologist prescribed Chlorithelidone 50 mg per day for lifetime and he said this will prevent stones in the future
My questions:
– Is my condition actually the Idiopathic hypercalciuria?
– In 2021-2022, I have been taking Vitamin D3 supplementation of 3000 UI per day.. I shopped recently. Could that be bad for me?
– Taking the Chlorithelidone for lifetime is a shocking news to me – what should I do? Should I just follow the instruction and take it for lifetime? Any follow-up tests that I should consider?
Thanks so much!
Fredric L Coe, MD
Hi Will Y, It would appear that you do have idiopathic hypercalciuria, and that treatment is long term. Perhaps with a lesser vitamin D supplement rate the urine calcium may fall, but I doubt it will become normal – you do not mention your serum 25D level. But chlorthalidone, though appropriate, need not be sole treatment, or perhaps even needed as diet can play a large role. Here is an article I like about treatment in situations like this one. Here is my recent book that has all the details. Regards, Fred Coe
Will
Dear Professor Coe,
Thanks so much for your quick reply – I will definitely read your new book! I can’t thank you enough for all what you are doing here to help people!!!
You mentioned diet change as a treatment vs. my urologist’s lifetime chlorthalidone treatment – how do I decide what to do with the options in front of me? How do I know diet treatment is actually working?
Thanks a lot!
Fredric L Coe, MD
Hi Will, The article points out low sodium and avoidance of refined sugar, high diet calcium, and of course 24 hour urine testing to be sure the sodium is low enough to prevent the calcium from raising urine calcium and stone risk. If there is bone disease you may need more, so be sure you get a routine DEXA scan to check it. The book expands on the site with regard to bone disease. Regards, Fred Coe
Anna
Dear Dr Coe!
Thank you so much for being so generous with your knowledge! I haven’t had any kidney stones in a while, but just found out that I excrete lots of Ca in my urine, and I am getting dangerously close to an osteoporosis diagnosis.
I am a 57 year caucasian female (grew up in Sweden), 115 lbs, 5’5” very physical active. No family history of kidney stones or hypercalciuria.
Dexa 2014 show osteopenia in spine, not in hips. Dexa 2022 show close to cutoff for osteoporosis in spine, and midrange osteopenia in hips. Menopause in 2015 at age 50.
I am on HRT, (estrogen patch/progesterone), since 2020. VitD,25-hydroxy is usually 21 to 29ng/ml. I take vitD 1000IU when I remember. Diet with lots of fruits/vegetables, full fat dairy, and some meat. On a normal day my intake is around 1000-1200mg of Ca, no supplementation. Staying away from high oxalate food. Trying to lower sodium.
Kidney stones in oct 2016 (ER visit), Dec 2016, Nov 2020, and Apr 2021. CAT scan 2016 showed biggest stone 3mm and the captured stone was calcium oxalate. Abdominal X-ray in 2018 and 2021 show 1mm stone which is no longer there in this year’s x-ray. I believe those kidney stones formed during 2016 when I was making smoothies with lots of spinach, almond milk and chia seeds and taking calcium supplement. I just didn’t know the danger.
Saw urologist in 2016 after first stone, see results below. He recommended fluids, less oxalate, and did not mention hypercalciuria or made me aware of osteoporosis risks even though my Ca was high in the 24hr test.
Visited new urologist this summer and have two new 24 hr test results. I drink 3 cups+ of drip coffee everyday and have done so for years. I dropped my consumption to 1 cup a day for a month and then stopped completely for 2 weeks before my latest 24 urine collection.
Here is some of my data:
2016: Volume 2 L, Ca 320mg, pH 6.2, sodium 51.8meq, oxalate 14.1mg, PTH 41.7. Fasting serum Ca 9.5mg/dl
2022 august: Volume 3 l, Ca 449, pH 5.9, sodium 76 ,oxalate 22, brushite 1.14. Fasting serum Ca 9.1 (in May 22)
2022 September: Volume 3 l, Ca 490, pH 6.9, sodium 101, oxalate 25, brushite 4.75
PTH was checked once in 2016. My calcium excretion didn’t change after stopping coffee, but my pH level and brushite levels increased. Clearly I have excreted too much calcium since 2016, and I wish I had known then. As a side note, I have had very nervy and tingly hands and feet for the last 8 years, and my body aches a lot at night. Limbs often get numb, and after exercise it feels like my bones ache the whole night, sometimes also without exercise. This is not muscle soreness, I know what that feels like. I have seen doctors for this, one of them a neurologist. Since I am thin and in shape and feel fine during the day most of the time, they don’t take me seriously. So I have started to ignore it but it doesn’t get better. Could it be Calcium related?
