Of all the knowledge on this site, a tiny nugget of three well established facts has explosive power for patients and physicians. Put to actual use they let you prevent idiopathic calcium stones and preserve bone mineral.

If you do not want to read the article, I have made a VIDEO to tell you the story in about 13 minutes. On my iphone the video opens well and looks better horizontal. Please let me know if it does not work well for you. 

I have not been shy nor secretive. Article after article speak about the three, but always in context so other facts can distract one, as can superb but unmagical paintings from a few masterpieces hung on the same wall. I know some patients, some physicians, have fully grasped the crucial importance of the three, and put them to use. From the many comments I read weekly, I know many have not. So I am taken with a passion to redress matters.

Les Demoiselles d’Avignon, Picasso, 1907, Hangs in MOMA, NY. It is my choice of masterpiece. I deliberately cropped into the center as I love the abstraction and also want metaphor for limiting attention to a few essentials in the midst of a richness of details.

Because Spring has come to cold Chicago, I used my picture from some Springs ago. Partly it is the green ivy, partly reminiscence.

This is About Idiopathic Calcium Stone Formers

Cystinuria, uric acid stones, struvite stones – all these are to one side. Calcium stones from systemic diseases likewise. Physicians detect these and manage them. My focus is on the vast mainline of patients who form calcium stones without systemic disease.

The Three Essential Facts

Diet Sodium Controls Urine Calcium

If I could I would paint this on the sky, draw it on sidewalks across the world. It has been demonstrated by scientists for at least 70 years,

and how it happens is reasonably well known. I made this picture using published data from many sources, and I placed the original data and references within this site. The blue points are from calcium stone formers, the red from normal people.

Urine sodium is diet sodium, because we absorb almost all the sodium we eat, and excrete it in the urine. Urine calcium is not diet calcium. We absorb only 18 – 35% of the calcium we eat, and that absorption is regulated by the intestines, and by hormones like vitamin D. 

Stone formers absorb a higher percentage than normals, but that is not why their urine calcium is higher. It is higher because they have idiopathic hypercalciuria and their kidneys do not retain calcium as well. At the heart of idiopathic hypercalciuria is what this graph shows – urine calcium is abnormally sensitive to diet calcium. As you lower diet sodium from the average US value of 150 – 200 mEq ( 3500 – 4600 mg) to the present ideal diet sodium of 65 mEq (1500 mg), their urine calcium (blue) falls into the normal range. 

Not rarely my own patients seem disappointed when I begin their treatment with lower diet sodium. It seems so mundane, so like the common nostrum that we all eat too much salt. Many have had multiple 24 hour urine tests, and I make a crude pencil graph of urine calcium vs. urine sodium and show them their own behavior. That works, sometimes. Otherwise, they agree to so alter their food lives, but – I sense this – wonder at coming all the way to a professor for a dull seeming advice. They do not sense the power sodium has, even if I show them this graph – or their own.

Diet Calcium Controls Urine Oxalate 

I made this messy but remarkable graph from work other people have done and put the name of the main author below their dots. These were experiments with variations of diet calcium, on the horizontal axis, measurements of urine oxalate on the vertical axis and diet oxalate as the size of the symbols. The smallest symbol means 50 mg/day of oxalate, the largest means 200 mg/d, the middle size is 100. In the main article using this I placed links to the original data.

The data scatter but above 1,000 mg of diet calcium all four authors found only modest urine oxalate, 35 mg/d or less as mean values. Average US calcium intake is about 500 mg/d or less, which permits a much higher swing in urine oxalate. 

People with idiopathic hypercalciuria, the reason for high urine calcium in idiopathic calcium stone formers, absorb diet calcium more efficiently than normal, so a higher diet calcium supply will raise urine calcium and stone risk.

But, low diet sodium will offset this, improve kidney calcium conservation, so urine calcium can stay low even though diet calcium is high enough to lower urine oxalate.

This is part of the magic and the peril. You must lower diet sodium first and show it is low by another 24 hour urine. Then you can raise diet calcium to block diet oxalate. If you do it right, and keep the diet sodium low, urine calcium will rise little if at all with a higher diet calcium.

Diet Sodium and Calcium Control Bone Mineral

Only one trial proves this, and only in one kind of person – perimenopausal women. We could use more trials. But this one was so perfectly done, and so dramatic, we can for the moment use it as out guide.

Each woman ate each of four diets, high and low sodium, high and low calcium, and in a random round robin fashion. Specifically, the sodium levels were 1600 and  4400 mg/day, and low and high calcium (518 and 1284 mg/day. On each diet, each woman participated in a full balance study so bone mineral uptake or loss could be quantitated.

The four diets are on the horizontal axis. Calcium balance of bone is the black bars scaled on the vertical axis in mg/day, and it can be negative – bones are losing – or positive – bones are gaining calcium.

