This may be the most important article – to me – I have written thus far.

It is a plea and argument that stone patients need more from us than prevention of stones, because often enough they harbor significant diseases that associate with stone forming and require their own treatments. We need to treat the patients, not just their stones.

The magnificent Garden of Earthly Delights (Hieronymus Bosch, 1450 – 1516) hangs in the Prado. I chose it here as it contains the whole world, which is to say that every patient is that self same.

Stone Formers Have Other Disease Risks

When you look at the data, kidney stones belong to a manifold of diseases that run together: Bone disease, kidney disease, hypertension, and stones themselves. This is to say that forming stones identifies someone as having a pattern of increased risk, modest risk, certainly, but well worth considering.

Renal and Cardiovascular Risk

For example, in Olmsted County about 1.2% of people eventually came to need dialysis or transplantation, but rates were 2.4% for those with stones. In other words low risk is amplified a bit. On the other hand, over 18 years, about 18% of people developed stage 3 chronic kidney disease (CKD) vs. 25% of stone formers. You might say modest CKD poses little threat to life, but in reality this kind of disease associates with higher rates of cardiovascular disease such as heart attack and stroke.

The same for hypertension. Having even one stone raises risk by about 1.5 times the rate for non stone formers.

While it is tempting to string these together in presumed causal linkages – e.g. stones damage kidneys, which leads to kidney disease and hypertension, etc – one may be better off to accept the simple fact of their association and act accordingly. Science will ultimately sort out what causes what.

Bone Risk

Likewise for bone disease. Whereas vertebral fracture in later life affected about 5% of people in Olmsted County, rates were over 20% in stone formers. I believe idiopathic hypercalciuria and low calcium diet massively contribute to this bone problem, but I am limited to my time and the future may show us more.

So What?

It is a matter of long term risk assessment and reduction. Stones tend to peak at younger ages, CKD, hypertension, and fractures come later in life. Both reduce life’s quality, and even longevity. If the final risk and type of damage is modest, risk mitigation seems equally so. Just a proper diet and – when needed – thiazide and potassium citrate should do wonders for stone reduction and improvement of health in later years. That self same diet acts against obesity, insulin resistance, diabetes, and osteoporosis. That is why the stone diet so much resembles the diet recommended for all Americans.

Systemic Diseases Can Cause Stones

One reason for all these associations may be that stones can arise from established systemic diseases that themselves affect kidneys, or bones, or blood pressure. For example, uric acid stones form because urine is too acidic. But that acid urine often comes from obesity, diabetes, or bowel or kidney disease, or insulin resistance, or metabolic syndrome. That will tend to associate stone forming with hypertension and bone and kidney disease when one looks at population studies. Likewise, cystinuria is an inherited disorder of kidney function, and chronic kidney disease is a common outcome. Renal tubular acidosis and Dent’s disease are other examples. Primary hyperparathyroidism is perhaps the clearest possible instance. It causes calcium stones and bone disease, and high serum calcium can damage kidneys and raise blood pressure.

In each case, disease causes stones and stones can add more injury on top of diseases that have preceded them. No one needs be surprised that hypertension, bone disease, and kidney disease accompany stones under such circumstances.

Idiopathic Calcium Stones Have Added Risks, Too

By contrast, common idiopathic calcium stones seem to arise from a complex interaction between genetics and our particularly bad modern diet so rich in salt and sugar and protein, and low in calcium and veggies. Such an interaction would fit with the familial nature of stones and the success of diet changes in reducing new stone formationAs an added pathway of injury, calcium deposits in the kidneys could raise blood pressure and cause kidney disease, and disorders like idiopathic hypercalciuria promote bone disease

This scenario posits that increased vulnerability to the bad effects of our modern diet may cause stones, bone disease, raise blood pressure, and by a multitude of pathways lead to kidney disease. In other words having stones is the mark of multiple vulnerabilities to a diet too rich in salt, sugar and protein, and low in potassium. Even though the linkages may be deeper and less apparent than this, stones become an all too obvious sign of what may be a manifold of disorders each of which deserves attention.

Preventing Stones Is Not Enough

Given this reasoning and the facts that have lead to it, proper care of stone patients cannot be stone prevention alone.

