MeUp to this point we have considered only increase of urine volume as a means of stone prevention. The effect of increased urine volume is to reduce urine supersaturation with respect to stone forming salts and therefore reduce the risk of crystal formation which is the basis for kidney stones.



Supersaturation with respect to the calcium stones depends upon urine concentrations of calcium, oxalate, phosphate, and citrate, and, in the case of calcium phosphate stones, or uric acid stones, urine pH. Giving citrate salts can reduce urine calcium excretion and increase urine citrate. Urine citrate binds urine calcium in a soluble citrate complex, which reduced calcium salt supersaturations. Citrate inhibits crystal formation, growth and aggregation. The alkaline citrate salts can raise urine pH.

relative risk vs urine citrate from Curhan control file in stone bookEpidemiology

In a prospective study of two nurse (red) and one male physician cohort (blue) Curhan found that relative risk of kidney stone onset (vertical axis) rose as urine citrate excretion (shown in hexiles along the horizontal axis) fell. Below 400 mg/day of urine citrate risk was – compared to above 800 mg/day) increased by nearly 2 fold. Mean relative risk is at the ends of the shaded bars. The upper 95% of risk is at the tops of the filled bars. Even though the average risk (end of crosshatched bars) remained below 1.



Although I had quibbles with some of the comments it included, I believe the recent American College of Physicians (ACP) review of kidney stone prevention trials was done properly, and therefore have selected for review here those they felt were technically adequate.

Below is a detailed presentation of the five studies. Here is a link to my spreadsheet with all of the numbers. It also contains my references for thiazide treatment.

Ettinger et al (J Urol 158:2069-2073, 1997).

Sixty four patients with at least 2 stones in the past 5 years and at least 1 within the past year before the trial were given placebo (33 cases) or potassium magnesium citrate (63 mEq citrate, 42 mEq as potassium and 21 mEq as the magnesium salt in combination pills) – 31 cases. Each pill contained 21 mEq of citrate; 2 pills were taken 3 times a day. The trial was designed to last for 3 years. There were 5 and 9 women in the placebo and treatment arms. Urine citrate excretions were not different before treatment (549 and 587 mg/day, respectively, nor were urine volume, pH, calcium, oxalate, or any other stone forming risk. After a one month grace period in which new stones were not counted, any passage or radiographic appearance of new stones, or growth of previous stones was considered a treatment failure. During the trial, 15 subjects left the treatment arm, 8 the placebo arm.

New stones or growth of old stones occurred in 63.6% (16 cases) of the 25 placebo cases who finished the trial and in 12.9% (2 cases) of the 16 treated cases who finished the trial. If the 6 subjects who left the treatment arm because of drug adverse effects are added in as treatment failures the drug effect remained significant (8 of 22 or 33%).

Of note, this particular formulation is not available in the US. A version of the supplement is available OTC but the dose per pill is so low that it is impractical for anyone to use it. So the trial is part of a proof of principle, but not actually applicable to clinical practice in this country.

Lojanapiwat et al (International Braz J Urol 37:611-616, 2011)

Unlike the Ettinger study, which concerned spontaneous stone formation, this study concerned new stones or growth of residual fragments after shock wave lithotripsy (SWL) or percutaneous nephrolithotomy (PERC). Their subjects were 80 initial patients, all 8 weeks after either procedure, and either stone free or having no residual stone fragments >4mm diameter (Numbers are in the Table). Hypocitraturia (<325 mg/day) was present in 20/39 who received citrate and 15/37 who did not.

  SWL PERC  Total
STONE FREE 24(8)  15(5)  39(13)
RESIDUAL STONES 26(17)  11(9) 37(26)
Total 50(25)  26(14)  76(39)

They were randomized into 39 treated and 37 placebo treated groups and followed for one year which 76 of the original 80 completed. Numbers receiving citrate in each group are in parentheses. Sodium potassium citrate was given as 81 mEq/day in 3 divided doses).

