Chapter Eight: Uric Acid Stones

Uric acid stones, to me, means not just pure uric acid stones but any uric acid in stones. If this seems fey, let me explain. Uric acid is a peculiar kind of crystal. Low urine pH causes them and treatment that raise urine pH prevent them altogether. Whether they form combined with calcium stones or pure, treatment is the same.

Why then scruple over percentages? If I find uric acid in any stone, I look at urine pH with a yellow eye. Should it be low I treat it surely and on the moment so at least that crystal be banished forever.

The Profligate Punished by Neglect, Edward Penny 1774 catches the common motif of diet excess, obesity, diabetes, and gout – the joint manifestations of uric acid crystals. Note the abdominal fat denoted by his overly tight vest. All of these states can lower urine pH and lead to uric acid stones.

This article has a pragmatic leaning and eschews excessive scientific details. I have written a more mechanistic article that explores how the low urine pH might arise and cause uric acid stones. Read this one first unless you are already reasonably expert.

Who Are Uric Acid Stone Formers

Stone Analysis

Given my prior reasoning, I call patients who have any uric acid in their stones uric acid stone formers but reserve the right to use compound names when needed. If all stones are only uric acid, I call such patients pure uric acid stone formers. Those whose stones contain uric acid and other crystals I call mixed uric acid /x stone formers: mixed uric acid calcium oxalate, mixed uric acid calcium phosphate stone formers, as examples.

These niceties of naming have the practical value of calling to mind the perpetual need for dual or multiple treatments – for uric acid but also for whatever crystals might be present.

Radiographic Evaluation

Commonly uric acid stones show poorly on routine flat plate x rays having only carbon, nitrogen, oxygen and no heavier atoms such as calcium. On CT scans they do not look different from calcium stones but radiographic density can be measured and tends to be lower. As this article points out, machines differ in their results and evaluation may therefore be less than perfect. Dual energy scanners are more precise, but also prone to many potential artefacts. Multiple reports, by contrast, indicate that CT measurements of radiographic density can reliably distinguish uric acid stones from calcium stones.

A reasonable present view is that lower radiographic density is an excellent clue to uric acid in stones, but far from definitive as stone analysis is. I hesitate to classify a patient on scanning evidence alone.

Signs and Symptoms of Uric Acid Stones

Pigmented Stones and Crystals

Being stones, uric acid stones cause the usual problems of pain, obstruction, bleeding and infection. But they have some special features. The most obvious is stone color – red to orange because the crystals take up a variety of pigments mostly derived from hemoglobin breakdown. Recently scientists have determined the structure of one of these – urorosein.  Sometimes, coarse or fine orange or red gravel passes, made up of uric acid crystals.

Rapid Crystallization, and Stone Growth

Because the crystals form not as a complex lattice like calcium with oxalate or with phosphate but simply as uric acid crystallizing with itself, the process can be swift to begin and require very little supersaturation. Said more technically the energy required to create the crystal is relatively low. This means the upper limit of metastability – the supersaturation needed to initiate crystal formation is not far from solubility, so values above 1 even if below 2, could suffice. Practically it means that bursts of supersaturation during the day can bring on showers of gravel and growth of stones.

Also, urine contains a lot of uric acid. Common daily losses of oxalate approximate perhaps 25 – 50 mg, compared to 600 – 1,000 mg of uric acid. The sheer amounts available when coupled to the rapid and facile crystal formation and growth allow stones to enlarge rapidly and achieve very large sizes, enough to fill the renal pelvis and calyces – so called staghorn stones.

Acute Uric Acid Nephropathy

Very uncommonly, sudden lowering of urine pH coupled with low urine volume can cause crystallizations in the terminal collecting ducts with acute kidney failure. This was once not uncommon during treatment of malignancies, but modern attention to uric acid surges from tumor killing has made it rare indeed. Today, one does not expect to see it apart from unusual situations

Uric Acid Supersaturation

I made the figures for this section anew but from a lovely data file constructed some years ago by Joan Parks, who was my scientific colleague from 1976 until her retirement about 8 years ago. Her legacy of curated data files sustains a lot of my public writing, now, and she deserves a place in it. 

