CoeTie4At the end of it all, the science, the medical visits, the surgeries, what we really want is to prevent new stones. That is the main goal. Modern surgery is a blessing for those with stones. But no surgery is far better than even the most skilled and effective surgery.

Prevention of stones is orderly and occurs only over time.

Here is how to do it.

This article is designed to go with my other one which tells how to organize your medical visits so as to achieve these steps. 

What is the Science of the Five Steps?

Stones are made of crystals.

Supersaturation drives crystal formation and growth – this is a physical law that must always apply.

Supersaturation measurements are widely available from commercial vendors.

Because people who are actively forming stones are forming crystals their supersaturations are too high – crystals are forming – with respect to those crystals.

Lower the relevant supersaturations and you must lower formation and growth of those crystals in their stones.

With respect to the most common stones, calcium oxalate and calcium phosphate, and uric acid, supersaturation in urine depends mainly on volume, calcium, oxalate, citrate, and pH. You can lower supersaturation by altering any or all of these in a given person and so far as crystals are concerned the effects are much the same. 

1. Know the Stone Crystals

Stones are made of crystals: No crystals no stones. Prevention is prevention of crystals.

Analyze Stones

The proper way to know the crystals is analysis of stones and their fragments. Stone analysis is not expensive. If imperfect, it is the best we have, so use the service liberally. Stone crystals can change, and therefore prevention can need to change direction. There is no reason to discard a stone without analysis just because we think we know the answer.

Uric acid stones are remarkably easy to treat by raising urine pH and require little more discussion.

Cystine stones arise from hereditary kidney transport disorders and require special management.

Struvite stones arise from infection and require special combined surgical medical management.

Drug stones, ammonium acid urate stones, and rare stones – eg. 2,8 dihydroxyadenine stones require special management.

The vast proportion of kidney stones are calcium oxalate and calcium phosphates and uric acid, and this article refers mainly to them.

Guess if You Have To

Red or orange stones probably contain uric acid. Likewise, stones that do not show up on simple abdominal flat plate x rays are probably uric acid. These are easy to prevent, and recurrences are unnecessary.

Allow me to elaborate on this. Pure uric acid stones are almost all due to an excessively acid urine pH, and will stop if you raise that pH. Potassium citrate tablets, 10 mEq size, 2 twice daily is almost always enough. Sometimes it takes 2 tabs 3 times a day. Crystal light lemonade has in one liter about the same amount of alkali as two of the tablets. I could say that there is little excuse for another uric acid stone.

If stones contain uric acid and other crystals, those other crystals need to be dealt with on their own. They may not respond to higher urine pH, and could be worsened.

Yellow stones are probably cystine, and due to cystinuria, a complex disease with its own special treatments. Because almost all kidney stone panels include a cystine screening test, cystinuria is almost never missed. A positive test, however, can reflect cystine trait and the stones can be something else. So it is the negative test that is fully informative.

Small black stones are probably calcium oxalate, and large very homogeneous hard stones are probably brushite. But one cannot be sure.

Big stones that fill up the interior of the kidney are usually cystinestruvite – from infection, or calcium phosphates from alkaline urine and hypercalciuria.

But guessing is not a good way to achieve prevention. Find out whenever possible what crystals you are trying to prevent. Any stone fragment can be analysed. Never pass up an chance to be sure.

2. Obtain Proper Blood and 24 Hour Urine Measurements

I prefer two 24 hour urine kidney stone risk panels as a minimum along with at least one set of fasting blood measurements.

Screen for Systemic Diseases

Here is a table of systemic causes any physician can follow using the blood and 24 hour urine testing. This is not something a patient can do anything about except see that it is accomplished.

Revised Table for Evaluation for Systemic Causes of Stones

The bowel diseases that cause enteric hyperoxaluria – small bowel resection, malabsorption, are usually obvious, as are ileostomy and bariatric surgery.

Medullary sponge kidney and nephrocalcinosis are complicating features physicians need to deal with. Medullary sponge kidneys actually form tiny micro crystals in their dilated ducts. Whether these grow to become clinically important is not clear.

Nephrocalcinosis simply means many crystals are present on x ray images. During ureteroscopy these crystal deposits can be sorted out into real stones and plugs within the terminal ducts of the kidneys. Pain without obstruction is widely described in both of these conditions which complicates management.

Measure Urine Supersaturations of the Stone Crystals

Standard 24 hour urine kidney stone risk panels give supersaturations along with the urine chemistries that control those supersaturations. These are the keys to prevention. Supersaturations control crystallization and can be measured reliably in people. If crystals are being formed the supersaturation is too high and we need to lower it.

Read Your 24 Hour Urine Reports

Your physician will take care of you but a prepared and educated patient can make that care vastly more effective and reliable.

You can understand your 24 hour urine tests and follow along with your physician during your visits and when treatment has been introduced and your urine chemistries change as a result. The details of interest are different for calcium stones and uric acid stones, so I have put them in two separate articles. Do not be put off by all the numbers. Follow the articles with your test panel in hand and you will find things are not so difficult.

