CITRATE TO PREVENT CALCIUM AND URIC ACID STONES

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.

WHY CITRATE

Mechanisms

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.

CALCIUM STONES

TRIALS

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.

GRAND SUMMARY

  NEW STONES
  YES NO TOTAL
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.

QUALITY OF EVIDENCE

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.

ROLE OF TESTING

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?

SERUM

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.

24 HOUR URINE TESTING

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.

URIC ACID STONES

Do We Need a Trial for Uric Acid Stone Formers?

NO

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.

WHY NOT?

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.

TRIALS ARE UNNECESSARY

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.

CALCIUM PHOSPHATE (CaP) STONES

Do We Need a Trial for CaP Stone Formers?

YES

WHY?

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.

 

 

 

220 Responses to “CITRATE TO PREVENT CALCIUM AND URIC ACID STONES”

  1. Cheri

    Hi: I am a frequent kidney stone sufferer since I was in my mid 20’s, I am now 49. I have been diagnosed with an over abundance of bile salts since my gallbladder was taken out 6 years ago and have had terrible diarrhea since then. This was causing me to not absorb any nutrients. The doctor told me to start taking Calcium Carbonate 600 mg with 800 mg of D3 added. This has worked wonders for the bile salts and has given me my life back over the course of 1 1/2 months of using it, but since then, I have passed at least 2 black stones in my urine. I HAVE to take the calcium carb/d3 supplements for the bile salts, so what are my options for the kidney stones that will not affect the calcium carb/d3 that I need for the bile salts? Please Help!!!!

    Reply
    • Fredric Coe, MD

      Hi Cheri, The D3 is not the problem, it is the calcium. But, if you take it will your meals it should not cause stones. Try this: get 24 hour urine stone risk analysis – your physician can arrange – when you are using the calcium with your larger meals. If your urine calcium is still high lowering diet sodium will lower the calcium. Mention this to your physician and see what she/he says. Regards, Fred Coe

      Reply
  2. J.D.

    Hi Dr. Coe,
    I have been suffering from kidney stones for 10 years, I am 25. My last 24 hour urine came back with 2.36 volume, 421 calcium, SS Cap 3.89, urine pH 6.753, and Urine Uric Acid being at 0.924. I make calcium oxalate stones. My doctor told me to drink lemon juice to lower My pH. I am seeing that lemon juice actually raises pH. What should I do to prevent my stones? I had my parathyroid checked, it was fine. Thanks, J.D.

    Reply
    • Fredric Coe, MD

      Hi J.D., You have marked hypercalciuria and an alkaline urine. I am surprised that your stones do not contain appreciable amounts of calcium phosphate as well as calcium oxalate. Lemon juice or any fruit concentrate will indeed raise urine pH, as you have found out. The only proper approach for you is to be sure you know exactly what is wrong. Do you have simple idiopathic hypercalciuria, primary hyperparathyroidism – PTH is not enough, or what. Here is a good approach. Check it out and be sure about each step. Then, treatment will become clearer. Regards, Fred Coe

      Reply
  3. Cindy kramer

    I am a chronic suffer of kidney stones. I have been taking potassium citrate for years and have had success with minimal kidney stone growth and when I do pass them they are much smaller. But my potassium levels have been going up. What citrate alternatives are there that don’t contain potassium?

    Reply
    • Fredric Coe, MD

      Hi Cindy, I wonder why your potassium is rising. Usual causes are drugs – ACE ARB etc. Others are diabetes or kidney disease. If these are causes, one can maintain urine citrate with fruits and veggies – five servings daily will provide about 4500 mg of potassium. Another question; if serum potassium is rising what is the urine potassium? Regards, Fred Coe

      Reply
  4. Mark

    I had a kidney stone removed on March 23, 2017. It was 10% calcium oxalate and 90% uric acid. Two weeks ago I has a urinalysis as part of a yearly checkup at my FP’s office. My urine PH was 5.5. Six months ago it was 6.0.

    I have been taking Losartan Potassium (50mg) for high blood pressure since June 3, 2015. I recently read and article https://www.ncbi.nlm.nih.gov/pubmed/9010643 that stated “Losartan potassium increases uric acid secretion and lowers plasma uric acid levels, which may be of benefit when losartan potassium is combined with a thiazide diuretic, but which may otherwise lead to uric acid stone formation and possibly to nephropathy.”

    Would you please comment on whether this drug could be responsible for my kidney stones? Thank you.

