Up 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.
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.
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
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.
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?
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 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.
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?
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.
372 Responses to “CITRATE TO PREVENT CALCIUM AND URIC ACID STONES”
I’ve had red gravel off and on in my urine for several years. Is red gravel exclusively uric acid? Or could it be calcium? I’m going to see a doctor when the new insurance kicks in in the new year, but thought I’d get educated before. Because I jog I’ve been taking potassium and magnesium supplements, worried that I might be sweating out too much. About a year ago I had a bladder stone removed. But never got a clear answer from the doctor about the type of stone.
Fredric Coe, MD
Hi John, red gravel is the very mark and make of uric acid crystals/stones. But certainly collect some and get it analysed – medicine is based on whatever certainties we can marshall! When UA ia proven – even before – add alkali. It can be potassium citrate 10 mEq tabs 2 twice a day or more depending. But this all requires both crystal confirmation and 24 hour urine testing to determine just how overly acid your urine is, and also your tolerance for potassium (there is blood work, too) and other factors that cause stones. Here is what to get done. The article you wrote on has the treatment options. If it is uric acid, and if your treatment is sufficient, and if uric acid is the only crystal, and if there are no other stone risks in the 24 hour urine, alkali should be a cure – so long as you take it. Regards, Fred Coe
But how did my citrate get so low (<47) to start with? I eat primarily plant based, 3 servings of fruit, 3-9 servings of veggies a day, 2 servings of fish a week. 10-15g sugar, 1200-1700mg sodium. With k citrate and lemon juice, it's up to 297, but still a long ways from 500. And everything else is now normal. So, is there some systematic problem somewhere else?
Do you have any malabsorption issues from illness or past surgery? Have you consulted your doc about why your citrate might be on the low side? Were they able to provide some answers?
80 yeas old with an ileostomy and years of kidney stones with several lithotripsy procedures. Recently passed a 5mm kidney stone and multiple weekly smaller stones. Oct. 5, hospitalized with blood infection plus a 6 mm kidney stone blockage, stent was placed. Stone analysis just received.. 80% Uric acid dihydrate; 20% calcium oxalate dihydrate. Currently on daily deptomycin antibiotic infusion until November 25 for blood infection (pacemaker had to be removed and had vegetation on mitro and tricep valve). What would you recommend to reduce the incidence of these stones?
Fredric L Coe, MD
Hi Herbert, Ileostomy usually produces uric acid stones and they can be abolished with alkali. Usually I use simple OTC sodium bicarbonate tablets because GI sodium losses are significant and the pills reliably make the urine alkaline so uric acid cannot form. Do not begin these pills without discussing them with your physician as there may be other issues, Potassium citrate is the usual prevention for uric acid stones. If you have low blood potassium and need more potassium your physician may want to use them. You must have 24 hour urine testing to be sure the dose of alkali is sufficient to raise urine pH above 6. Typically this requires 2 OTC 10 grain sodium bicarbonate tablets 4 times a day. Be sure to discuss this with your physician, as I am not the one responsible for your case and he/she is. Regards, Fred Coe
This area of science has been a confusing minefield of sometimes-conflicting data, and certainly inscrutable advice at times, even though I’m certain it all comes from a place of care and trying to be helpful.
Quickly, my story, and then my questions(s):
I was diagnosed with Type 1 Diabetes in 2019 and immediately turned to a low-carb diet as a way to best manage my condition. This low-carb diet, in hindsight, also meant a high-oxalate diet (large amounts of almonds, almond flour, peanuts, peanut butter, raspberries, etc. as my primary snacking foods).
Then, in early 2022, I was diagnosed with low blood platelets and low HDL cholesterol. So, turning to the internet to get some natural solutions, I started loading up on spinach, wheatgrass, and chia seeds as well, on an almost-daily basis.
Then, in May 2022, I passed my first stone. And the CT scan in the ER showed another stone in my lower left pole of my let kidney as well. So, suddenly, two stones. Turns out, I passed 2 stones over a 72 hour period, yet the stone in my lower left pole is still there, so I do not know where that other stone came from! In any case, I got one of the stones tested and it was Calcium Oxalate.
I immediately went on a low-oxalate diet, and a few months later did the 24-hour urine analysis and found that my citrate levels were low (189mg), my oxalate levels were high (65mg), Ammonia was high (63mEq), and Uric Acid was high (980mg). The rest of the metrics were within range.
With this, I went to a Nephrologist and he recommended the following treatment: 15mEq potassium citrate 3x/day and a low dose of hydrochlorothiazide (which I am having at least some initial adverse reactions to).