Stone prevention is long term and involves changes in diet and behavior and, often, medication use. If you can read your own report you will have a first hand sense of why your treatments are good for prevention and whether your treatments have achieved what they were designed to achieve.

3. Lower By Half the Supersaturations for the Crystals in Stones

There is no one way to reduce supersaturations. Every patient will have a characteristic pattern of abnormalities and supersaturation can be lowered by changing any number of those abnormalities present. Below is my general strategy, but it may not apply to you. If your urine volume is already very high, for example, to raise it would be silly. So consider my ‘strategy’ a general set of rules, easily modified to fit the individual situation.

Raise Urine Volume as High as is Practical

Above 2.5 liters daily is ideal. The site is very rich in advice for fluid treatments. How to drink more. How to get variety. How to avoid low flow periods. Being without cost or risk, fluids are always my first choice.

Reverse Urine Abnormalities Raising Supersaturations for the Crystals in Stones

urine calcium oxalate volume and citrate vs risk of stones from Curhan plotted with identical risk axesIdentify the factors in the 24 hour urine beside volume that are raising supersaturations for the crystals in stones, and act so as to reverse them toward normal. Common ones are high urine calcium, high urine oxalate from diet, low urine citrate, and low urine pH – for uric acid stones. High pH is a risk factor for calcium phosphate stones but one cannot lower urine pH under most circumstances.

Bang For the Buck

A vulgar phrase, if you think about it. Here are the relative risks of becoming a stone former in the three cohorts of nurses (red) and physicians (males, blue) Dr. Gary Curhan followed. You might say relative to what. For each risk factor it is different: Calcium – less than 100 mg/day; Oxalate – less than 20 mg/day; Citrate – less than 300 mg/day; Volume, less than 1 liter.

The average relative risk is at the end of the crosshatched bars. The ends of the solid bars are the 95th percentiles. When the solid bars are above one risk is certainly present, so you can see the safe ranges for calcium, oxalate, citrate, and volume. Because the plots all have the same risk ranges you can compare these four risk factors. Calcium has the widest  effect range. Oxalate is next and increases risk at even 25 mg/day. Citrate causes risk only when below 400 mg/day, and volumes above 2 – 2.24 liters lower all three cohorts into a low risk range.

Although urine volume confers relative risk equivalent to high urine calcium and oxalate only when below 1.25 liters daily (see graph at left), one always wants to raise it as much as is possible because such treatment is without risk or cost. Above 2.25 liters daily is ideal. The site is very rich in advice for fluid treatments. How to drink more. How to get variety. How to avoid low flow periods.

Obtain New 24 Hour Urines to be Sure Supersaturations Have Fallen

There is no point to changing diets or medications without proper follow up to determine if what was done had the desired effects. Six weeks is a good time for the first follow up measurement. Continue measurements until the supersaturation goals have been achieved.

4. Obtain more 24 Hour Urines if New Stones Continue

Crystals follow physical laws and supersaturation is what drives them to form and grow. Continued stones with reduced supersaturations means either supersaturations need to be lower, the 24 hour samples are not being taken on representative days, or the days themselves have periods of low urine flow or other breaks in treatment.

Crystals do not sleep nor do they make mistakes. Any chances they get, they use.

Physicians are trained to ferret out the details of a patient’s history that matter here. It is my main clinical expertise. 

Patients are not trained but they are the ones sitting up close at the 50 yard line. So they know more than anyone else. They just may not know what is important for stone prevention.

5. Follow Up Every Year Thereafter Even If Free of New Stones

OH, you might say, those urine measurements cost money.

They do, hundreds of dollars for each one.

The merest surgery can cost near to or even above ten thousand dollars when you consider the total of medical, operating room, anesthesia, and pre and postoperative imaging costs, and the inevitable emergency room visits that provoke the surgery in the first place. This is not to mention lost time from work.

And, did I speak about pain, misery, infections?

It it time for blunt talk. Lab measurements are the compass and altimeter. Flying blind is silly.

A Good Way to Get All This Done

You cannot do the five steps alone, your physician is crucial. He or she cannot do them either; you are crucial. In case you missed it, here is my view on how a patient and physician can best partner for stone prevention

That’s It

This site is far from complete but it already has a lot of what one needs to carry out these five critical steps. Do them and new stones will cease altogether or at least greatly reduce in frequency. If it does not work, one or more of the steps need correcting. After nearly 45 years preventing stones, I have become bold enough to say this, and mean it.