    Reply
    • Fredric Coe, MD

      Hi Mark, No Losartan does not ever cause uric acid stones. The review article writer lacks knowledge. ON first use losartan can cause a brief outpouring of uric acid, but bicarbonate comes out with it, so uric acid cannot form. In fact I did the work showing this. Given you form 90% uric acid stones I doubt your 24 hour urine pH was 6; spot urines are not reliable. Be sure and get several 24 hour urines to be sure of your pH and other risk factors. You can read it yourself. Here is my main uric acid article. Alkali is for you. Enough to raise urine pH above 6 in the 24 hour urine. Regards, Fred Coe

      Reply
  5. Adrienne

    Hi Dr. Coe,
    I was a recent participant in one of Jill’s courses. You might recall my “impressive” (not in a good way) sodium number from my first Litholink tests: 327. Thought you would like to know that on my follow up test my sodium came back at 77 🙂 They tested twice to be sure there wasn’t a mistake at the lab 😀 Unfortunately, on my follow up results my citrate has gone from around 400 down to 292 and my pH is down to 5.322. I’ve read about the pills that could help my citrate number – potassium citrate. My question: Is there a direct correlation between the potassium that we eat and the citrate number on the test? I continue to work with Jill and I know the next part of my journey is to get more fruits and vegetables in more regularly. If I can do this, will it have a direct effect on my citrate number?

    Reply
    • Fredric Coe, MD

      Hi Adrienne, I do remember and you did very well. More fruits and veggies sounds good to me. See how far they can take you and then make up the rest with some supplements. But do it in that order. Best, Fred Coe

      Reply
  6. Roger Diggle

    I have read several articles, summarizing studies that indicate calcium supplementation increases stone formation, while increased dietary calcium reduces stone formation. My perception is that there is a missing piece in all these articles: None of them indicate whether the calcium supplement used in the study was carbonate, citrate, or something else.

    After reading the article above, which explains that citrate is very good at blocking crystal formation, I wonder whether there is an appreciable difference between supplementing with calcium citrate versus calcium carbonate. Is it possible that calcium citrate could be beneficial as both a citrate source and a calcium source, reducing stone formation? Or is some other, overriding effect involved that causes an increase in stone formation even when a calcium citrate supplement is used?

    Thanks in advance for any wisdom you may be able to bestow!

    Reply
    • Fredric Coe, MD

      Hi Roger, A perceptive reader! Calcium with meals that contain oxalate blocks oxalate uptake. So food calcium – that tends to be with meals – is effectively reducing urine oxalate. Supplements often miss meals – taken in the morning or at random, so oxalate is not blocked. Calcium supplements tend to rapid absorption vs with meals, too, making spikes. We need a trial perhaps, of supplements with or between meals, but alas I know of none. As for citrate, the citrate creates bicarbonate and that can raise urine citrate, citrate is a good anti stone material. So perhaps it is a better supplement, although most calcium supplements have alkali so I am not so sure. Regards, Fred Coe

      Reply
      • Roger Diggle

        Many thanks for your reply.

        It makes sense to me that if a calcium supplement is not taken with meals it won’t be effective. If no advice is being given to supplement with meals, then it sounds like that may be the real reason that calcium supplements perform poorly – rather than that there is something superior about food calcium sources.

        Reply
  7. Paul Smith

    Dear Dr Coe,
    I require acetazolamide for treatment for a neurological problem. After 1 year at 500mg per day I passed a kidney stone. CT showed one small remaining stone in the other kidney. A 24hr urine test revealed very low citrate of 39 mg/day. Most everything else was in the green zone except for low urine volume, and somewhat elevated calcium oxalate, brushite and sodium urate. My urologist put me on potassium citrate 15MEQ 3xday plus >2.5l of water per day. After 3 months, another 24 hour urine test was done. It showed citrate raised to 122 mg/day but oxalate urine went from 35 to 75mg/day, uric acid urine went from 732 to 956 mg/day, PH urine went from 6 to 7.4. My Dr was concerned that these numbers didn’t seem accurate so he said wait a year, have another test and lets wee what happens. 9 months later I pass another stone (literally one year to the day from the original stone passing). CT showed 4 stones remaining in left kidney (2 medium sized, 2 small) and 2 small in the right. I recently had another 24 hour test and I am awaiting the results. It seems that the citrate treatment has accelerated the stone formation instead of reducing it. I fear these are CaP stones that are forming due to the high urine PH. My question is, if we take as a given that I can’t stop taking acetazolamide (I really can’t function without it), what would be the best way to manage this situation? Should I take more Potassium Citrate to raise urine citrate higher, or will that make things even worse for forming CaP stones? I searched hard for literature describing how to manage stones for patients on acetazolamide but I could not find anything useful. If you have any references for this it would be greatly appreciated.
    Best regards, Paul

    Reply
    • Fredric Coe, MD

      Hi Paul, You pose quite a problem. Of course, the drug causes perpetual delivery of alkali downstream into the terminal nephrons, so pH is high and SS calcium phosphate likewise. As serum potassium falls – as usual- or even not, and serum bicarbonate falls, urine citrate falls and will remain low. Potassium citrate cannot help because the extra bicarbonate from metabolism of citrate simply moves into the urine raising pH and worsening CaP SS. The rise in oxalate does not seem germane, the rise of pH is expected. I would not pursue more alkali. Very low sodium intake might reduce distal bicarbonate delivery and potassium chloride would repair the potassium deficiency that almost always occurs with the drug. Of course, your neurologist might be asked for a more imaginative alternative – surely by now a new drug has come along. Regards, Fred Coe