He also said that there’s no convincing evidence to-date that low-oxalate diets impact future stone creation — that it’s far more about getting these “break down” components (like citrate) readily available (along with plenty of fluids) to do the work that needs to be done to ensure no crystal formation happens.
I am surprised by these recommendations (esp the lack of data supporting low-oxalate diets!), and I was curious what your perspective is on this regimen that has been prescribed for me.
Any insights deeply appreciated!
Fredric L Coe, MD
Hi Jon, There are some complexities you mention, and I do not know enough about your particular case to make any strong statements. The low platelets must have a cause, and I do not know what that is. I understand you ate considerable amounts of high oxalate foods, had a high urine oxalate level and that despite a ‘low oxalate diet’. The usual reason for high urine oxalate despite attention to high oxalate foods is too low a diet calcium. Another is a very high protein intake, for which you offer some evidence – high urine ammonia and uric acid; the former is a common response to the acid load from cystine and methionine in meats (or legume species), the latter is from the purines in DNA and RNA, both high in the same sources. The low citrate may be from the acid load or an additional problem for which I would need a lot more data. I can understand the use of alkali and possibly a thiazide, and I understand that there is a miscommunication as well. There is no trial data for low oxalate diet per se, merely a strong epidemiological link between higher urine oxalate levels and new onset of stones. But I am sure that lowering urine oxalate would be reasonable. Yet your whole diet is so biased toward acid load! Another issue is your diabetes. Diabetes alters acid balance, lowers urine pH, but does not generally raise urine ammonia. One could have to relate your urine ammonia total acid excretion to fully understand things, and you do not offer enough information for that. Your nephrologist will know all this, and probably has already considered the diabetes effects, as the research group at Dallas SW medical school has published a lot on the subject. I hope this introduces at least some of the issues, and explains why there seems to be a conflict. Regards, Fred Coe
Hi Dr Coe,
Just wanted to let you know that I appreciate your writing. My urologist doesn’t have time to talk in detail, so being able to read your articles is very helpful. Thank you for sharing your knowledge with the wider community – it’s important to have this information from a vetted Urologist resource such as yourself on the internet open and free to all. Thank you, Julie
Fredric L Coe, MD
Thank you, Julie. Fred
Hi Dr. Coe
My pshiquiatrist recommended i take magnesium for helping with my burnout. I was wondering which would be best for me, magnesium citrate, magnesium oxide or magnesium glicinate. I tend to make kidney stones, although they are so small i cannot seem to find them. Thanks
Fredric L Coe, MD
Hi Maria, the form I most urine is magnesium oxide. As for the stones, you might collect some and get them analyzed so you know what they are made of, and prevention might be of value. Magnesium oxide is not likely to cause or worsen stones. Regards, Fred Coe
Thank you so much.
I have 300 mg magnesium oxide pills to take. Am taking one per day.
I think my stones are more sand and although I use a strainer, I have not been able to catch any. 🙁
Hi Dr Coe.
Many thanks for this article. I am not at all a scientist, much less a chemist, so I hope that you can be patient with me! You talk about Citrate, but – just to be clear – are you saying that taking Calcium Citrate will reduce the instance of Calcium Oxalate crystals in the urine/kidneys etc? Why would the Calcium element not lead to greater instance of crystals?
Many thanks in advance
Fredric L Coe, MD
Hi Mark, I said potassium citrate (or there is a typo I need to fix). The citrate you take is metabolized to bicarbonate and the latter signals the kidneys to release citrate into the urine. Regards, Fred Coe
Hi Dr Coe. I have mostly uric acid stones with a tiny bit of oxylate. I have tried potassium citrate, sodium bicarbonate and moonstone. I can’t tolerate them. I am dairy free and get very little calcium. My urologist said to try citracal calcium 2 times a day. It has zinc, manganese , copper and D. Will this supplement prevent uric acid stones?
Fredric L Coe, MD
Hi Holly, Uric acid crystals form at low urine pH and dissolve at a higher one so anything you do to raise pH will stop them. Crystal Light lemonade will raise urine pH, a diet rich in veggies and fruits will help – try putting both together. Calcium citrate is also fine and the calcium will be good for bones. If you cannot tolerate potassium citrate or sodium bicarbonate as treatments, perhaps you could tolerate smaller amounts to use on top of the lemonade – one OTC sodium bicarbonate 4 times a day is not much but this would give you about 20 mEq of alkali. Mix and match till urine pH is about 6 in a 24 hour collection. Regards, Fred Coe
I’m 60 year old male who just developed his first kidney stone after moving from Chicago to Arizona (the Stone Belt I’m told). Lithotripsy last week seemed to work well as I’m passing small stones (probably calcium oxalate). Besides drinking a lot more water, could you impart one other recommendation to lessen the chances of another stone? Magnesium and B6 are often mentioned. Thank you.
