CASE 2: A Calcium Oxalate Stone Former


A man in his fifties formed his first stone in the early 2000’s and his last 6 months ago. There was a single passage event a year or two after the first stone at which time he was Megiven hydrochlorothiazide 25 mg daily. A right SWL procedure was performed 1.5 years ago because of a stone attack, and  potassium citrate 10 mEq twice daily was added in treatment. A right sided URS procedure was performed 8 months later but was not completed because of bleeding. A right URS 6 months ago is said to have left his right kidney stone free, but some stones were seen on the left. I did not have images to review when I saw him. He believes that all of his passage events were on the right. Stone analysis of material removed at his last procedure showed 60% COM and 40% COD.

Apart from hepatitis A at age 13 and a disc injection he had no significant medical history. But, oddly, at a routine screening colonoscopy there were signs of Crohn disease which is said to have been verified at biopsy. He was and is devoid of any symptoms or other signs of this disease.

His mother has stones but not his father or three brothers. His father has adult onset diabetes. He has an extremely high level position that requires 10 hour working days, many working weekends, and meetings that occupy perhaps half of every working day. He need not become dehydrated during these meetings which he runs. But if he ‘forgets’ he does become dehydrated, and forgetting is not rare. Prior to the stone attack 1.5 years ago he believes he was frequently dehydrated during work. He flys 20 – 30 times a year for his work and is away from home at night but the trips are mostly domestic.

Breakfast is oatmeal with yogurt and pumpkin seeds. About two days a week, lunch is for business and at a restaurant. The other days he ‘grabs a sandwich’ at McDonalds or another local takeout place. Supper, at home with his family, is typical US cuisine with a lot of meat. He avoids spinach and nuts but in the past was a heavy user. He eats a lot of sugary foods if they are handy.


Outside routine blood measurements from 2 months ago showed normal values except glucose was 141 mg/d; but he may have been not fasting. On review of this finding be mentioned that some prior HbA1c levels have been around 6 or so.

His 24 hour urine studies were performed at Litholink and are dated in months before my visit with him – to protect confidentiality. All three were performed while taking hydrochlorothiazide 25 mg daily, the most recent with potassium citrate, 10 mEq twice daily, as well. Because of the high urine oxalate, he was placed on pyridoxine prior to the most recent urine collection.

-3 6.7 0.30 0.69 2429 4.3 283 204 1070 94 5.7 900 64 51 1.4
-9 8.3 0.59 0.35 2519 3.6 242 198 1177 100 6.1 800 65 52 1.3
-13 6.2 0.17 1.5 2211 3.2 147 97 841 92 5.5 1107 71 78 1.4

All values apart from SS are mg/24hr, mEq/24hr Na, SO4 and NH4, or l/24 hr, VOL.


General Principle

I follow what I have called the fundamental premise of stone preventionThe urine supersaturations of an active stone former are too high in relation to the crystals in stones forming. Lower them.

Application to This Patient

Is my patient an active stone former?

I do not know. His surgeries were complicated and presumably aimed at a stone passage event and the reducing his renal stone burden. As is not rare, I did not have his CT images at this first visit, but even if I could it would have taken many serial images to decide if he had been active within any one period. I do not care anymore about that period of time, except in an academic way. Since his last surgery there may have been new stones in the right kidney, a question I will have to take up when I next see him. Clearly he had active enough disease in the past to amass a considerable stone burden, but he knows he was more prone to dehydration then than now and he stopped eating high oxalate foods, as well.

He is someone in whom it is important to determine stone activity, yet CT scans involve considerable radiation. I will presumably have to rely on renal ultrasounds from his urological surgeon. My decades of reading tens of thousands of simple flat plate radiographs have made me a powerful sceptic; much of the time I could not tell if stones were present or not.

Do we know the crystals in stones forming?


We know the crystals in stones that formed in the past, and they are calcium oxalate mono and dihydrate with no reported calcium phosphate.

Do we know his urine supersaturations?

We know them in his altered state of awareness – by which I mean his urine volumes are very high and yet he tells me he was not rarely dehydrated during the years before his present stone burden. I can guess, and I can extrapolate, but I cannot know what his supersaturations were when he was an active stone former. His samples were obtained during working days according to my calendar – I know the real dates.

Laboratory Analysis

Supersaturations. All three CaOx SS are high enough to support  crystallization, and would be very high if his urine volume were in the more common range of 2 liters/d instead of 3 – 4 liters as they are now. But that is meaningless in that the values are not related to active stones. CaP SS are trivial and would remain low even if urine volume were lower. Uric acid SS are low apart from the first one and not relevant to his stones.

Judging from the creatinine excretion, urines are consistently collected.

Urine Volumes are consistently high, far above the common risk level of below 2.5 liters.

Urine calcium excretion is high enough to pose risk of stones, and is crudely correlated with urine sodium as one expects. As there is no systemic cause, it is surely idiopathic hypercalciuria, and his mother may well have the same.

Urine citrate is very high, far above the risk level, and is not much higher in the most recent urine, when he took potassium citrate, than in the other two when he did not take the drug. Diabetes is associated with increased urine citrate, although some have found insulin resistance is associated with reduced urine citrate (and also) and suggested here by his borderline blood glucose and HbA1c levels. I must say I have often found that early diabetes is associated with high urine citrate excretion but have not published the observation.