Effects of Urine pH

Uric acid crystals form like all crystals because of supersaturation. In this instance, that supersaturation varies remarkably with urine pH.

In the figure, supersaturation ranges from 0.01 to 10 fold. The dashed line at 1 represents equilibrium, or saturation, the level where crystals neither form nor dissolve. The horizontal axis shows urine pH. The dashed lines at 5.5 – acid urine and 6 neither acid nor alkaline urine are for visual reference.

The tiny points each are one 24 hour urine from patients and normal people. Like an ancient Persian scimitar, points curve downward from 8 to 0.03 as pH rises from 4.5 to 7.5.

Effects of Urine Volume

Urine volume matters. Low volumes (red) 0.5 to 1 liter/day give higher supersaturation than 1 to 1.5 liters/day (green), and 1.5 to 2 and above 2 liters/day (blue and black) lower supersaturation progressively.

But pH trumps volume. At pH 5.5, the whose distance from red to black varies supersaturation between about 2 and 5 fold (use the lines for averages) whereas raising pH from 5.5 to 6 brings almost all the points down below 1. Below 5.5 virtually no points are below 1 at even above 2 liters of urine volume daily.

Effects of Uric Acid Excretion

In speaking about excretion of uric acid we need to insert a note about the molecular species involved.

Form of Uric Acid in Urine

Uric acid is a weak acid, which means it can take up or donate a proton to water. When it has its proton, that proton neutralizes much of its charge, so water molecules cannot themselves form charge bonds with it to keep it in solution. This means that the molecule becomes very poorly soluble and tends to crystallize.

When it loses its proton into solution, it has a charged site for water to relate to and also requires a counterion, which in urine will be sodium, potassium, and ammonium ion. These ‘salts’ of urate – the name for uric acid when it has given up its proton and is a charged ion – can themselves form crystals just like calcium and oxalate form a salt – calcium oxalate – that can crystallize. But all three salts have much higher solubility than uric acid itself.

Effect of Uric Acid Excretion on Supersaturation

When we measure and report urine uric acid excretion we show the sum of all salts and the acid in one number. Obviously this total should affect supersaturation, but the effect is relatively small because so much depends on pH that sets the percentage of uric acid per se – the fraction that has its proton and is therefore poorly soluble.

Here, red, green, blue and black stand for below 500, 500 to 750, 750 to 1,000, and over 1,000 mg/d of urine uric acid excretion respectively. As for urine volume, the total amount of uric acid matters; a fivefold increase from below 500 mg to over 1,000 mg/day raises supersaturation at pH 5.5 from about 1.2 to about 3 fold.

Urine pH of Stone Formers

One presumes that urine pH of uric acid stone formers must lie below that of other kinds of stone formers, and numerous reviews and case descriptions have proven this true.

My own collected data make the point as well as any.

The dot distribution just below shows individual 24 hour urine pH measurements for calcium oxalate (blue), calcium phosphate (green) and uric acid (red) stone formers. Here I include among uric acid stone formers those with both pure and mixed stones.

Calcium oxalate stone former pH ranges widely with an average at about 5.8 pH units. Calcium phosphate stone formers average a lot higher – around 6.4.

Uric acid stone formers lie in an acid range. Their average is about 5.3 – 5.4 and only a tiny scattering of points range above 6. So uric acid stone formers produce a very acid urine compared to other stone formers, and the pH is exactly in the range to produce supersaturation that can drive formation of uric acid stones and hold them steady or cause them to grow.

To see this, just look back on the graphs showing supersaturation vs. urine pH. Below 5.5 values almost all lie above 1 – solubility – meaning that crystals can form and grow.

UA Fraction in Stones

The General Pattern

I have said that any uric acid in stones means pH should be raised because at least that portion of the stone burden might dissolve or at leasts not grow.