      Reply
      • Paul Smith

        Dear Dr. Coe,
        I will definitely investigate alternative treatment, although it appears that in Neurology, there is not a good understanding of why certain drugs work, which makes finding alternatives difficult, particularly if the consequences of the drug not working are severe.
        Prior to taking taking Potassium Citrate my urine PH was 6.0, is this considered high?
        You note that you would not pursue more alkali, but do I understand correctly that you would eliminate the current level of potassium citrate supplementation?
        There is a slow release version of acetazolamide that I am not taking. Would you expect any reduction in stone formation by using the slow release version? i.e. is it only the average PH that really matters, or is it better to avoid high swings from larger punctuated medication doses?
        How helpful is increased fluid intake in this situation? In the first year of treatment, which produced only two quite small stones, I had very low urine volume (~1.3l/24hr) and did not control Sodium intake particularly well. It seems that at a minimum I could make an impact on stone formation relative to that first year by maintaining the high urine volume i have now and reducing sodium. Does this make sense?
        Thanks so much for your help.
        Regards, Paul

        Reply
        • Fredric Coe, MD

          Hi Paul, Higher volume could help, and perhaps low sodium diet but that would require multiple 24 hour urines to monitor. Potassium citrate will not help well because it adds more bicarbonate. Potassium chloride might be helpful in case the drug has caused potassium depletion. Slow release etc might help, but I have no experience with it. So we are left with lots of water and low sodium. About this, with the drug blood sodium could fall, so have your physicians informed so they can monitor it. The best would be another drug. Regards, Fred Coe

          Reply
  8. JAKSHAY

    HELLO SIR, MY NAME IS JAKSHAY. I WANT TO TELL YOU HELATH QUES.ABOUT MY 3 MONTH SON VIHAAN.A FEW DAY AGO,BLOOD COME IN URINE OF SON.SO,I WAS GONE TO OUR PED.DOCTOR.DOC.SAID FOR USG & URINE RM REPORT.SO,WE DONE BOTH.IN USG REPORT MULTIPULE (3 TO 4 IN EACH KIDNEY) STONE OBSERVED IN BOTH KIDNEY WITH LARGEST SIZE IS 4MM & IN URINE RM REPORT RBC NOTICED 35 TO 40/HPF, CRYSTALS OF CALCUIM OXLATE NOTICED.SO,OUR PED.DOCTOR SUGGEST US TO CONSULT A PED. NEPHROLOGIST FOR OPNION FOR SUCH FORMATION OF STONE.SO,WE CONSULT A PED. NEPHROLOGIST IN OUR CITY, SHE DONE 24 HRS URINE REPORT OF MY CHILD.AFTER REPORT COME SHE SAID THAT YOUR BABY HAVE HYPERCALCURIA & REASON FOR HYPERCALCURIA IS EXCESS DOSE OF VITAMIN D3 & CALCUIM SYRUP.SO,PRESENT SHE GIVE US k-CIT SYRUP(3 TIMES IN DAY) FOR ONE MONTH AS A TREATMENT & ASKING TO F’UP AFTER ONE MONTH WITH USG & URINE RM REPORT.SO,SIR I WANT TO KNOW THAT WHAT IS THE REASON OF HYPERCALCURIA OCCURED IN BABY EVEN WE ALWAYS GIVE THE DOSE OF VITAMIN D3 & CALCUIM SYRUP AS SUGGESTED BY OUR PED.DOCTOR & ALSO WANT TO, KNOW THAT WHAT IS CHANCES OF NORMALIZE OF THIS HYPERCALCURIA WITH ABOVE TREATMENT.IT IS DENGERS DISEASE OR NOT?

    Reply
    • Fredric Coe, MD

      Hi Jakshay, Of course this is a very serious problem. Hypercalciuria can occur in infants. I doubt vitamin D is the reason, and would suspect idiopathic hypercalciuria or another genetic cause. Also be wary about urine oxalate, as primary hyperoxaluria can be present. This is so complex and I am so far away I can only urge your peds nephrologist be very careful about diagnosis and consider genetic testing as well as urine testing. There are a lot of stones! I would be remiss in saying more. Regards, Fred Coe

      Reply
  9. Sarah

    I have had bouts of uric acid stones in the past and my dr. has prescribed one Potassium Bicarbonate effervescent tablet (25mEq) twice a day. I haven’t had any kidney stones since I began taking it 3 years ago, have had a hard time getting my two doses in each day. Would Crystal Light work the same/as well? And how would I know? Measure the pH of my urine myself?

    Reply
  10. sandeep shanker

    Hi,
    recently I have got kidney stones and I could arrange the stone analysis. the analysis for the stone indicated it as CALCIUM CARBONATE stone of 2mmx2mm size. one stone of 5mm is still present in my right kidney. What are the dietary controls I have to take and what medicines to dissolve this undelivered stone.
    thanks
    sandeep

    Reply

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