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. John V.

    Hi, I recently had my second round of kidney “gravel”. The first was one year ago. The first stones were not analyzed, but the recent stones came back 80% calcium phosphite and 20% oxalate. Two to three years ago we installed a sodium based water softener. Our water was fairly hard, so the salt in our water greater than the average water softener. I drink a lot of water, around 3 liters a day. Do you think that my sodium consumption change could be significant to the formation of calcium phosphite crystals?

  2. DClewett

    Hi Dr. Coe – I had a 10+mm stone back in July. Unfortunately my urologist at the time never got the stone or its fragments tested for composition. I am now seeing another urologist. In September I passed another small stone which was diagnosed as a uric acid stone. I later did a 24hr urine test, and all results were good except pH was 5.0. I have been taking 4 – 10 meq potassium citrate tablets daily, and my pH is still less than 5.5. My urologist said I should now take 6 – 10 meq potassium citrate tablets daily, but he would not recommend increasing the dosage over that amount. What if this new dosage does not raise my pH? What will be my options then? Thank you for your time.

    • Fredric L Coe

      Hi DClewett, Your urologist is doing what I would do in that 60 mEq of K citrate is a reasonable dose when urine pH stays low. Often, one needs even more alkali, and sometimes that needs to be sodium alkali if potassium becomes limiting. Of course your next 24 hour urine will tell you if more alkali is needed. If it is, then your physician will have to choose more potassium citrate – and follow serum potassium closely for a while – or add sodium alkali. One way or another urine pH will rise and uric acid disappear. Regards, Fred Coe

  3. Jen

    My husband has a history of large kidney stones, this February he had surgery to remove large13 mm stone and one from his bladder. In November, he again had a bad stone attack and had to go to the ER they found two stones measuring 7mm and 8mm with a number of small ones. The surgeon told me after surgery that he was concerned he suffered from Cystine stones. They also are afraid his left kidney may have suffered serious damage and may need removed. It has at least two large stones measuring 1.2 cm and is atrophic. We are awaiting test results as well as our follow up appointment 12/10… but the stone analysis came back Calcium Oxalate Dihydrate (Weddellite) 30% Calcium Oxalate Monohydrate (Whewellite) 35% Carbonate Apatite (Dahllite) 35% and the 24 hr urine came back with very low citrate and magnesium. The test results mention Hypocitraturia . To me it seems like he’s an oxalate stone former. Wouldn’t cystine show up in one of those results..? Urologist is recommending lifestyle change of plant based based on cystine stones in order to keep right kidney healthy. Just want to be prepared with questions to ask. My husband has never really delved into why he gets them. This is new for us. So want him to begin to take ownership of his health. He’s 42. Thanks.

    • Fredric L Coe

      Hi Jen, Your husband forms calcium phosphate / calcium oxalate mixed stones and not cystine stones. He needs a full evaluation as to the cause of these stones. Here is a reasonable starting place. Of his physicians are entirely responsible for his care, but I would submit that testing be complete and treatment based on the results. The atrophic kidney may have been damaged by chronic obstruction from a stone or perhaps was never properly formed at birth. Either way he has only one normal kidney so prevention is paramount. I would view his situation as very complex and potentially high risk in the case of new stones on the right – the good side. Perhaps these comments may be of use to his physicians, but of course they know far more about his case than I do being distant and without any more information than is in your note. Regards, Fred Coe

  4. Cindy

    Hi Dr Coe. I have been diagnosed with Cystinuria about 4 years ago now. I’m on many different types of medication to help stop formation of stones and to avoid them growing to big. I’ve had 9 laser surgery a to remove the stones and a kidney removal since diagnosis. I’ve just been put on effercitrate tablets (two, three times a day), instead of Sodium Bicarbonate! Which one do you believe helps alkaline the urine better? Thanks

    • Fredric L Coe

      Hi Cindy, Treatment of cystinuria depends on a lot of changes – high fluids, alkali, reduced protein, and meds. Potassium alkali is preferable to sodium as higher sodium loads can raise urine cystine losses. If stones persist your physician might want to consider having you evaluated at a stone center to be sure treatment is optimal. Regards, Fred Coe

  5. Meagan

    Hi Dr. Coe,

    I have recently been prescribed potassium citrate 30 meq/ 2x a day for calcium stones and I’ve been trying to find information on how long patients typically stay on the medication. I’ve seen you mention that it may be months, years, or decades. How often do you recommend testing to determine efficacy/safety? And under what circumstances do you continue or discontinue potassium citrate?