Of the 13 cases who were stone free and received citrate, 12 remained so vs. 15 of the 26 given placebo. Of the 26 who had retained fragments and were given citrate, 8 were stone free vs. 1 of the 11 controls and 16 others given citrate showed no change (13) or reduction in size (3) vs. 2, no change and 2 decreased size among the 11 placebo. These differences were judged significant at the p<0.05 level by the authors.

Soygur et al (J Endourology 16:149, 2002)

This trial considered 90 patients after SWL for lower pole stones who had residual stones <5 mm or were stone free. They were randomly assigned to potassium citrate (50 mEq/day in 3 divided doses) or placebo (Table). The trial lasted one year. The end

  Citrate  Placebo  Total
STONE FREE 28(0)  28(8)  56(8)
RESIDUAL STONES 18(0)  16(6) 34(6)
Total  46(0)   44(14)   90(14)

points were stone free or not and residual stone size increased or not.

New stones occurred (parentheses) in none of the citrate treated stone free patients and in 8 of the placebo treated patients. Among the residual stone group, the fragments disappeared in 8 treated cases and failed to grow or shrank in the others vs. growth or new stones in 6/16 placebo cases. The differences in growth or new appearance were all significant.

Of course, both of these post treatment trials are subject to the biases of a radiography study, but observers appeared to have been suitably blinded to the patient groups.

Hofbauer et al (British J Urol 73:362-365, 1994)

In this trial, an equimolal sodium / potassium citrate was given in doses that maintained urine pH in the range of 7 to 7.2 vs. placebo. Therefore, although patients were allocated randomly to active treatment or placebo, the trial could not be blinded. By the three year endpoint, 22/25 placebo and 16/25 active drug subjects remained. New stones occurred in 16/22 placebo and 10/16 active drug subjects. This difference was not significant. This study is the only one with a negative outcome. It is also the only study that was not double blinded.

Barcello et al (J Urol 150:1761, 1993)

Stone formers with urine citrate excretion rates below 643 mg/day (3.4 mmol/day) were allocated to potassium citrate 60 mEq/day in 3 divided doses. Their mean urine citrate excretion was 359 mg/day. At the end of three years of followup, 20/28 placebo treated and 18/27 citrate treated subjects remained. New stones occurred in 14/20 placebo and 5/18 treated cases, a significant departure from chance.


TREATED  20  115 135 
NOT TREATED 77 71  148
TOTAL  97  186 283 

Despite the variability of design, one can, with nerve, simply ask about the beneficial effects of citrate salts across all the trials. In all five trials 283 people completed the desired treatment period. Of these, 97/283 (34%) formed new stones or, in the case of the post procedure trials showed growth of retained fragments. Among all patients who were given citrate salts, 20/135 (14.8%) formed new stones or showed growth of retained fragments vs. 77/148 (52%) of those given placebo.

I have not added back the 6 cases from the Ettinger trial who left because of drug side effects.

From this we can reconstruct a sense of the value of the treatment as applied to the mixed practice of post surgical management and overall medical prevention.

Let us assume these numbers will hold for the future.

For every 1000 cases like the ones in the trials, 520 untreated cases will form new stones or show stone growth after a procedure vs. 148 cases/1000 cases with citrate, a savings of 372/1000 cases overall.

I realize I am not calculating in the most satisfactory manner as a statistician, but I rather like the coarse grained, even vulgar nature of my count me up.


A Personal View

The trial community exhibits the kind of methodological fussiness one expects and applauds in any scientific situation. Among their ilk the citrate effect is viewed as modest at best, the evidence, by their likes, fair.

I am sure they are right according to the mores and social instincts of this discipline, but I do not come from nor inhabit that discipline, and therefore have an altogether different way of counting – for that is all one does after the impatient and often indifferent subjects have played out their roles in the work.

How likely is it, I ask myself, that citrate salts do not prevent new stones or fragment growth?