The figure below shows urine pH associated not with the kind of patient – calcium oxalate, calcium phosphate or uric acid stone former, but by the fraction of a given stone made up of uric acid.

Blue means no uric acid at all. Red means 100% of the stone is uric acid, and pink and green lesser amounts. With a scattered few points as exceptions, stones made of mainly uric acid go with urine pH values mostly below 5.5.

The graph makes a point we often speak of but rarely show. Oxalic acid has a very low pKa – is a strong weak acid. So it has charges available for binding to calcium that very hardly at all with urine pH all the way down to 4.5, about the lowest value human kidneys attain. So these stone crystals are indifferent to pH.

Paucity of Mixed Stones

I makes another point, too, one that a patient emphasized in a comment to this article and that I failed to mention in the original version. Of all stones that contain any uric acid, at least in my collection of data, most are mainly composed of uric acid. See where the red – pure uric acid – stones make up the largest mass in the figure just above?

This is not to say that patients are uncommon who make both calcium and uric acid stones – mixed stone formers. The graph shows the stones themselves. People who make both kinds of stones need treatment with alkali so they will stop making uric acid crystals. They also may need treatment against their calcium stones. Stones that contain both uric acid and calcium – usually calcium oxalate – mean the patients may need treatment against both their uric acid stone formation – that would be alkali, and for their calcium stone forming.

So in the final analysis, whether the stones are mixed, or patients form both uric acid and calcium stones the answer is the same: Treat against both crystals.

Who Produce Uric Acid Stones?

Low pH Without Intestinal Disease

Genetic Factors

In identical twin studies, urine pH had only a 60% concordance compared to over 90% for calcium excretion. In a larger study urine pH seems as heritable as urine calcium excretion. Of interest, such dietary traits as sugar, calcium, and protein consumption that could influence stone formation also had significant heritability.

Systemic Disorders

Historically, uric acid stones have been linked to gout. A recent but brief review repeats that fact. Likewise, another review.

Given low urine pH drives uric acid crystallization, one has to ask whether some kinds of patients might be expected to produce acid urines. In answer, those most common are obese, older, diabetic, hypertensive, and prone to modest reduction of kidney function. Obesity itself, without necessarily overt diabetes correlates with lower urine pH in a progressive manner – as obesity increases urine pH falls

Resistance to the actions of insulin – so called insulin resistance – is often invoked as a general paradigm to encompass the general class of abnormalities that lower urine pH. Metabolic syndrome, a mix of insulin resistance with lipid and vascular abnormalities is linked to kidney stones. But not to uric acid stones per se. Attempts to link uric acid stones to gut bacteria – use of the genetically defined biome -failed in a tiny study to disclose any species unique to uric acid stones.

Kidney Physiology

At least one specific abnormality that produces the low pH is an inadequate production of ammonia with which kidneys can remove acid. I plan another article on uric acid stone formation that will review the underlying disease mechanisms, and do not wish to burden this text with more detail. The linked articles from the group at UT Southwestern Medical School give access to the best current work on the subject. Essentially uric acid stone formers respond to acid load with less ammonia than normal people. Insulin resistance probably produces the renal tubule abnormality.

The issue is complex, as illustrated by a recent publication that found no evidence for low urine ammonia in uric acid stone formers. But the conditions of that study – mere measurements made in uric acid stone formers with comparisons to normal ranges hardly have any power to test the ammonia hypothesis.

In an elegant analysis of a single patient, Kamel and his colleagues point out two matters I use in my own work. Urine ammonia needs to be viewed in relation to urine sulfate – the net acid load. Likewise, the low urine ammonia of their case was accompanied by a high urine citrate – this occurs when proximal tubule cells consider themselves in an alkaline state that would cause a fall in ammonia production

I have allowed myself a bit more about the urine pH than perhaps is ideal, and will end here. Either I will write another article on this subject or expand this one with my own data on ammonia and citrate.