    Thank you for your time!

    • Fredric L Coe

      Hi Meagan, Great questions. I guess if stones have been a problem and the drug has reduced that problem importantly I would keep it up for years. Repeat 24 hour urine testing yearly, and blood likewise, is a prudent idea. If stones recur despite the drug I always look at repeat studies to figure out why, and change treatment as I need to. After a long while, most patients stop meds, but given how benign this one is, I am slow to do that if the benefit has been obvious. Regards, Fred Coe

    • David K.

      hello Doc,
      urine retention for 3 years now. detrusor muscle works fine, the lower spincter is the issue. possibly related to lumber L2 to L5 nerve issues the foley in dwelling over the last 3 years plugs up with calcium dust and chunks requiring frequent change outs.
      irrigation just pushes it all back in to the bladder.

      has the scope run into the bladder a week ago and 9 stones were pulled out . dark grey in color. 3 years of growth . largest one was 8 mm size\

      the kidneys were scanned and are fine no stones .

      Question : will potassium citrate help keep urine ph lower and slow down calcium dust and new stones from forming at a slower rate. ?

      please advise. thank you.

      • Fredric L Coe

        Hi David, You need to get the crystals analysed and figure out if they are calcium phosphate, uric acid, struvite – from infection. Without knowing what it is how can one decide how to prevent it? Potassium citrate will raise urine pH, so that would help if it is uric acid. Regards, Fred Coe

  6. Mary young

    Dr. Coe,. I have two uric acid kidney stones in my left kidney. I produce kidney stones of uric acid . I’ve had my Stones analyzed several times and they’re always uric acid.. My kidney doctor is trying to dissolve the stones with potassium citrate. My uric acid level in my blood is normal. I am taking 45 meq of potassium citrate daily. My Stones continue to grow. I now have one at 1.57 cm and one at 1.3 CM both in my left kidney. My doctor won’t do surgery on me cuz I’m a very high risk. I have left side heart failure, pulmonary hypertension and I’m 300 lb. Is there anything else we can do to get rid of these stones? I can’t do laser cuz he says I am too fat. If my urine is alkali at 6.25 to 7 pH why is the stones still growing?
    Any help at all is greatly appreciated.

    • Fredric L Coe

      Hi Mary, If your urine pH is above 6 and the stones are growing they are not uric acid. They may have been but uric acid is not stable at so high a pH. Since the stones are so large ask him/her to measure the hounsfield units of radiographic density of the stones on your CT images, uric acid is very low compared to calcium stone crystals. Another matter, is your 24 hour urine pH over 6 or are these spot urines? The latter are misleading as long periods may have lower pH. Regards, Fred Coe

  7. Paul

    Dr. Coe, I am 52, male, 5’0″, 115lbs, lifelong joint damage from severe juvenile rheumatoid arthritis. Last month I began excreting anywhere from 5 to 15 stones with ‘gravel’ per day every morning for weeks. A urologist later deemed them to be ‘bladder stones’ as there has never been any pain associated. While waiting to see this urologist I lived on the internet trying to understand what was happening. To help my bones and joints I had been taking a daily combination of 5000iu of Vit.D3, 40mg collagen powder, Vit.K, Meriva(curcumin concentrate), magnesium, hyaluronic acid, and in hindsight maybe too little calcium in proportion. I stopped all supplements and nothing changed. I then tried adding some very basic supplements. When I tried a 280mg dose of potassium citrate the stones stopped over night! The PC makes me flush and a mild headache. I have arrived at the lowest effective dose being 210mg day. When I saw the urologist I asked him if I can make stones in 24 hours. He said not possible, it takes a while to form them and that the stones would be sitting in there for a while. I asked him if that’s the case then why does taking PC make me stop excreting them? He didn’t know. I’ve read forums where several people say they can form uric acid stones within hours. After an ultrasound he wants to do a cystoscopy as he said it showed a thickening of the bladder wall and a shadow which could be a stone. I’ve spent a total of 30 minutes with this doctor and I’m headed for a cystoscopy with no hematuria over 5 different samples, no 24 hr urine and no analysis of the 4mm and 5mm stones I brought him. His info says he’s been doing this for 19 years. I’m leaning towards a second opinion. It feels like him “not knowing” is him dismissing me. Is it that odd to be able to stop/start visible stones that quickly with PC?