Fredric L Coe, MD
Hi Mike, The only reasonable approach is to get fully evaluated. I presume you have long harbored stone risks and the move has brought them into the daylight. Please do not guess, the workup is cheap compared to even one stone surgery. Regards, Fred Coe
Hi Dr. Coe,
You wrote in one of your respnoses to a question here that magnesium citrate will raise urine PH. I have uric acid stones. My urine PH iis almost always between 5.0 and 5.4. I’ve tried potassium citrate, but unfotunaely, couldn’t tolerate it. Would supplementing with magnesium citrate be a good alternative? Thanks..
Fredric L Coe, MD
Hi David, I did not mean to say that magnesium citrate is useful for uric acid stones, but perhaps I wrote in error. Given these stones you need alkali. If K citrate is not acceptable mere sodium bicarbonate tablets – OTC, 10 grain, 2 three – four times a day – is acceptable. There are new OTC mixtures like Moonstone and perhaps the taste etc will work for you. Crystal light lemonade is high in potassium citrate, and a liter daily will help raise urine pH. Since raising urine pH to about 6 cures – prevents – uric acid stones, you really should want to achieve that goal. Regards, Fred Coe
Thanks, Dr. Coe..
With regards to the magnesium citrate, you wrote in your 7/2/21 response to KimO on this page that “Magnesium citrate will raise urine PH as will potassium citrate….”. I’ve taken about 270 mg of the citrate daily for 2 days. According to the dosing instructions on the pill container, that’s about 2/3 of the recommended daily allowance. I know that’s not a huge dose and I know taking it for 2 days isn’t a long time, but after 8 tests with a PH meter over that period of time, my urine PH has risen from a range of 5.0 to 5.4 to a range of 5.7 to 6.2. Could this rise be a result of the magnesium citrate intake or most likely the result of something else? As I mentioned in my original post, I have uric acid stones and am hoping a rise in PH will prevent new stones from forming. I plan to continue testing.
One other question… If I’m diabetic and have stage 3 kidney disease, would magnesium citrate be safe to take on a daily basis? I was reading that it may not be for someione who’s in renal failure. Thanks..
Fredric L Coe, MD
Wow, good reader! I had forgot the comment. Magnesium citrate nonahydrate has a mw of 613, so you take 270/613 or 0.44 mmol but with a valence of 3 giving 1.3 mEq of alkali. That seems way too small to raise urine pH. Trimagnesium bicitrate may be in these OTC materials,, MW is 451 so you are taking 1.9 mmol with a valence of 3 for 5.76 mEq of alkali. I suspect that is the material, and this amount of alkali could raise urine pH a bit. Most magnesium is in cells, and even with mild renal insufficiency I am not overly concerned about 2 mmol/d. But uric acid stones are worrisome, and why use an odd preparation like this when potassium citrate is so much more effective (a lot more alkali)? My concern is that 24 hour urine pH, the real force for crystal formation, will not rise to 6 or more and you are getting just time samples – for example think about overnight. Regards, Fred Coe
The 270 milligrams of magnesium citrate I’ve been taking daily only keeps me in the 5.8 – 6.2 PH range for about 10 hours, so I’m planning to increase the dose to see if I can maintain that range for a full 24. Unfortunately, I wasn’t able to tolerate the potassium citrate or the sodium bicarb for very long.
On Tuesday, I’m scheduled for a utereroscopy to remove a number of kidney stones, the largest, 1.6 mm. This will be my 2nd utereroscopy in the past 2 years. At 57, it seems I’ve become a stone former. This makes me sad. After my last utereroscopy, my urologist had me take a couple 24 hour Litholink tests to determine my stone risk. The first test, about a month post surgery, The second, about 6 months later. Each test result showed a urine PH below 5.5. My urine volumes were also both low, under 1.4 liters. My urologist wanted me to increase my water consumption. Doing that, unfortunately, didn’t increase my urine output, It only raised my blood pressure. Now, I only drink when I’m feeling thirsty.
Fredric L Coe, MD
Hi David, Your story illustrates the real complexity of working out a prevention program. If, for example, increased water intake raised your blood pressure, then there is a need to consider why – this is not a common outcome. Likewise, if you cannot tolerate even sodium bicarbonate, why not and what can be done as an alternative. Given uric acid stones and perpetual low urine pH and volume, of course risk of new stones remains. Rising blood pressure from water increase is not common, but needs to be gotten around. Perhaps, your physicians might with to consider seeking additional consultative input from somewhere convenient to your location. Regards, Fred Coe