Since I don’t seem to actively make kidney stones any more, should I still go on medication? Since I can’t know if my bone loss is due to estrogen loss (5 years in menopause before staring HRT) or hypercalciuria, or something else, I am worried about my diet and also about intense exercise. I don’t even know if my bone density is stable or if I am constantly loosing bone mass. Would thiazides be recommended and would they help for bone loss or should I first ask for a parathyroid test? Imaging of my kidney?
I am going back to my coffee habit, but will stick to 1, sometimes 2 cups a day.
What type of doctor do you recommend I see, stay with my urologist (who is now on maternity leave), go to Sutter’s kidney stone department, or find an endocrinologist? Any suggestions for the San Jose/Palo Alto Ca area? Should I set up video appointment with someone in your department?
Thank you again!
Fredric L Coe, MD
Hi Anna, Here are your results (in order of year): Sodium 51, 76 101; here are the corresponding calcium excretions: 320, 440, 490. If you make a graph, the two correlate. I suspect you have genetic hypercalciuria, which exhibits this kind of sodium response, and have bone disease in part because of the excessive kidney calcium losses. Thiazide is bone friendly and often used to stabilize bone. Since your values are fallen rather far, your physicians might wish to consider a bisphosphonate. Sutter is certainly a fine group. If your physicians believe telehealth with me would help, I can certainly do that. Regards, Fred Coe
Anna
Thank you so much for your quick response. I have been thinking hard about your response and my situation after your comment. Maybe a bit too much!!! I have started to track my food intake, and my urologist have given me one more chance of a 24 hr urine test. I am lowering my sodium now, trying to stay below 1200mg/day. I realize that my attempts earlier wasn’t serious enough. I know I probably can’t fix my issues through diet alone but I want to try since I don’t seem to create new kidney stones. The thiazides scare me because I am already on the low end of blood pressure, 109/67 last time it was measured, and a low resting heart rate of about 43. I easily get head rushes and dizzy.
My GP has told me I can have another Dexa scan in a year, so I am hoping I won’t cause to much damage by waiting one more year before deciding on medication and instead focus on serious strength training (with supervision), continue my HRT, some careful supplementation, as well as a better natural diet for bone health. I really need to gain weight but it is difficult for me while still eating healthy.
I assume I have had the hypercalciuria all my life? Or is this something you can develop? I have never been on any medication except birth control and the HRT. My 87 year old mom is healthy and broke her first bone (in the wrist) last summer after a nasty fall and my dad never broke any bones and he lived till 91. None of them ever had a Dexa scan or any tests for hypercalciuria unfortunately. Neither have my two older brothers but there has been a few fractures between them, but always due to falling from bikes, while skiing, or slipping on ice.
Thanks again, I am so grateful that I have your website to learn from!
Fredric L Coe, MD
Hi Anna, If you do indeed have idiopathic hypercalciuria it was present at birth. Although 1/2 of first degree relatives usually have it, many do not form stones. Bone disease arises from so many causes – low calcium diet, menopause. I do not know your medical situation, so please do not undertake long term bone oriented treatment simply from my note. Your physicians are responsible to you for your care. If they believe reduced sodium + normal diet calcium – 1000 to 1,200 mg/d from foods will help fine. If they want bone oriented medication, I urge you to follow their advice. Regards, Fred Coe
Mihaela C
Hi Dr. Coe,
Please, I am hoping you can shed some light on my situation too.
I am 50 years old, in good health, proper weight (63kg) and I lead an active lifestyle (mother, wife, teacher), living in Montreal Canada. I’ve had a number of stones in the past 20 years – five of them have passed ( the one analysed in 2003 was Oxalate – CA 40% and PHOS.ca Hydroxy 60%) with pain and no medication and some are still waiting. The largest ones that I have now are 5.5 mm on one kidney and a 5mm on the other plus many smoller ones.
I was diagnosed with hypercalciuria 448mg/L, PTH 5.9, hypophosphatemia 0.78 and the conclusion of a thyroid ultrasound: ‘A mixed primarily cystic lesion is noted inferior to the left lobe of the thyroid with increased flow within the solid peripheral wall component. In view of the clinical history, this is suggestive of functional parathyroid cystic adenoma. Further evaluation with parathyroid scintigraphic scan is suggested. Bilateral millimetric TI-RADS 2 thyroid nodules of no significance.” The nefrolog that directed me to have the tests decided on the second apointment to send me to have the operation. I really want to try everything else before and leave the surgery as last choice.