    • Paul

      Also, now that I’ve streamlined to just PC I’ve tried stopping it several times to experiment. If I don’t take PC the stones return the very next morning. I can literally stop/start it that quickly. Urine pH on PC has been 7.0 every time.

      • Fredric L Coe

        Hi Paul, Nice experiment. Surely they are uric acid, and I have already offered my main suggestions. Fred

    • Fredric L Coe

      Hi Paul, I guess the stones are uric acid, and the K citrate raised urine pH enough to stop their forming. You should have the stones analysed to be sure. UA stones tend to be red or orange, but not always. The sudden stopping with alkali is good evidence. Your dose is very low, so you may be at the threshold of forming them, and that is convenient for you. Of course uric acid stones form suddenly and can grow rather fast. I am not your physician so I cannot comment about cystoscopy. That is a decision for your physicians of record and there are considerations beyond stones. Regards, Fred Coe

  8. Donna F.

    Hi, my daughter was subjected to toxic mold at school. She saw a Functional MD who gave her physician strength Glutathione to bring about the mycotoxins for a urine mycotoxin test. My Daughter started having severe stinging pain in bladder area after taking 500 mg a day for a week. Any thoughts on what happened? People are telling me oxylates dumping, mast cell activation caused Interstitial cystitis, ect. I need a cure for this pain, this kid has been bedridden since January 2019. Im thinking she could not detox the mycotoxins properly because she has MTHFR a1298c. Please help, thank you. P.S all lab tests and ultrasounds have been done to rule out UTI, STI, candida, ect all normal. Binders have been used since end of January to help remove the mycotoxins but this pain is still there and debilitating.

    • Fredric L Coe

      Hi Donna, A review on PubMed of glutathione trials shows no evidence of bladder side effects. Oxalate dumping is a myth, such a thing does not occur. Glutathione does improve immune system function, but I found no papers describing mast cell activation. But I must add that as a professor I am broadly speaking here, as neither toxic mold not glutathione supplements fall within my area of specific expertise, and neither is related to kidney stones – which I actually do know about. Regards, Fred Coe

  9. Richard Chapman

    After 50 plus calcium oxalate stones in 3 years, my nephrologist put me on 60 mEq of potassium citrate (taken in two doses daily). I had been passing (or not) a stone or two, every three to four weeks. After starting potassium citrate therapy, I have been stone free for 6 months! It is cheap and effective, and as far as I know has no side effects.
    The question would be, are there any side effects that I need to look out for?

    • Fredric L Coe

      Hi Richard, you are lucky: Good physician and the drug is effective for your particular situation. No risk. Regards, Fred Coe

  10. George Coffin

    My urologist has me on 40 MEQ Potassium Citrate daily to prevent formation of uric acid stones. This is after the formation and eventual removal of a 6mm uric acid stone last year. My rheumatologist recently told me to start taking 400 – 500 mg of calcium daily to help deal with my osteopenia. Is it possible to replace the potassium citrate with calcium citrate to “kill two birds with one stone” so to speak and if so what would be the appropriate dose of calcium citrate to meet the two dosage objectives?

    • Fredric L Coe

      Hi George, 400 mg of calcium is 10 mmol, or 20 mEq, so it will at best be half of the 40. But I am not sure if this is even right because you will not absorb all the calcium, probably only about 20%, so I am not sure if you will get anywhere enough citrate. You can try but I am not very optimistic. Regards, Fred Coe


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