Not at all likely.

Why assume anything but that blinding was performed when specified, that radiograph readers were competent and blinded to the groups patients were in, that stone events were counted fairly and compared to radiographs to estimate new stones? If we make these assumption of honesty and skill, the marked downward skew from alkali is just too large to be by chance.

My bet will be on the drug, and if I bet that way, I will always win.

Do We Need More Trials For Calcium Stone Formers?

For me, no. It would seem a waste of money.

Some trials treated patients with reduced urine citrate, others did not. Some trials looked at new stones over 3 years, others at residual fragment growth one year after urological procedures. Will another 50 or even 100 cases be likely to change the outcomes? If so, in what way, and why?

It is true that one trial showed no effect and that trial was not blinded. It is actually a drag on the results as I did not remove it.

We Do Need a Trial of Citrate for Calcium Phosphate Stone Formers?

I do not know how often this must be said. Calcium phosphate stone formers must lurk in each of the trials I have reviewed, but I do not know their outcomes. One trial insisted stones be at least >50% calcium oxalate. That means perhaps a few had considerable phosphate is stones.

Calcium phosphate crystal formation is sensitive to urine pH whereas calcium oxalate stone formation will not be. The reason is that calcium phosphate supersaturation requires divalent phosphate be present, and the pKa for the second proton is about 6.8. Citrate salts can raise urine pH, so they can raise supersaturation with respect to calcium phosphate salts. On the other hand, citrate is an inhibitor of crystallization both because it is calcium binding and because it directly affects calcium crystal growth.


The very same ACP report from which I derived the studies shown here presented an annoying set of comments that infers we might as well just give a drug like potassium citrate without knowing stone composition, or doing serum or urine testing that concerns stone pathogenesis.

For this reason, I offer some remarks on that subject. This is in the special context of citrate treatment. I have made more general remarks of a negative sort about the APC comments.

Does Stone Analysis Matter?

How can it not? I have already mentioned the problem of phosphate stones. Do we not have to exclude struvite is stones? The odd patient with cystinuria who has slipped by? Drug stones? Conversion from calcium oxalate to calcium phosphate stones?

Do Serum and Urine Testing Matter?

How can they not?


Do we want to give potassium loads to people with reduced renal function?

Having prescribed potassium, do we not want to monitor for serious increase in serum potassium; some patients are older, some diabetic, some take ACE or ARB medications, some age or change drugs over the years we treat them.

Do we not want to diagnose primary hyperparathyroidism? You cannot without serum testing and 24 hour urine testing to be sure calcium excretion is not low.


If we do not obtain and measure 24 hour urine samples, how can we know anything? Some patients may have very high urine citrate levels. Some may have very high urine pH values.

Here and there urine oxalate is very high, from primary hyperoxaluria, or occult malabsorption syndromes, or very odd food habits.

People change their habits and develop diseases.

Moreover, people do not always take their citrate. Fall in urine ammonia in relation to urine sulfate, and rise in urine potassium assure one they are taking the drug.


Do We Need a Trial for Uric Acid Stone Formers?


No one really questions that alkali salts will raise urine pH, nor that raising urine pH will reduce uric acid supersaturation and prevent stones. It is common practice. I doubt anyone will pay for or perform an RCT to test this question.

That they will not is very important, because it raises an unexpected question.


We Know the Chemistry

Uric acid is a large flat mainly hydrophobic molecule with most of its charge on a single proton receptor site. The protonated from has a very low solubility in urine of around 90 mg/liter whereas 24 hour urine uric acid excretion ranges from 400 to over 1000 mg daily depending upon diet purine loads. The pKa of the proton receptor site is about 5.3 in urine. 

Given these facts we can calculate uric acid supersaturation from the urine concentration of total uric acid and the pH, along with minor adjustments for the effects of ionic strength on the pKa. High supersaturation will lead to a snowstorm of uric acid crystals. Raising urine pH to above 6 will generally reduce supersaturation below 1 and end uric acid stone formation.