Of course we want to prevent stones. They are dangerous, painful, and utterly disruptive to a normal life. But beyond the stones, we want to treat or prevent the diseases they travel with. Because stones single out people with multiple disease risks, we need to treat the whole patient, not just prevent kidney stones.

Evaluate Every Patient

Systemic Causes Can be Hard to Diagnose

When they know about them, physicians are apt to treat systemic diseases effectively. But they may not know for some time.

Consider primary hyperparathyroidism. Mild increase of serum calcium can be lost in the noise and confusion of blood samples not always drawn fasting, not always drawn well, and not always run by highly precise labs. Vitamin D deficiency and even modest reduction of kidney function can mask primary hyperparathyroidism.

Intestinal  malabsorption may have few symptoms yet produce hyperoxaluria. Primary hyperoxaluria itself is not evident unless a 24 hour urine has been obtained. If stones are lost, or not analysed, uric acid stones and even cystinuria can be missed – for a while.

The rare genetic diseases – Dent’s disease, renal tubular acidosis as examples, can be colorful and odd looking but mainly we diagnose them from coordinated serum and urine laboratory measurements. The not uncommon and unfortunate tendency to restrict 24 hour urine testing to recurrent stone formers can much delay diagnosis.

Uric acid stone formers are rarely ‘idiopathic’ in that the low urine pH they require is not a normal finding. I already listed the panoply of underlying disorders one usually encounters. Almost never do they lack systemic problems, so almost never is it enough to just prevent more stones.

Likewise for struvite stones that bacteria produce. These infected foreign bodies need special surgical care. Often, struvite forms over calcium stones of idiopathic etiology, so two problems need attention.

Evaluate All First Time Stone Formers

Detect Systemic Diseases

Consequently, no stone former should be let go without a proper evaluation. You simply cannot diagnose systemic diseases without fasting blood and 24 hour urine testing combined with considerable clinical acuity. Of course stone analysis is paramount. How else to discover uric acid or cystine, or dreaded struvite – from infection. Explicitly, even first time stone formers cannot be left untested and told to drink more. That approach that invites mistake.

Improve Treatment Outcomes

Idiopathic calcium stone formers are diagnosed by exclusion. That means no one can be so classified without serum and 24 hour urine studies and stone analysis. Once identified, they are best off with immediate multimodality treatment. The more stones formed, the less effective our treatments. Just high fluids ignores the need for changes in diet calcium and sodium to protect against bone mineral loss, reduction of refined sugar as a hedge against insulin resistance and metabolic syndrome, as examples. It ignores the need to manage against bone and kidney disease, and high blood pressure.

Promote Healthy Diet

How can I best say this? Every first time stone former deserves serum and 24 hour urine testing. Period. Why wait? To neglect systemic disease is sinful. If idiopathic, stone prevention begins simply with a healthy diet that otherwise might have been put off for convenience’s sake, but followed from necessity contributes to a healthier life not only for the patient but the family as well.

Said perhaps more aptly, stone prevention based on a proper diet and medications when needed reduces risk of later life fractures, as well as high blood pressure, chronic kidney disease, and their associated increased risk of cardiovascular diseases such as heart attack and stroke.

Canary in the Mineshaft

Put another way, most patients will have idiopathic calcium stones.They are lucky in having no overt systemic diseases. But just because their idiopathic calcium stones bring patients to physicians for care, the stones cannot be all we attend to.

Bone Disease

Every stone clinic is a bone clinic‘ – Professor David Bushinsky.

Find It

Stone formers fracture more commonly than others do. I think idiopathic hypercalciuria and low calcium diets are a main reason why. But whatever the real reasons turns out to be, we want to lower that risk.

Given established idiopathic hypercalciuria, a bone mineral density (BMD) scan seems reasonable, and insurance carriers may pay for it. Multiple studies document reduced bone mineral density in IH. We do not have enough clinical data to advise a bone scan for other idiopathic stone formers, yet. Even so, I favor scans given a history of low calcium diet or of family fracturing. Obviously, we need more data about bone disease in non hypercalciuric calcium stone formers.