Intestinal Causes

Intestinal Diseases

Any organic cause of diarrhea can lower urine pH because the fluids contain appreciable bicarbonate, the main blood buffer. In turn kidneys increase acid excretion in compensation. This requires both an increase of ammonia excretion and lowering of urine pH. Common situations include small bowel resection for such conditions as Crohn disease and partial or complete loss of colon. The latter, ileostomy, can cause marked alkali loss with acid urine and uric acid stones.

Chronic intestinal fluid losses also deplete body sodium and potassium. The 24 hour urine is very valuable for assessing both as excretion rates fall with such losses. Repletion with a mixture of sodium and potassium alkali is often valuable.

Bariatric Surgery

Howsoever valuable, these can result in both enteric hyperoxaluria and chronic alkali loss so calcium oxalate and uric acid stones do occur. The former are more common. This recent and excellent review details new stone frequencies but stone analyses are not widely reported so I cannot state the balance between calcium oxalate and uric acid crystals. Treatment with potassium alkali is recommended to increase citrate and pH.

Overuse of Laxatives

By increasing Gi fluid and alkali losses one might think these drugs would cause uric acid stones. In fact, a recent review of reported cases – not many! – suggests that mainly low urine volumes from fluid loss causes calcium stones. Not uric acid, in fact, but ammonium urate stones have been documented. I presume they represent induction of ammonia production by the potassium depletion from the diarrhea. As ammonia increases urine pH can rise despite loss of alkali and the higher pH would favor the ammonium acid urate salt.

What Happens With Treatment

Changes in Urine pH

In principle, potassium alkali in the proper dose will raise urine pH and abolish uric acid formation. The reality of practice has a bit less perfection.

These are data from my own work.

The original pretreatment urine pH values are at the top of the figure, for reference, in red. Below them, in pink squares the treatment data show a large shift toward high urine pH so that a majority of values lie above the pretreatment ones. But some patients did not take their medications, and in some I miscalculated the dose needed.

Even with this natural variation in physician intent and patient willingness, the shift of pH with treatment was drastic in my own practice.

Given the powerful dominance of pH over supersaturation, I decided to not add a figure showing that supersaturation fell – it would be redundant.

Treatment Complexities


Although potassium alkali – potassium citrate or potassium bicarbonate preparations are an obvious and widely used treatment, the kind of patients involved – often older, diabetic – may not tolerate large amounts of extra potassium without increasing serum potassium. Especially, common and effective blood pressure medications such as angiotensin converting enzyme inhibitors or receptor blockers can worsen the risk. Typically most clinicians are aware of the problem and proceed based on serum potassium level and whether kidney function is normal or not. Sometimes I use a low dose of thiazide diuretic along with potassium citrate – the diuretic to foster renal potassium loss. This can enable patients to get more alkali without risk of raising serum potassium.


In the intestinal diseases, sodium depletion may be great enough one wants to use sodium alkali. I prefer inexpensive sodium bicarbonate tablets bought over the counter, being cheap and easy to use. Two provide about 13 mEq of base.


I almost always begin with 40 mEq daily and repeat the 24 hour urine measurements. Spot urine pH testing with pH paper never impresses me as very useful because results scatter and, after all, what most matters is average supersaturation over the day. These crystals can form and dissolve rather rapidly, and one hopes to achieve 24 hour average SS below 1. Overnight is clearly a high risk because of lower urine volumes so a nighttime dose of alkali before bed seems reasonable. If I need to I increase dosing in 20 mEq/day increments.

Effect on Uric Acid Stones

Uric acid in stones has a different meaning than we attach to calcium oxalate or calcium phosphate, or even cystine. This crystal can be prevented by raising urine pH within the common physiological range between 4.5 and 6. This means that simple alkali treatment should and will prevent such crystals in stones. Likewise, lowering supersaturation below 1 must eventually reduce kidney stone mass. Put another way, not guile or special knowledge but simply persistence with alkali use must inevitably stop uric acid crystallization.