Everyone Knows Alkali Work

There is a lot of uric acid excreted every day, so uric acid stones can grow rapidly. Uric acid gravel has an orange red color and is often seen. When alkali are given, the gravel goes away only to come back if patients miss doses. The absence of new stones is obvious.

No One Treats Without Stone Analyses

Who can be sure of stone composition without stone analysis? Even during treatment of someone who has produced uric acid stones, calcium oxalate or calcium phosphate stones may begin. So people know the stone type, and proceed by custom.

No One Treats Without Testing Serum and Urine

Uric acid stones are common in diabetics and people with reduced renal function; potassium loads are potentially dangerous. Perhaps this is more obvious among uric acid stone formers than calcium stone formers, although given wide spread use of ACE and ARB drugs and NSAIDS, potential risk is everywhere.

The amounts of alkali needed can be variable, and the only reliable way to ascertain is 24 hour urine testing. Likewise for compliance.

Therefore routine practice monitors before and during potassium citrate treatment of uric acid stones.


IN this situation, no one has and probably no one will propose a trial of alkali for uric acid stones. But, there is an almost exact parallel situation for calcium phosphate stones, yet such certainty as pertains to uric acid stones certainly does not exist.


Do We Need a Trial for CaP Stone Formers?



We Know the Chemistry

Calcium cannot combine with mono-valent phosphate but only with the divalent form. The pKa for dissociation of the second proton of phosphoric acid is about 6.8 in urine, although the precise value varies with ionic strength. Given the molarities of total phosphate, calcium, citrate – which binds calcium – and other ligands that have modest effects, the supersaturation of brushite – the usual initial urine CaP phase – can be calculated as well as we can calculate the supersaturation for uric acid.

Like uric acid, phosphate and calcium are abundant in urine, so the amount of crystal that can be produced in a day is similar to that of uric acid. Therefore stones can, and do, form rapidly and become large.

As in the case of uric acid, high urine CaP supersaturation can produce snows storms of crystallization; though certainly not common, patients can recognize this as white urine.

On physical chemical grounds, to lower CaP supersaturation below one and keep it there is to prevent CaP stones as surely as one prevents uric acid stones by raising urine pH and lowering supersaturation below one. Why, then, is not this treatment as self evident as alkali for uric acid stones?

Everyone Does Not ‘Know’ Treatment Works

We have no drug corresponding to alkali.

We can raise urine pH safely but cannot lower it.

Acid loads raise urine calcium losses and can be detrimental to bone mineral balance. Higher protein intake is a possible way to lower pH, but not all kidneys respond to acid with a prompt fall in pH. In some cases urine ammonium ion excretion will rise. In others, acid retention may occur. Urine calcium will tend to rise.

So treatment is not as transparent as for uric acid.

But Treatment Must Work Exactly the Same Way

We can lower CaP below 1 with fluids and measures – reduced diet sodium and thiazide – that reduce urine calcium, and we can monitor supersaturation as we monitor urine pH and uric acid supersaturation.

Furthermore, patients can tell if white urine has ceased.

Moreover, because stones are often actively forming, effective treatment is reasonably obvious.

However, these measures may be difficult to achieve. Thiazide is not always tolerated, reduced salt diet not always maintained.

Citrate is a powerful inhibitor of crystals, and it would be good to know if it were beneficial for the CaP stone former.