Good Luck, Fred Coe


  1. Richard Rosenbaum

    Hi Dr Coe:
    Thanks for the excellent website and for all of your work on kidney stones. I’ve had multiple CaOx stones… 68 y.o. radiologist with ileostomy (colon Ca 40 years ago), low urine citrate and low urine pH. I take Tricitrates solution (Kcitrate/NaCitrate/citric acid) 15 cc (15mEq) twice daily (Kcit tabs don’t seem to get absorbed) and 2 liters of water daily (trying for 2.25!). Also CaCarbonate (750 mg) heartburn chew daily. Have Stage 3 CKD (Cr=1.7, BUN=24), mild DM2 (taking 500mg metformin daily), borderline anemia and hyperlipidemia (on rosuvastatin 40 mg and lovaza 1 g). HBP controlled with metoprolol (25 mg) and lisinopril (20 mg). K has been gradually rising since beginning ACE inhibitor (now 5.4). I’m considering taking CaCitrate instead of Tricitrates (to avoid K intake and horrible tasting solution) since HBP meds seem to be working well otherwise (I’ve read that ARBs may cause less K rise and could be better for CKD?). I see cardiologist and nephrologist at JHU but few folks have such specific interest and knowledge as you. Do you have opinion re: CaCitrate or other advice? Thank you.

    • Fredric L Coe, MD

      Hi Dr Rosenbaum, With ileostomy, sodium loads are usually irrelevant – large sodium losses – so I use sodium alkali with abandon. Your 24 hour urine studies can confirm if this is true. If so, you would need neither calcium or potassium as a counter ion. Sodium bicarbonate tablets work, too, and are easy to use for many. Take a look at the article I wrote on this topic. I like Arbs more than ACEs, as a rule, but suspect the rising K is partly from the diabetes. Even so, there is no need to potassium loading. The article shows our published renal pathology in ileostomy, the plugging of tubules is significant and probably contributes to reduced kidney function. So effective reduction of supersaturations is really important. Regards, Fred

  2. Becca

    Hi all. I noticed a question about the MTHFR polymorphism. As a genetic engineer (NOT a physician) with a family that has the C677T polymorphism I know this definitely leads to kidney stones especially in males. I have 100 years of family data. Those that are homozygous for this polymorphism- in my family – ALL have horrible stone issues. Luckily it can be treated effectively. My homozygous son began forming stones at age 8. Appropriate probiotic and methyl B-12 and methyl folate (B-9) supplements completely solved the problem. A good and experienced functional medicine physician will be able to help. If possible obtain the services of a doctor that suffered/s from this same problem and overcame it!!!

    • Fredric L Coe

      Hi Becca, Thank you for responding about this gene variant. On the OMIM site, I could not find kidney stones in this genetic disease complex. Likewise for the NIH Rare Disease site. Can you point me to a reference about kidney stones and this variant so I can post it for others? Thanks very much, Fred

      • Rebecca

        Hi Dr. Fred,
        My son’s kidney stones are the result of a mitochondrial disorder of the liver. He has hyperoxaluria – three types of PH have been elucidated but unfortunately we have yet to determine the exact genetic difference/defect that is at play in our family. The heterogeneity of mitochondrial disorders is astonishing- even within my family. Given his MTHFR polymorphism – a poor methylator- we bypass the metabolic gridlock by giving him methyl-B12 injections SubQ and L-methylfolate PO. In addition I apply magnesium sulfate cream tid to support sulfation metabolism that is critical for oxalate detox. I give him probiotics and keep him on a special anti-inflamatory diet to ensure that his gut is sealed so that dietary oxalates do not escape out into his bloodstream as he is already overburdened with oxalates- Many professionals studying this think that the MTHFR gene drives the mtDNA damage/dysfunction in a complex epigenetic way. Initially my son was Dx with “autism” that was actually hepatoencephalopothy. Many of these autistic kids have extremely high levels of oxalate in their urine wether or not they get stones. Scientists are just now beginning to look at these kids and see that in a quite large subset of autistic kids there is a true biological metabolic illness at work & these kids are NOT just mentally defective. So far since the installation of the above medical interventions, he has remained stone free for five years although his urinary oxalate is always high. I know my family’s situation is rare and probably doesn’t apply to your patients but I just wanted to let everyone with a MTHFR polymorphism know about what we’re doing in case it might help.

        • Fredric L Coe

          Hi Rebecca, Primary hyperoxaluria is a serious disease. Can you say how high his urine oxalate level is? I do not know about high urine oxalate in autistic children; can you please provide a reference so I can read it and put it up on the site. That would be very valuable. Fred

      • Rebecca

        It would be so wonderful to have a urologist with your experience and desire to really help others study renal disease in these children. They suffer so much! I am just now figuring out how to help my children. If you can direct me to any research you think could help- I will be eternally thankful!

        • Fredric L Coe

          Hi Rebecca, Thanks for the reference. I cannot get the full paper as it is protected by copyright and my institution does not participate in the consortium. This paper is later and does some more serious work on what high serum oxalate might do about iron binding, which may also be abnormal in autism. But it is about serum, not urine oxalate. I will try to get access to the full article you mention, if possible. Regards, Fred Coe


Leave a Reply