Even so, data are hard to come by. This small report says that 91% of 24 uric acid stone formers treated with potassium citrate had no recurrence after a mean of 31 months.

No Formal Trials

A look on PubMed found no prospective uric acid stone prevention trials.

(For the purists, this was my search: ((“prevention and control”[Subheading] OR (“prevention”[All Fields] AND “control”[All Fields]) OR “prevention and control”[All Fields] OR “prevention”[All Fields]) AND (“uric acid”[MeSH Terms] OR (“uric”[All Fields] AND “acid”[All Fields]) OR “uric acid”[All Fields]) AND (“calculi”[MeSH Terms] OR “calculi”[All Fields] OR “stones”[All Fields])) AND Clinical Trial[ptyp])

I am not surprised. Given all we know can we assign such patients to a control group that does not receive alkali? Given the ease of use should one even try to do so?

I say not.


160 Responses to “Chapter Eight: Uric Acid Stones”

  1. steve mecke

    Do I need a prescription to get Potassium Alkali. If so, can I do enough OTC Potassium Citrate on my own to get comparable results or any benefit? Thank you for the courtesy of your reply.

    • Fredric L Coe

      Hi Steve, Many people buy food grade potassium citrate and a home scale that can weight out in grams. A single 10 mEq potassium citrate tablet contains 1.080 gm of potassium citrate and that is the dose form physicians use. But this requires you work with your physician who says how much and agrees to home weights. Potassium can be dangerous, so she/he is crucial in all this. Regards, Fred Coe

  2. John Rius

    Hello Dr Coe,
    I am a 66 year old male with a history of occasional kidney stones in the past. Last January 2019 I suffered heart AFIB and have been ok since. I take lipitor for cholesterol, losartan and carvediolol for blood pressure.
    In the last several weeks I noticed that I am passing on almost a daily basis kidney stone gravel. Had this analyzed and was told by the lab that they are 80% uric acid Dihydrate and 20% calcium oaxalate Monohydrate.
    Before the lab test I had started taking B6 – 400 mg per day thinking that these stones were mainly oaxalate, but the lab test corrected my assumption, although it probably would not hurt to continue this to prevent oaxalate issues, I imagine.
    The ultrasound shows only one 5mm calcification on the right kidney that may represent a peripheral calculus or vascular in nature in the kidney. No hydronephrosis and no masses. Otherwise both kidneys are normal.
    As I stated I pass gravel daily; for example today, I passed about a dozen little stones already and it is only 4pm here in Florida. Very concerned about this daily gravel passing situation.
    I see that in your article it mentions potassium citrate as a treatment to raise urine ph, and will start on that right away. How much should be taken daily?
    I would really appreciate any other suggestions you may have to increase my ph and other ways to resolve this issue.

    Thank you for your consideration of my email. Have a great day.

    • Fredric L Coe

      Hi John, You are reading the right article. The uric acid gravel will vanish when you take enough potassium citrate to raise urine pH to about 6. You need 24 hour urine testing before treatment, as the dose depends on the urine pH – how low it is, and the urine ammonia excretion. That is for your physician to consider. Generally 20 to 40 mEq/d of potassium citrate works, but I have used as much as 80 or more, depending. Your physician needs to supervise everything as your tolerance for potassium is also a consideration. But uric acid vanishes when pH reaches 6, and you are done. Regards, Fred Coe

  3. Kerry

    Hello, Dr. Coe. I am a little confused by what I am reading here and in other places, and wondered if you might help me understand better.

    I have, within just the last couple of years probably, developed uric stones. These have caused me a bit of trouble, including several laser liths and sepsis from obstruction. While I had some calcium-based stones years ago, these stones have come back tested as 100% uric.

    I didn’t appear to form them – or at least notice them – until I went on a low carb, somewhat keto diet a couple of years ago when my husband became diabetic. Your article seems to indicate that this type of diet doesn’t have much affect on uric stone formation, but much of what else I read says it really has an effect.