  1. Mary Young

    My urologist is a doctor of very few words. We’re trying to dissolve a uric acid Stone in the lower pole of my kidney. He just did a 24-hour urine test and a blood test. The uric acid in my blood is normal however in the urine tests its high. How could blood uric acid be normal but urine uric acid be High? Thank you

    • Frederic L Coe

      Hi Mary, Uric acid stones form because urine is too acidic – pH to low. Blood uric acid can be normal, as can the amount of uric acid in the urine. SO treatment is to make the urine more alkaline. Here is a good article on the matter. The amount of uric acid in the urine is itself of little concern once the urine pH is raised above 6. I a quite sure your physician knows all this. Regards, Fred Coe

  2. Mary Young

    Hello dr.,
    My urologist wants me to try to dissolve my uric acid kidney stone . It is 1.3 cm. He told me to take 15 meq of potassium citrate. This seems kind of low. Could you tell me what is the average dosage of potassium citrate to dissolve a stone of this size? Also what is the success rate? He says it’s less than 50%. Thank you

    • Frederic L Coe

      Hi Mary, It is seemingly a low dose. But one always does a followup 24 hour urine to see if the pH has risen to 6 or more. If it has, the uric acid can dissolve. What he/she means about 50% is that the stone is large and dissolves from its surface, so it is a slow process. As it dissolves, the stone may fragment, necessitating stone passage or possible surgery. But worth a try. For long term prevention, it is a necessity. Here is a better article for you. Regards, Fred Coe

  3. Amit

    What about Struvite stone with highly alkaline urine. Litholink test shows 24 hr urine citrate is low at 187 with urine pH 7.855. Will K-citrate be useful in this case?

  4. Mary Young

    I have 80% uric acid Stones 20% calcium oxalate. I have a 1.3 CM down in my left kidney lower pole. With heart and lung disease my doctor does not want me under general anesthesia. What is a safe way to get rid of the Stone. Thank you

    • Frederic L Coe

      Hi Mary, The uric acid stone will dissolve with alkali treatment to raise urine pH, so one possible route is just that – see if stone bulk decreases. Of course you need 24 hour urines to determine the dose of potassium citrate and also other stone risks related to the calcium oxalate – which will not dissolve but may grow if not managed. I do not know if spinal anaesthesia is effective for ureteroscopic stone removal, but that also seems an option. Regards, Fred Coe

  5. Ray

    Hi Dr. Coe, I was wondering if you could give me your opinion.
    I have been told that my citrate is low, I have done 3 urine collections is the past 12 months
    after having a calcium oxalate stone.

    1st collection:
    Volume 2479ml
    Oxalate 452 umol/24h
    Citrate 0.5mmol/24h *L
    Calcium: 6.06mmol/24h

    2nd collection:
    Volume 4000ml
    Oxalate 678 umol/24h *H
    Citrate 1.1mmol/24h
    Calcium: Lab error

    3rd collection:
    Volume 2230ml
    Oxalate 401 umol/24h
    Citrate 0.9mmol/24h
    Calcium: 8.31mmol/24h *H

    Currently I am taking magnesium/potassium citrate (2 tablets a day)
    each 1 contains:
    1072mg potassium citrate
    412mg magnesium citrate
    15.8meq citrate
    10.5meq potassium
    5.3meq magnesium

    My calcium went up on the last collection, however I have increased
    dietary calcium (is this a concern?) my oxalate has lowered as a result though I think.
    The citrate certainly keeps the PH of the urine very high when I check my urine with the dip strips
    which I’m told will avoid urine to get too concentrated.

    Many thanks

    As per the citrate, do I necessarily need it judging by the results? If so, Is it safe at this dose and would it be safe
    to take everyday, forever?
    Blood magnesium and potassium were checked recently and
    were fine.