I was told that I’m leaking calcium, and that diet alone would not address my problem. Please read some key values from recent lab results and guide me throught this labirint.
May 2021 March 2022 Val Ref
PTH: – 5.9 1.2 – 8.4
Ca: – 2.45 2.15 – 2.62
Phosphore: 0.79 0.78 0.80 – 1.45
HbA1c 0.052 0.04 – 0.06
G.B: 3.59 3.6 4 – 11
Urine Ca: 8.09 11.2 (448mg/L) 2.5 – 7.5 (=30
Urine pH: 6.5 7.0
Ca Endocr: 2.43 2.45 2.15 – 2.62
Bone density : – normal
They are many more but they are in normal limits.
I can maintain a specific diet (I do not drink sodas and I cook with no salt and I realy, realy rarely eat procesed food. Thanks to Jill Harris I stopped eating the top oxalate foods.), and would be happy to do so as I know what exactly can help me. I would like to know if the lab numbers offered above indicate a case where diet and treatment (?) would help or the next step is surgery.
I look forward to your thoughts on my case.
Thank you very much!
Fredric L Coe, MD
Hi, I believe this is a duplicate and that I answered the question. Fred
Mihaela C
Hi Dr. Coe,
Thank you so much for your work. Please, I am hoping you can shed some light on my situation too.
I am 50 years old, in good health, proper weight (63kg) and I lead an active lifestyle (mother, wife, teacher), living in Montreal Canada. I’ve had a number of stones in the past 20 years – five of them have passed ( the one analysed in 2003 was Oxalate – CA 40% and PHOS.ca Hydroxy 60%) with pain and no medication and some are still waiting. The largest ones that I have now are 5.5 mm on one kidney and a 5mm on the other plus many smoller ones.
I was diagnosed with hypercalciuria 448mg/L, PTH 5.9, hypophosphatemia 0.78 and the conclusion of a thyroid ultrasound: ‘A mixed primarily cystic lesion is noted inferior to the left lobe of the thyroid with increased flow within the solid peripheral wall component. In view of the clinical history, this is suggestive of functional parathyroid cystic adenoma. Further evaluation with parathyroid scintigraphic scan is suggested. Bilateral millimetric TI-RADS 2 thyroid nodules of no significance.” The nefrolog that directed me to have the tests decided on the second apointment to send me to have the operation. I really want to try everything else before and leave the surgery as last choice.
I was told that I’m leaking calcium, and that diet alone would not address my problem. Please read some key values from recent lab results and guide me throught this labirint.
May 2021 March 2022 Val Ref
PTH: – 5.9 1.2 – 8.4
Ca: – 2.45 2.15 – 2.62
Phosphore: 0.79 0.78 0.80 – 1.45
HbA1c 0.052 0.04 – 0.06
G.B: 3.59 3.6 4 – 11
Urine Ca: 8.09 11.2 (448mg/L) 2.5 – 7.5 (=30
Urine pH: 6.5 7.0
Ca Endocr: 2.43 2.45 2.15 – 2.62
Bone density : – normal
They are many more but they are in normal limits.
I can maintain a specific diet (I do not drink sodas and I cook with no salt and I realy, realy rarely eat procesed food. Thanks to Jill Harris I stopped eating the top oxalate foods.), and would be happy to do so as I know what exactly can help me. I would like to know if the lab numbers offered above indicate a case where diet and treatment (?) would help or the next step is surgery.
I look forward to your thoughts on my case.
Thank you very much!
Fredric L Coe, MD
Hi Mihaela, Your serum calcium appears normal, so I have much doubt about primary hyperparathyroidism. To be sure, I would suggest at least three fasting, morning serum samples for calcium and PTH. I predict all three will have normal serum calcium and PTH. You do indeed have marked high urine calcium and stones with low serum phosphate. Your care might be enhanced by genetic testing for a NaPi2c gene variant of significant consequence that could explain the low phosphate and high urine calcium. A serum 1,25D would be expected as well. If this is what you have, then oral phosphate supplement could much reduce the urine calcium. Perhaps your physicians might wish to consider this possibility. Regards, Fred Coe