Treat It

We obtain a scan and estimate fracture risk. What then?

If fracture risk is modest, high calcium, low sodium diet should be reasonable. You might say it is also proper for IH as a way to prevent stones, and I agree. So in treating the one we help treat the other. Likewise for thiazide: proper to lower urine calcium and reduce new stones, known to improve bone mineral balance and reduce fractures.

I hear you saying, ‘so why measure BMD?’

Sometimes, we will find advanced bone disease at the beginning, and treat it with bone specific medications. If BMD is only modestly reduced we know we need to repeat the scan after some period of diet treatment. Should all be well – stable or improved BMD – we have done well. But if not, further treatment can be offered, such as bone specific medication appropriate to fracture risk.

What we gain is precious time, a baseline to work against, and a bone oriented follow up we might have otherwise not performed.


You might say, every primary care physician looks for hypertension, finds it, and treats it. But that cannot be. The fraction of people with high blood pressure under control from treatment has been estimated at only about 50%

Because stone formers are at higher risk than normal, we need to be sure about blood pressure. To me, this means not only making a measurement at clinical visits but also looking at what others have found. If values seem suspicious, the cost of home blood pressures is virtually negligible compared to the benefits of early recognition.

Once again, treatment of stones usually involves low sodium intake, high potassium from fruits and veggies, thiazide, and reduction of sugar intake – which will tend toward weight loss and improvement in insulin sensitivity. All of these measures can lower blood pressure and may suffice.

If it does not, we can augment medical treatment ourselves or work with primary care physicians to have it done if pressures remain above ideal despite the kidney stone diet and thiazide. Because we know risk of kidney disease is increased, we may be more vigilant than others.

Kidney Disease

It Happens

I am surprised kidneys fare as well as they do given repeated obstruction from stones, infections, and procedures like shock wave lithotripsy and percutaneous nephrolithotomy. All of these offer possibilities for kidney tissue injury and inflammation. Virtually all stone forming kidneys harbor calcium deposits. Tissue cannot but recognize them and react.

Years of work have established that resilience has its limits. Stone formers do progress to chronic kidney disease and even serious kidney failure at higher rates than normal.

We Can Help

One cannot reduce this complex matter to a few clinical nostrums. Say instead we have the responsibility for wary observance and care to mitigate. I mean by this attention to even slight reductions of eGFR and to stone related events that can damage kidneys. Obvious examples of the latter: contrast agents; dehydration from vomiting when NSAIDS are being used for stone pain; multiple shock wave procedures; painless and therefore missed stone obstruction.

Our basic stone prevention diet – low sodium, moderate protein – helps protect kidneys, as does attention to blood pressure. Likewise for reduced sugar intake that helps stave off obesity, insulin resistance, and diabetes. But stones themselves and the procedures to visualize or remove them can deceive us. The very urgency of a stone attack may divert attention from the need to protect against kidney injury, however inadvertent.

My Message to Patients

Stones are bad enough, but they may signal risk for as bad or worse. Shun monotherapies like ‘lots of water’; low oxalate diet as panacea; lemon juice; or nostrums found on the web. They are often ineffective and do not speak to all that may be wrong.

Demand blood and 24 hour urine testing after even one stone.

Ask about bone disease, blood pressure, kidney function.

Learn and follow the kidney stone diet. It has a good scientific base and matches what all US people are advised to eat anyway. The diet, supplemented with thiazide or potassium citrate when needed, helps protect against bone and kidney disease, and hypertension, as well as more stones.

Offered procedures, ask about kidney protection, risks to kidney function. Know what your kidney function is, and always ask about changes in it, if any.

Know your blood pressure and see it is kept in proper limits.

If your bone mineral density has been low, be sure it is re-measured at intervals, and that you get treatment, if needed, to stabilize it.

My Message to My Fellow Physicians

Stones can be the first sign of systemic diseases. Find them early.

Shun single modality remedies. Because they do not protect against bone or kidney disease, or against hypertension, they are wrong at their core: too narrow for a population at higher than normal risk. Especially first time stone formers, so numerous as they are, deserve a proper initial evaluation for systemic diseases, bone disease, hypertension, and kidney disease.