    • Ray

      * forgot to say, I started taking the citrate supplement after the 2nd collection, around 3 months before the
      most recent (3rd collection),

    • Fredric Coe, MD

      Hi Ray, your urine citrate is indeed low, low enough to pose a statistically increased relative risk of stones. I gather these low citrate levels were found despite taking potassium citrate – I judge about 20 mEq/d. The urine pH is not mentioned but you find it high at home. I do not know enough about your case to say too much except that if your stones are calcium phosphate, and citrate raises urine pH and fails to raise urine citrate it may not be ideal to use it. Your urine calcium is indeed high. Perhaps your physician and you might want to be sure of an ideal diet and use meds over that base. Sometimes a better diet irons out your kind of problems, and allows for a clearer view of what more is needed. Regards, Fred Coe

      • Ray

        Hi Dr. Coe, apologies for the delay in replying.
        Yes, these citrate levels are despite the supplement containing both magnesium and k citrate.
        My stones are calcium oxalate.
        My intake of protein the day of the 24h urine was pretty high (100g+), so that might explain the calcium level
        which until then has always been normal. I have my consumption now.
        Below is the last set of results:
        •Parathyroid Hormone (pmol/l) 17/01/2019 5.51
        •Albumin 17/01/2019 48
        •Calcium 17/01/2019 2.41 2.08-2.65 mmol/L
        •Adjusted Calcium 17/01/2019 2.37
        •Phosphate 17/01/2019 1.19 0.80-1.50 mmol/L
        •Alkaline Phosphatase 17/01/2019 79 30-130 U/L
        •Albumin 17/01/2019 48 35-50 g/L
        •Total Bilirubin 17/01/2019 19 0-20 umol/L
        •Alkaline Phosphatase 17/01/2019 79 30-130 U/L
        •Alanine Transaminase 17/01/2019 38 7-40 U/L
        •Magnesium 17/01/2019 0.88 0.70-1.00 mmol/L
        •Serum Sodium 17/01/2019 141 133-146 mmol/L
        •Serum Potassium 17/01/2019 4.4 3.5-5.3 mmol/L
        •Serum Bicarbonate 17/01/2019 31* 22-29 mmol/L
        •Serum Creatinine 17/01/2019 65 62-115 umol/L
        •Estimated GFR 17/01/2019 >=90

        •Colour UA, POC 17/01/2019 Light Yellow
        •Clarity UA, POC 17/01/2019 Clear
        •Glucose UA, POC 17/01/2019 NEG
        •Bilirubin UA, POC 17/01/2019 Negative
        •Ketones UA, POC 17/01/2019 NEG
        •Spec Grav UA, POC 17/01/2019 1.015
        •Blood UA, POC 17/01/2019 NEG
        •pH UA, POC 17/01/2019 7.0 PH meter 6.13
        •Protein UA, POC 17/01/2019 NEG
        •Urobilinogen UA, POC 17/01/2019 3.2
        •Nitrite UA, POC 17/01/2019 Negative
        •Leukocytes UA, POC 17/01/2019 Negative
        •Urine Oxalate:Creatinine Ratio 17/01/2019 40* <33 umol/mmol
        •Urine Calcium 17/01/2019 2.72
        •Urine Creatinine 17/01/2019 2.881
        •Urine Calcium/Creatinine Ratio 17/01/2019 0.94 Should be less than 0.7
        Suggest maintain normal calcium in diet, add effercit-K 2 tabs at lunchtime.


        • Fredric Coe, MD

          Hi Ray, You give no new citrate so I suppose it was in the prior note. With very high protein intake citrate will fall and calcium will rise. I would never lower diet calcium, as oxalate will rise, and you have a skeleton. Here is a proper diet. As for the potassium citrate, I see nothing wrong with it. There are no other special abnormal values in your list as you yourself can see. Regards, Fred Coe

          • Ray

            Thank you very much for the diet link and the info regarding the potassium citrate and protein.
            Regards, Ray

          • Ray

            Hi Dr. Coe,

            Is there a difference between potassium citrate and other citrate such as magnesium citrate In helping with increasing urinary citrate levels ? Reason I ask is that I’m feeling a little bit anxious lately and I’m not sure whether it might be linked to my potassium citrate supplement. Alternatively i could try getting citrate from natural dietary sources. Many thanks , regards Ray