    Am I misunderstanding something on either end? My very recent 24-hr urine came back with a bit high uric (around 1200), and I had a slightly elevated serum calcium level. I have been working to reduce my animal protein intake.

    I have upcoming appointments with both my endocrinologist (for my thyroid issues, but she works with stone formers) and the urologist. I’m just trying to understand how a higher protein diet may or may not affect uric stone formation before I discuss things with my doctors, since that diet seems to have affected me in this way.

    Thanks so much for your guidance to everyone.

    • Fredric L Coe

      Hi Kerry, You are reading the right thing. At a urine pH above 6 the solubility of urate species is so high that the total urine ‘uric acid’ excretion has no significance at all. This is because the solubility of a acid form is 95 mg/liter, that of the sodium or potassium alkaline form is over 1000 mg/l. Allopurinol, low protein diet, all as basically silly as compared with alkali enough to raise the urine pH above 6 on a steady basis throughout the day and night. The only failure possible is not enough alkali, a bad choice of alkali, or poor timing, and your physicians can certainly tend to that. You also speak about an elevated serum calcium level. That is something else altogether and separate as a problem. If serum calcium is high, fasting, on repeated measurements, you certainly have something that needs treatment, like primary hyperparathyroidism. That is not a cause of uric acid stones but of calcium stones, and nothing prevents you having two problems. Low diet protein can have no effect on serum calcium. Regards, Fred Coe

      • kerry

        Thank you so much for your reply. I suspect both physicians will be looking at allopurinol because it’s been brought up before, but I didn’t have the opportunity to do any research before I had the sepsis issue. I’m glad to know this information before my appts because I’m certain the uric level/diet will be brought up. I continue to see much reference to the keto diet “keeping urologists in business”. I will read more to learn how to work with these stones.

        My fasting calcium came back at 10 this time – first was not fasting. Usually I’m in the mid 9’s fasting. So hopefully that non-fast higher one was just a one-off. 🙂

        Thank you again for your generous guidance. Much appreciated.

        • Fredric L Coe

          Hi Kerry, The keto diet, by being deficient in sugars, stimulated ketone acid production. Urine pH falls but does not stay at its minimum long term as urine ammonia production rises. But given 24 hour testing we never need to guess. The 24 hour urine pH is low enough <5.5 or so, to permit uric acid crystallization or it is not. Potassium alkali – see article you wrote on – is enough to bring the pH to 6 or more, or it is not. Urine uric acid excretion is what it is, but the pH matters most. I did not mention the matter, but of course you always want 2 liters of urine or more. Regards, Fred Coe

          • James Gallagher

            Hello Dr. Coe,

            I saw an earlier comment that you responded to and I had a few follow-up questions. Here is the thread:

            Thanks so much, Dr. Coe. I’m trying to get a sense of what you mean by “rapidly.” Could uric acid crystals form in only one missed day of citrate treatment? During my first stone episode 9 months ago, I did see small red crystals in my urine but have not seen anything since.


            Fredric Coe, MD
            July 16, 2017
            Hi Kim, Yes they can. Uric acid crystallized when urine becomes acid, and in a day red crystals mean uric acid. Take your med. Regards, Fred Coe

            I have seemingly had rapid formation, all seemingly on days where my salt intake was higher than normal. I eat very low carb (<20g/day) mostly beef and eggs. I drink only water and black coffee (once in the morning). I've been eating this way for over 18 months and the little red/orange gravel has only started in the last 3 months here and there. I can go weeks without any and then 1 will appear. Sometimes a few. If I increase my water intake they go away – though the last one I was surprised as I had consumed a good bit of water that day.

            How does salt intake effect formation of crystals?

            Does the Ph of the water I drink have any influence?

            Thank you. This site is amazing.