At minimum, every stone patients should follow the ideal US diet – which is indeed the ideal kidney stone diet. What possible reason can we adduce for acting otherwise?

The hypertension, bone disease, and kidney disease in our stone formers are our responsibility simply because we have ongoing treatment relationships centered around stones. Stone prevention modalities can benefit bone, blood pressure, and, consequently, kidneys. Stone passage and surgical interventions pose risks of kidney injury.

My Message to My Fellow Clinical Investigators

We lack important data concerning bone disease, hypertension, and kidney disease in idiopathic calcium stone formers. These are compelling problems. It is not for me to say what we need, it is for you to think about what we need to practice better, and help as best you can.

My Message to NIH – NIDDK

Shun and discourage thoughtless management of idiopathic stones as if stones were THE problem. Stones are part of a larger problem.

Lots of water, or lemon juice, magic enzymes and bacteria, or obsession over diet oxalate may reduce stone recurrence for a time. But such monovalent remedies are no service to patients who might have more benefitted from a better diet they do not understand and embrace because of distraction and false security.

The ideal stone diet follows the ideal national diet shaped by your peers in government service. We need funds to foster that diet in stone prevention because it also acts against bone disease, hypertension, obesity, and diabetes, crucial issues to stone patients at risk for fractures, hypertension, and kidney disease.

We need research that helps physicians detect and manage bone disease, hypertension, and kidney disease in stone formers in ways that are austere, efficient, comprehensive, and effective. That would be a dignified and thoughtful use of public funds.


  1. Taiwo owodunni

    Hello sir,
    I am an hbv patient with normal lft. I have been having pain for over 2months on my left side/admonen that radiates to back and also make my left leg tingle.Done several ultrasound,ct scan and colonscopy nothing was found. I was placed on medications for colitis but pain didn’t stop.So I did another ultra sound few days ago because the pain was spreading from the left side to the right abdomen with pinching feeling on my right side close to the armpit and found out that I have bilateral hydronephrosis/mild hydronephrosis.Prior to the scan I had done eucr and urine mcs with the result below
    Sodium 138,potassium 3.6,chloride 99,bicarbonate 26,Urea 45,creatinine 0.9. So I went to see an urologist which confirmed that I have kidney stones.i don’t understand why ct and previous scans couldn’t pick it?how can I get the diet plan,please I need your insight and to be sure if its really a kidney stone or calyces as some sonograph people pointed out

  2. Eliot Godofsky

    Dr Coe
    Could ou comment on the role of vitamin D supplementation and the risk fo stones in various scenarios ie caOxalate formers etc. I realize this is a complex question but, supplementing with Vit has become more popular in light of “suggestion” that covid-19 risk “might” be mitigated by supplementing people with relatively low levels etc. Also were one to consider, would weekly or even monthly dosing of Vit D (any form preferable?) be better for potential stone formation than daily dosing. A lot there , sorry but thanks in advance

    • Fredric L Coe, MD

      Hi Eliot, Ordinary dosing with D supplements – 1000 to 2000 U/d are not known to promote stones. Serum D levels below 50 likewise. I know of no studies comparing daily vs other dosing. Fred

  3. Kim Murray

    Aged 41 now and I got my first stone at age 14. Had sporadic stones through my twenties but after the birth of my daughter in 2013 (Age 35) I have been producing non stop stones, bilaterally. 24 hour urine shows elevated calcium but Doc has me on Thorazide and bananas. Too soon to tell if it’s working but had approximately 9 ER visits and 4 surgeries, including a failed PCNL and an emergency stent removal due to blood clot complications following my umteenth ESWL all in 2019 (The blood clot, stone, stent combo was thee absolute worst pain I have ever experienced in my life).
    (A quick recall of 2015-2020 – probably close to 25 procedures and matching ER trips to match…. anywhere from 6 to 12 weeks out of work each year since 2015 on FMLA and many, many dollars spent).
    Love my Urology team but I’m wondering if they are missing Hyperoxaluria?! How do I get tested?
    All other results always come back normal…. kidney functions, no hyperthyroidism, and plenty of output. I do produce calcium oxalate stones. At this point I’m surprised my kidneys haven’t just totally giving up on me.
    Currently have 2 in the left and pieces in the right. Had Cysto yesterday with stent placement … this is following major Spinal surgery on 3/11 as well…. Anterior Corpectomy with Dissection and Fusion (ACDF) which came out of left field and I actually thought it was radiating kidney stone pain my shoulder!!!
    Any and all help you can offer for my stone saga would be greatly appreciated!
    Thank you!!