            • Frederic L Coe

              Hi Ray, Mg citrate has limited GI tolerance, and no special advantage. Fruits and veggies give you lots of potassium along with anions that are converted to bicarbonate like citrate is, and 5 servings a day can substitute for as much as 40 mEq of K citrate pills. None of the agents affect the brain, or cause anxiety. Regards, Fred Coe

  6. George Coiner

    Hello Dr. Coe. I am 60 years old and have had kidney stone surgery treatments on three occasions once in a water bath 30 years ago, a shockwave procedure perhaps 3 years ago then most recently a treatment where a device was sent up inside my bladder and urethra to breakup and remove the stones last year 2017. I believe my stones have been calcium oxalate. An interesting thing occurred this year after I went in for a colonoscopy. After taking the preparation called Golitely a polypropylene glycol mixture. I was cleaned out and went for the colon test. A day or two after the test I started feeling kidney pain of perhaps 6 out of 10. I passed a small stone at home but then decided to go to emergency room and while I was waiting had a strong urge to pee. I then passed a 11mm then 9mm stones but only felt pressure upon the release…not tearing, scaring pain like was previous stone symptoms. Looking at the stones they appeared to be tan, smooth surfaced and shaped like footballs instead of crystalline and sharp. Could I have stumbled upon a way to “melt the surface of these stones” so they could be passed naturally without further surgery? Being a commercial helicopter pilot requiring annual physicals it is in my best interest to find a solution to my kidney stone issues if possible. I suppose the latest stones could have been Uric acid in nature also?
    Thanks so much for your comments.

    • Fredric Coe, MD

      Hi George, I do not think so. The propylene glycol is not absorbed and would not be in the urine. It will not melt calcium stones. Get the new stone analysed to be sure what it is made of. Regards, Fred Coe

  7. Donna Shure

    I was put on Potassium citrate for uric acid stones (in the past I had calcium oxalate stones) I was very sick from the meds (very upset stomache which lasted weeks even after stopping the meds) They want me to try sodium bicarbonate now Can this help and do you recomnend? Thank you

    • Fredric Coe, MD

      Hi Donna, Sodium alkali work for uric acid stones but the sodium load can raise blood pressure. If your physician can deal with that, the approach is perfectly sound. Regards, Fred Coe

  8. Bev Thomas

    My daughter has had kidney stones in both kidneys. In the last 5 months we have had 2 surgeries and was just informed that the
    Third surgery in needed but they are not sure that they will be able to reach the stones.
    Getting very concerned as to why we keep developing stones in the matter of weeks. I am beginning to think the doctors are lost for words. We did a 24 hour urine which showed her stones are made of calcium phosphate. She drinks 72 ounces of water a day which has created issues at school.
    Asking for some advice … is there any meds we can go one ?

    • Fredric Coe, MD

      Hi Bev, 24 hour urines cannot disclose the kind of stones – you need to analyse the stones themselves. The urines help determine cause and focus treatment. I suspect her urine calcium and pH are high. The amounts of water show why monotherapies are not ideal. Just 2.5 liters of urine a day are enough and the other problems can be fixed as well so she relies on more than one treatment approach. Here is my favorite article on prevention. Regards, Fred Coe

  9. Savannah Shockey

    Hello, I was told by my doctor to take calcium citrate after every meal and snack. That seems excessive, I just want to make sure I’m not taking toooo much. Also, I read about Alkali and is that just an alkaline supplement to take additionally with calcium citrate? I reread a few times and I just wasn’t able to find the answer above. Thank you for your time!

    • Fredric Coe, MD

      Hi Savannah, The article is about potassium citrate; calcium citrate is a form of calcium supplement that had alkali content but is intended to provide extra calcium. I am guessing you have calcium oxalate stones and high urine oxalate, and your physician is attempting to lower urine oxalate with increased diet calcium. That is a workable strategy. Possibly s/he intends treatment for bone disease. Either way, the calcium is the intent in use. You should discuss this with your physician. Regards, Fred Coe


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