            • Fredric L Coe

              Hi James, Thanks for providing the thread. What I said to Kim is as best I know. The pH of drinking water matters not at all as water has no buffering capacity. Sodium has no role either. It is all urine pH and treatment is all potassium alkali, either citrate or bicarbonate. Regards, Fred Coe

  4. Joe Faraci

    Hi. Dr. I am a uric acid stone former 80/20 the 20 being calcium Oxalate. I take 30 meq pot citrate twice a day but my urinary ph rises to 6.8 only for about two to three hours after I take the potassium and then back to a low 5 ph. . Is this enough time to dissolve the crystals? I’ve been asymptomatic for 15 months but

    • Fredric L Coe

      Hi Joe, the dosage is not right given what you are saying. If your pH dips to 5 after only l3l hours ask your physicians if you might not be better off with taking 20 mEq three or even four times a day. Uric acid does dissolve, but if it is forming and dissolving that is not as good as just not forming at all. Regards, Fred Coe

  5. Charlotta Matson RN

    Dr. Coe,
    I am so impressed with this website and information disbursement need it supplies. The questions and answers section is almost as important as the articles themselves – discussion/clarification is always good. There is not enough reliable sites and sometimes information is conflicting.
    I am currently wanting to do diet coaching, and I have a friend that wants to lose weight, but I don’t want to misinform him. He is obese class I with kidney stone issues (mixed uric acid and oxalate stones but mostly uric acid) He currently takes allopurinol for an elevated uric acid blood level. He does not have a problem with gout, only kidney stones. At first he had strange side effects with this medication (such as involuntary muscle movements that creeped him out, for lack of a better expression!). Is this an effective treatment for uric acid stones? I am not sure he takes a urine alkalizing agent or not, but he mentioned eating alkaline foods. Can diet be enough to correct urine pH. He stopped exercising last spring when he passed copious amounts of stones (in the hundreds according to him), in fear of “knocking stones loose” or creating more of them. I have read as far as weight loss not to lose to fast as this could precipitate an attack. What are your thoughts about diet/exercise regarding these types of kidney stones? There is so many ” don’t eat this and don’t eat that , when you look at low-purine and low oxalate diets that there would be nothing left to eat. My friend sure likes his meats and limiting that to 6 oz/day as some places recommend, would almost devastate him. He does have hypertension, and has had cardiac problems such as pericarditis. No sign yet of diabetes yet, but did have a slightly elevated fasting bloodsugar level (under 110 mg/dl). As I understand in your comments, diet restrictions are only minimally helpful in preventing these type of stones, is this right? I am not sure if he takes any urine alkalizing medication, but as I understand, diet alone is not effective enough!? If you could recommend a reliable source for diet recommendations and your thoughts on diet, exercise and weight-loss for people with these problems would be highly appreciated. Thanks!

    • Fredric L Coe

      Hi Charlotta, I did not realize in the earlier question below that you were a nurse. Allopurinol is useless for uric acid stones, because they arise from protonation of the urate N-9 site that is the only polar region on the uric acid molecule. The pKa for this site is 5.3, so when urine pH is below 5.7 or so the concentration of uric acid begins to exceed that of urate, and uric acid per se is very insoluble – 90 mg/l or so. No amount of allopurinol will lower uric acid so low, and the drug has risks. I never find diet sufficient to raise urine pH in uric acid stone formers. When renal function is adequate to tolerate potassium loads, I use K citrate 40 – 60 mEq/day seeking a pH over 24 hours of 6. Low protein diet, low purine diet, neither makes any difference. As for the diabetes, it is a notorious cause of low urine pH and uric acid stones, as is obesity – that lowers urine pH all by itself. Given his hypertension, lower diet sodium – to 1500 mg/d is ideal, but hard to attain. I hope this is useful to you. Best, Fred

  6. Becky

    Greetings, Dr. Coe.
    I have been prescribed Potassium Citrate ER, 10 MEQ, 4 pills, 3 x day for uric acid kidney stones and am concerned about taking too much. My pharmacist states that this can be a dangerous medication in that it affects all of the muscles in the body, and that this is the reason for frequent testing. The muscles in my arms ache, even when I sleep. When I wake in the morning, my legs feel “heavy.” Although I reside in the Chicago area, my doctors are at Mayo Clinic. The pH testing kit that I was instructed to get is extremely difficult to decipher. My internist retired and I’m about to meet with a new internist. Any thoughts on how I should approach my concern?