    • Fredric L Coe, MD

      Hi Kim, It sounds like a horrible lot of stones and procedures. Treatment of calcium oxalate stones is rather programmatic. Here is a good article on it so you can see if all the steps have been taken. Prevention is crucial for you! Regards, Fred Coe

    • John Paul

      Hi Dr Cole.
      I am a sufferer of Uric acid stone and I am unable to get potassium citrate pills where I am located however I do have access to it in the liquid form was wondering what you think is a good dosage to start at I am currently taking 10 ml 3 times a day but every time I test my urine it seems to only hold in a alkaline state for a short period of time. I also take 300 MG of allupurinol every night
      Thank you,
      John Paul

      • Fredric L Coe, MD

        Hi John, I believe it is you who has also requested telehealth consultation. Potassium citrate liquid is fine. Usually one wants 20 mEq 2 – 3 times a day and you need to collect the 24 hour urine to get average pH. Ideally, the pills are slow release and last longer. You can spread out the dosing to 10 mEq 4 – 5 times a day and perhaps get better coverage. Regards, Fred Coe

  4. Michael Kane

    Hi Dr. Coe,
    I was recently told by my Nephrologist that with my Urine Ammonium level at 52 and with my Protein (PCR) being at 0.9 my Urine Ammonium levels should be in the range of the 30’s 40’s, rather than 52. My previous (14) 24hr urine results over the past 5 years have averaged 58. My current PH is 6.9. I was told there is known cause for this condition, he did indicate it may be low potassium, but my blood potassium is 4.3. My current 24 Hr Urine results are as follows.
    I do have some concerns and questions that maybe you can help address. What causes a patient to have this condition?
    Is this something that I should be concerned about? What are the potential treatments (dietary, life style or medications) to help?
    Thank you very much,
    Mike Kane
    24 Hr Urine Results – 5-29-20
    Vol 24 – 4.18, SS CaOx – 2.10, Ca 24 – 213, Ox 24 – 25, Cit 24 – 429, SS Cap – 0.72, pH – 6.933, SS UA – 0.02, UA 24 – 0.273
    Dietary Factors
    Na24 – 46, K24 – 116, Mg 24- 121, P24 – 0.538, Nh4- 24 – 52, CL 24 – 119, Sul 24 – 30, UUN 9.13, PCR – 0.9

    • Fredric L Coe, MD

      Hi Michael, I am rather thrilled at a nephrologist who pays attention to urine ammonia. Most I encounter do not do this. Your urine ammonia is very high because your urine sulfate – part of the acid load that would drive ammonia production – is only 30, and ammonia is usually 2/3 of the sulfate. Apart from potassium depletion, which you do not have – serum K 4.3 urine K 116 mEq/d – infection with urea hydrolyzing bacteria is possible. The urea is broken down to ammonia, so pH rises and struvite stones can form. That is possible. A more subtle possibility is that you have calcium phosphate stones and over produce ammonia as the reason for a high pH and therefore calcium phosphate stones. The latter is our own work recently published. I would advise culturing the urine for bacteria that possess urease. Some are fastidious and grow only in anaerobic conditions on enriched media. These are best detected by genetic means. Others are vigorous soil bacteria – proteus, pseudomonas, enterobacter, klebsiella. My Guess the you are a calcium phosphate stone former. My respects to your intellectually superior nephrologist. Fred Coe

      • Michael Kane

        Hi Dr. Coe, thank you for your response. Some additional stone history, my 1st stones were in 2014, 2015, a few 2-3mm calcium oxalate stones in my left kidney, then two 8mm stones from my left kidney that were logged in my ureter in 2016 those too were calcium oxalate stones removed via lithotripsy. My urine sulfate average in the 14 pervious 24 hour urines is 38. Based upon your response, for a possible infection with urea hydrolyzing bacteria, with your advising to culturing the urine for bacteria that possess urease, is there a test available that I could request from my PCP or my nephrologist to order? Also are there any other assessments or testing that I should consider?