Absorption is plotted upward, meaning more for bone. Urine and intestinal secretory (‘endofac’) losses downward meaning potential losses for bone,

Balance was positive only with the high calcium + low sodium diet.

The amount of calcium absorbed was higher on the two high calcium diets, of course, and the urine calcium was lower on the low than on the high sodium diets.

As I have already said, the odd term ‘endofec’ means the amount of calcium secreted from blood into the stool by the duodenum, pancreas, and small intestines. This was measured using stable isotopes. If you look close, it was a fall in urine calcium and calcium secretion, both, that created the bone mineral gain from high calcium low sodium diet vs. the high calcium high sodium diet.

Also look close at the urine calcium. 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.

The Magic Works for Stones

This is the one trial of the magic formula. Low diet sodium to keep the calcium in the body and thence the bones, high diet calcium to keep oxalate out of the body and thence the urine. It works for bones. Does it work for stones?

Of course, why else would I put it here, and many other places on this site.

I made the graph very large so your could see the printing in the overlay. The patients were men forming calcium oxalate stones whose urine calcium exceeded 300 mg/d. Low calcium diet was 400 the high calcium 1200 mg/day. The low sodium diet was aimed at 1150 mg, the high at the usual level of about 4000 mg/day.

After five years, stones were fewer in the high calcium reduced sodium group – highly significant statistically.

The why of less stones is exactly what my prior graphs predict.

Of course urine sodium was lower in the low sodium diet group (2,800 vs. 4,600 mg/d, low vs. high sodium, respectively).

Urine calcium of the low and high calcium groups was virtually identical (248 vs. 236 mg/d, low vs. high diet calcium, respectively). Just like for the women in the bone study, one could triple diet calcium yet keep urine calcium the same by lowering diet sodium.

Are you not amazed by this? In two studies one can raise diet calcium three fold and urine calcium does not increase if you also lower diet sodium. Look at the power diet sodium has.

How about oxalate?

Both groups were told to avoid high oxalate foods – walnuts, spinach, rhubarb, parsley and chocolate. The high calcium diet lowered urine oxalate (333 vs. 411 umol of oxalate/d, high vs. low diet calcium, respectively). Supersaturation for calcium oxalate, the proven driver of stone risk, was 3.5 in the high calcium and 4.5 in the low calcium group.

Think about how the threefold magic formula worked. Low sodium diet permitted high diet calcium. The high calcium lowered the oxalate but could not raise urine calcium because sodium was so low.

How to Use the Three Facts

These are magical facts, but they must be used in the right order. It is exactly like casting a magic spell.

Lower Diet Sodium First

Make the change and then be sure you did it by getting a new 24 hour urine. Without the urine test you will never know if you succeeded. Ask yourself if what you did during the collection was like the usual for you and also ask if you really mean to keep the diet sodium as low as during the test. If you get tired of the low diet sodium, and urine sodium rises, all is lost.

Raise Diet Calcium Next

Once you know your diet sodium is low, raise the diet calcium and test again. Is diet sodium (urine sodium) still low? If so, is urine calcium low enough? Low enough is about 200 mg/d of calcium or less.

If so, you are done. If not, you need to keep changing diet sodium and calcium until you get there – high diet calcium, below 200 mg urine calcium.

Some people cannot make do with only diet. Their urine calcium remains too high. For them, we add thiazide to the diet, usually in a very low dose. But for most, this will do. You must keep the low diet sodium, so the thiazide works well at a low dose, and to avoid potassium loss.

Now, Consider Diet Oxalate

With high diet calcium in place, is urine oxalate high enough to raise risk of stones – above 25 – 30 mg/d. If so, it is time to get rid of the highest food oxalate sources. Not all food oxalate, but foods on the high end. I listed some just above. My site has the main ones on a graph. Work from the top down.

Diet oxalate is the last thing to worry about, never the first. One wants to remove what high diet calcium has not removed.

Of course, repeat 24 hour urines are the only way to know if success or failure has attended your efforts.

If You Have Bone Disease

If your bone mineral is deficient, these diet changes are good but you need a physician to be sure they are enough. You may also need medication. Do not rely on just diet. Repeat bone mineral measurements are essential. Be sure your physician is satisfied with your bone health.

If you do Not Have Bone Disease

You may not have looked. Get a bone mineral density. If it is normal, get another some years later. The diet is fine for you unless bone mineral declines. If it does decline your physician needs to manage things. The diet is still advisable, but may not be enough.

There is More but Focus Here, on the Big Three 

Diet potassium and protein matter, the former from from fruits and veggies. Diet refined sugars matter, they raise urine calcium. Diet protein matters, too much raises urine calcium. The kidney stone diet accounts for all of these.

Fluids matter. Urine volume should be above 2 liters/d, the point at which stone risk has been reduced. But fluids are never enough.

But the three way magic spell predominates over all else: – lower diet sodium, then raise diet calcium, then consider diet oxalate.  