    • Fredric L Coe

      Hi Becky, Uric acid stones are treated only by raising urine pH, but 12 pills a day seems high. I might be concerned, although I do not know the details of your particular condition. Since you are in Chicago, and if you are concerned, we can see you at University of Chicago 773 702 1475. If that is not possible, perhaps I can suggest alternatives, or you can journey back to Mayo Clinic which is certainly an excellent facility. Regards, Fred Coe

  7. Richard Weston

    Hello Dr. Coe – Great article. I recently passed a 6mm stone that was 80% uric acid and 20% calcium oxilate. Also a CAT scan revealed that I have two stones in my other kidney that are 16mm in size. I have Crohns disease and have had surgery for it so I’ve been told this is a major contributing factor to the many stones I get. Assuming that the two large stones are mixed uric acid stones like the one that passed can they be dissolved by raising the pH in my urine or will they most likely need surgery to be removed? The pH in my urine is 5.0 which is pretty low. I see a urologist about them in a month. Thank you!

    • Fredric L Coe

      Hi Richard, It is very important to raise urine pH so uric acid stops crystallizing. This can be from sodium bicarbonate, sodium citrate, or potassium citrate and your physician can help you choose the best for you. Uric acid will dissolve, calcium oxalate will not. The Hounsfield units of radiographic density of the stones on CT can help tell, and UA stones have low values in the 100’s of units. Regards, Fred Coe

    • Joe Faraci

      Hi again. I am the 80/20 uric acid calcihm Oxalate song former. I have Another question this time about magnesium glycinate. I started talking 500mg qd of this magnesium supplement along for another reason along with my K citrate. I have noticed however that my urinary ph is raised to seven which it has never been and for a much longer period of time. As I mention on 30meq k citrate extended released twice a day, the most I can get my urine ph to is 6.4-6.8 and that’s only for about two hours after taking the k citrate. While my ph is higher, there are conflicting thoughts on the effect of magnesium on stone formation. What are your thoughts. Thanks and happy Thanksgiving

      • Fredric L Coe

        Hi Joe, The magnesium itself has no effect on urine pH, but the glycinate will be metabolized as glycine taking up a proton and behaving as an alkali. Perhaps the addition of this extra alkali is causing the higher urine pH. Magnesium has no proven benefit for any stone type. Regards, Fred Coe

  8. Barry D Berger

    Greetings, Dr. Coe, from Deep South Texas. Is it ever appropriate for a urologist to advise consuming 1 tablespoon of sodium bicarbonate three times daily–yes, 1 tablespoon, which I verified with him the next day–to dissolve an 8 mm uric acid stone? He also prescribed Potassium Citrate ER 15 MEQ twice daily, which might be fine, but the Arm & Hammer stuff is kicking my butt. I’m a 61-year-old male on Ozempic 0.25 mg once weekly, Atorvastatin 40 mg Q.D., Lisinopril-HCTZ 20-12.5 mg Q.D., and Tamulosin HCL 04. mg Q.D. This is my second stone in four months, with the earlier stone being the first of my life. It was removed during a ureteroscopy (I believe) requiring no overnight hospital stay. Thanks for any guidance you can provide.

    • Fredric L Coe

      Hi Dr Berger, Whatever will raise urine pH to a 24 hour average above 6 will prevent uric acid stones and help dissolve present stones. Frankly I prefer potassium citrate, and in general need to use 60 mEq in 3 divided doses to get the effect I need. Sodium bicarbonate is cheap and will work but lots of patients hate it. Best, Fred


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