        Thank you very much,
        Mike Kane

        • Fredric L Coe, MD

          Hi Michael, given your stones are calcium oxalate with little or no admixed calcium phosphate – be sure this is true, often oral reports say calcium oxalate when 1/2 of the stone is calcium phosphate! – check the actual written report – then a urea hydrolyzing bacteria is probable. One orders a urine culture and asks for fastidious urea splitting bacteria. Regards, Fred Coe

      • Michael Kane

        Hi Dr. Coe, thank you for your response. Some additional stone history, my 1st stones were in 2014, 2015, a few 2-3mm calcium oxalate stones in my left kidney, then two 8mm stones from my left kidney that were logged in my ureter in 2016 those too were calcium oxalate stones removed via lithotripsy. My urine sulfate average in the 14 previous 24 hour urines is 38. Also my evening urine has had a sulfur type of smell to it. Based upon your response, for a possible infection with urea hydrolyzing bacteria, with your advising to culturing the urine for bacteria that possess urease, is there a test available that I could request from my PCP or my nephrologist to order? Also are there any other assessments or testing that I should consider?
        Thank you very much,
        Mike Kane

      • Michael Kane

        Hi Dr. Coe, thank you for your response. Some additional stone history, my 1st stones were in 2014, 2015, a few 2-3mm calcium oxalate stones in my left kidney, then two 8mm stones from my left kidney that were logged in my ureter in 2016 those too were calcium oxalate stones removed via lithotripsy. My urine sulfate average in the 14 previous 24 hour urines is 38. Also my evening urine has had a sulfur type of smell to it. Based upon your response, for a possible infection with urea hydrolyzing bacteria, with your advising to culturing the urine for bacteria that possess urease, is there a test available that I could request from my PCP or my nephrologist to order? Also are there any other assessments or testing that I should consider?
        Thank you very much,
        Michael Kane

        • Fredric L Coe, MD

          Hi, I think I answered this already. Please let me know if I did not. Fred

  5. Patricia Sammarelli

    Does Truvia in granules have oxalate? I know Stevia leaves does.
    Thx in advance,

    Patricia Sammarelli

  6. Brittany

    Dr. Coe – Your website is simply amazing. My mom had four kidney surgeries over the past year (two with Dr. Monga, who unfortunately is no longer at Cleveland Clinic). After each of them, she experienced bad infections and in November 2019 she was in ICU with sepsis. We recently learned she needs yet another surgery. I was in the process of enrolling her in your Kidney Stone Prevention Program, when a bigger issue arose… she works at our local hospital and she just tested positive for Covid yesterday.

    My mom has multiple at-risk factors, not the least of which is her kidneys. I read a few studies about how Covid is really bad on the kidneys (for example a May 4 article
    in the Journal of the American Society of Nephrology). I was wondering if you had any guidance or suggestions regarding this.

    My mom had blood in her urine and a temp
    two Sundays ago (May 3, 2020). She assumed it was a UTI and started taking Keflex. I am now concerned that the blood in her urine was actually Covid attacking the kidneys. Her right kidney was only operating at 23-33% before she contracted Covid.

    I came home to monitor her. I know what to look out for with regard to her breathing and pulse ox. But here are my question:

    (1) What symptoms or signs should I look out for with regard to Covid effecting her kidneys? How can we tell if it is causing AKI or blood clots to form in her kidneys before it’s too late?

    (2) I explained to her new doctor my concerns, but she wasn’t very receptive. Should I demand that someone check her kidneys now to make sure everything is fine? If so, what types of tests, imaging, etc. should I even be asking for?

    Again, I cannot tell you how helpful you and this website has been with quenching some of my fears in normal times, so I thank you.