Keep your mind on diet sodium and calcium first, and be sure they are set properly. Then go on, if you must, into the thicket and brambles of oxalate lists. Then control unhealthy sugars, excess protein, and get adequate diet potassium. They matter, I always attend to everything I can.

But always, I urge, stay on the main road. Perform the magic spell and see how far you can get.


  1. Terry Phelan

    I really appreciated how the video explained the article and would love to see a similar video that goes with this article “DIET PROTEIN AND POTASSIUM AND KIDNEY STONE RISK”. Thanks

    • Fredric L Coe, MD

      Hi Terry, thanks for the comment. Others have expressed a liking for the videos, and I will do one on the protein article – for you. Fred

  2. Amy

    Hi Dr. Coe,

    Thank you for these thorough and clear articles. Can you please comment on the intake of sodium in the context of a very low carbohydrate diet (less than 40g/day net). I am assuming that the studies above and elsewhere on your site were done in the context of a normal American carbohydrate load of between 100-300g/day. I have heard in the context of a ketogenic diet that sodium needs actually increase some. I am curious what you may know or studies you may know of that deal with urinary calcium excretion and net acid loads in the context of low fasting blood glucose levels. My husband (57) forms calcium oxalate stones ( 3 times since 45). He has a history of high fasting blood sugars but has now turned this around with a extremely low oxalate, very low carb (40g or less), higher protein (1.2-1.5g/kg day) diet. His fasting blood sugars are down from over 109 to 88 mg/dl. We are curious what effect on his kidney stone formation his lowered blood glucose might have and how that may or may not change the sodium recommendations included above. Thank you,

    • Fredric L Coe, MD

      Hi Amy, If the diet produces high ketone loads for excretion, the ketones can promote sodium and potassium losses being negatively charged ions. I do know know the data concerning urine calcium response to reduced diet sodium during high urine ketone losses, but suspect urine calcium will be higher from the ketones. This kind of complexity is why he needs attentive physicians, and they need 24 hour urine testing to determine what is happening. I would suggest that 24 hour stone urines be done for monitoring and that urine ketones also be measured. Day to day management has to be from his physicians because this is complex physiology, but I suspect reduced diet sodium will always be helpful. Regards, Fred Coe

      • Amy

        Thank you Dr. Coe,

        He is about to do another litholink test to see where he is in terms of urinary output of calcium, sodium, potasium, etc. I do not suspect he is actually particularly ketogenic with high urinary ketones despite the low carb intake because his protein intake is higher as opposed to his fat intake being higher as in a typical ketogenic diet. His diet is high meat(1.5kg/kg), very low carb( 40g) , high but not crazy high fat intake.

        I guess I am wondering if carb intake being exceptionally low influences sodium requirements or recomendations in the absence of ketones. He has been following a 90% carnivore diet. Mostly animal meat, a bit of onion, mushroom,etc, sometimes a few teaspoons of honey and a little fruit ( one serving or less per day). So his diet is not specifically ketogenic due to high protein intake but again blood sugars have been brought into healthy fasting ranges in the 80’s. The meat offsets the typical ketone production in such a diet.
        People who go on low carb diets typically feel better with additional salt intake ( especially during initial transitions).

        I guess I am just curious if you have heard of carb intake and higher blood sugar being a lever that affects calcium/sodium output. It is an unusual situation as so few people follow such a low oxalate ( near none), high protein diet. It is not well studied. The best resource I could think of for further info on such low oxalate, low blood sugar situations might be you and your team since you have done so very much with regard to treating stone disease through diet. I am very grateful for this by the way as there are so few doctors who focus on the effects of and are knowledgeable about the intricacies of diet in the diseases they treat. So thank you for any additional insight you might have.

        • Fredric L Coe, MD

          Hi Amy, the only link I know of between CHO restricted diets and sodium is via ketones – they are anions and obligate sodium and potassium loss. High protein without high fat or carbohydrate is a special case. It causes depletion of body fat stores and weight loss if CHO intake is very restricted, so ketones form from one’s own fat. Later on, it is not healthy – good reading here is what happened with Lewis and Clark, 5 pounds a day per person of Elk meat and they lost body fat and were starving. Regards, Fred Coe

          • Amy

            Thanks Fred! Great reference. Yes absolutely high protein low fat diets would cause starvation. Completely get that. Rabbit starvation situation. Elk can be extremely lean. Good to remember the importance of fat especially once body fat percentages get really low. I would assume lewis and Clark were in single digits by the time they did all that outdoor living and traveling. Thanks for reminding me. Well if the ketones create greater excretion of salt and potassium it must be why it is suggested to supplement salt while ketogenic. Again specific case here though while trying to fix stone formation. I guess litholink should be best guide here based on mineral excretion data. He has the test on order and will be very interesting to see where he is at. Thank you again for your response.


Leave a Reply