    • Fredric L Coe, MD

      Hi Brittany, Most likely the blood is from stones. Covid effects are most marked in increase of serum creatinine or increased urine protein excretion, but if she has bleeding from stones the blood will raise urine protein. So for the moment I would rely on serum creatinine as a gauge. If it rises, it could be Covid or possibly obstruction from a stone. I hope this is helpful. Regards, Fred Coe

  7. Jordan

    I have had several calcium oxalate/phosphate kidney stones causing symptoms of microscopic hematuria with occasional moderate hematuria 2+. I am on thiaziade medication and kidney stone diet. My last removal was a 10mm stone in my lower pole kidney but without obstruction via ureteroscopy and laser lithotripsy and my eGFR went down 20%. Urologist wanted to remove it as he said then I could avoid an emergency surgery later so I did so. The urologist wants to do x-rays annually to check my stone situation. My current thinking is to allow NO procedures ureteroscopy OR ESWL unless there is a blockage despite possible hematuria. Am I off base in my plan? Is there ever a good reason to remove a stone located in the kidney and not causing blockage but maybe a bit of bleeding?

  8. Tracy

    Hi Dr Coe
    I’m from Canada and I’m 45 yrs old I have had 7 kidney stone removal procedures in the last 5 years both sides and always more then 3 on each side some almost an inch and a half. Why do I get them every 6 months after being removed? They were tested and came back as calcium stones. Any real advice for me. I am so tired of nobody looking into this and going about this as a normal thing

    • Fredric L Coe

      Hi Tracy, Prevention is very important, and here is a good place to start. In Canada, 24 hour urine testing appears scarce and rationed – from comments I have had in the past – but such testing is crucial. Read through how prevention works and see if your physicians can get it done for you. Given so many procedures, cost consciousness alone should motivate everyone. For me, your situation demands prevention. Regards, Fred Coe

  9. Kendall

    Hi Dr Coe,
    I have hypercalcuria at 320 and sodium at 100. I just had a serum vitamin D test and it was at 32 and a Dexa that showed a normal z score of .3 and t scores ranging from .1 to -.5. My doctor wants to me try to reduce my sodium which I am doing based on your website. Also, he wants me to take a megadose of 50,000 IU of vitamin D2 three times a week for four weeks followed by 5,000 IU vitamin D3 per day for a month to get my vitamin D level up to 50. Is there any chance a megadose of D2 or even a daily 5000 IU level of vitamin D3 will worsen the hypercalcuiria? Is megadose of D2 have a better/worse or same affect as a megadose of D3? Lastly, could a more optimal serum vitamin D level of 50 result in better calcium absorption and reduce urine calcium? I am a bit skiddish of taking this vitamin D without comprehending the implications.

    Thanks for being a great patient advocate and sharing your knowledge,

  10. Sheryl Frankel

    Hi Dr. Coe,
    Thank you for the comprehensive website. I wonder if you would like to weigh in on my particular case.
    I am 57 years old. Ten years ago, while under treatment for another condition, approximately 20 stones were found in both of my kidneys. I have never passed any and haven’t had any complications from them. I go yearly to a urologist for an ultrasound and a check-up. I did go to a nephrologist about six years ago. My urine collection indicated oxolate stones. He had wanted to put me on a water pill and mentioned that it could induce pre-diabetes. As I am the grandchild of two diabetics with multiple amputations and daughter of a diabetic, I didn’t want to risk this, so I didn’t go back to him and then just put my head in the sand.
    Fast forward to late 2019. My internist had suggested a bone density test. It turns out I have osteoporosis with T scores in the -3 range. Some other facts about me: I don’t consider myself postmenopausal as I am still having some high estradiol readings. I am hypothyroid with Hashimotos Thyroiditis. I had achieved Weight Watchers Lifetime in 2015 and had been eating a low sodium and relatively low sugar diet. As I don’t drink coffee, I have at different periods in my life drank bottled ice tea, or Diet Coke or black tea for the caffeine content. Probably averaging about 20 ounces of the soda daily.

    I did just join up with the Kidney Stone Diet and look forward to my first conference call tonight. I do have appointments with a new nephrologist and an endocrinologist but aren’t able to be seen in until late March/April timeframes. Many thanks and looking forward to hearing from you.


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