Urine oxalate is remarkably high, in the range of primary hyperoxaluria or enteric hyperoxaluriaNothing in his history suggested this finding except the odd note about symptomless Crohn disease found incidentally during a routine screening colonoscopy. His physicians suspected a possible pyridoxine sensitive version of PH1, perhaps, but he showed no response to the drug – dose unknown at the time. 

Urine uric acid, sulfate and PCR values are consistent with his high intake of protein and purines from meats.

Urine pH varies in the low normal range, and with the high uric acid excretion rates causes variable UA SS. Urine pH of CaOx stone formers whose stones contain little or no CaP run a bit low – usually around 5.8.



In many ways this man could seem to be a commonplace kind of idiopathic calcium oxalate stone patient with mild sodium dependent idiopathic hypercalciuria complicated by a demanding career that imposed intermittent but significant dehydration over many years. As such, like his physicians before me, I would have recommended marked diet sodium reduction, reduction of high sugar foods, and hydration with a reasonable likelihood of successful prevention. If that was not enough to prevent new stones I would have used a low dose of a long acting thiazide like drug like chlorthalidone or indapamide

But given that his stone activity is as yet unknown, only hydration and reduced diet sodium are suitable. Bone mineral loss occurs in idiopathic hypercalciuria and lower diet sodium may well confer protection against this.

I would not use potassium citrate at this point. His urine citrate is very high, far above usual risk levelsHis stones contain no uric acid, and his urine pH, though modestly low, is high enough that risk of uric acid stones would not move me to use a second drug. If I needed to supplement with potassium because of losses from thiazide I would use potassium citrate, but generally I try to avoid supplementation by controlling diet sodium and by using amiloride 5 – 10 mg daily. (The review in this reference points out that this class of sodium channel blocker has independent benefits in blood pressure lowering for which they are under-utilized).

All of this is set to the side by the startling and unexpected high urine oxalate. His diet does not seem a likely cause by history and dietary hyperoxaluria is not usually this marked. A reasonable possibility is primary hyperoxaluria, which can present in adults. Another is enteric hyperoxaluria because of his diagnosis of Crohn disease. Essentially pursuit of the correct cause and treatment for the oxalate excess is the clinical business here.

Any number of approaches can be justified, from genomic studies to GI malabsorption studies. My thought, for better or for worse, was to see if calcium supplementation, an excellent way to lower urine oxalate in enteric hyperoxaluria, might reduce the urine oxalate. To prevent increase of risk from calcium I thought to couple it with reduced diet sodium.

Treatment and Follow up

For all of these reasons, I recommended using one TUM with lunch and supper taking care the pill is used directly with the meal. I pointed him to the oxalate lists on this site, which are as reliable as any presently available, and asked him to reduce diet oxalate as much as possible. I left the potassium citrate in place for the moment as doing no obvious harm, and with the intent to make as few changes as possible.

If the urine oxalate falls significantly that will point to bowel disease or perhaps an unsuspected diet peculiarity. If not, PH is a good bet and genetic analysis the most obvious and direct approach.

Our own work points to proximal tubule crystallization as an important mechanism for kidney damage in PH1, and that crystallization is fostered by increases in proximal tubule reabsorptionReduced diet sodium and thiazide diuretics will increase proximal tubule reabsorption. Therefore leaving him on thiazide and asking for less sodium intake – to balance the increase of urine calcium and SS CaOx from adding TUMS – is a calculated, or shall I say an intuitive choice. Followup measurements need to be fairly soon, not later, as we need to know. Even though things have gone well in terms of renal function – his is normal, PH1 is capable of producing rapid and severe kidney damage. Because the crystallizations are in the proximal tubule, fluids and other factors that reduce urine supersaturations are not likely to be protective.

I will update this case report as we get more information.

8 Responses to “CASE 2: A Calcium Oxalate Stone Former”

  1. Tracy

    Hello Dr. Coe,
    I have been reading your articles non-stop since discovering them yesterday in regards to kidney stones. If possible, I would like to give you a little hx about my son and get your input. He is a 19 y.o. division 1 long distance runner. His problems began the end of his high school senior year (May 2017). He had severe pain in bilateral thighs the final month of track and was dx with bilateral femoral stress fx in July of 2017. He rested the rest of summer, rehabbed in the fall once at college and was looking to be fully recovered by the end of year. It was thought that these stress fx’s were caused by common distance runner issues; overtraining, increased mileage, etc. Ortho dr. told him to start taking a Ca supplement of 1200 mg and 1000 i.u. vitamin D daily. His return to training seemed to be going well over the fall, but then in early Jan 2018 he sustained 2 sacral stress fx and was then out for rest of season. This was devastating news for all of us. The school ortho dr. then referred him for a bone density test in February and he has since been referred to an internal med dr. I will give you the results we have to date:

    Bone density: Z scores were lumbar spine -0.9, normal; femoral neck -1.0 early osteopenia; proximal femur 0.1 normal

    Blood work/24 hour urine 3/30/18: All blood results came back WNL, including PTH, ionized Ca, Na, testosterone
    In urine abnormal results include: Vit D 25-OHD3 was 27, Creatinine/24 h 2,257, Calcium 396. BP was also 146/84
    *At this point, dr. told him to stop calcium supplement as he may be overdosing on Ca and to start taking 2000 i.u’s of Vitamin D and a recheck would be done in 3-4 months.
    6/30/18: Lab work was redone inc. 24 hr urine (urorisk), calcium ionized, Comp metabolic panel, PTH, Mg, P and Vit D
    All blood work came back normal with exception of SGOT (AST), which was 72, Vitamin D increased to 38.9 (averaging taking 1000 i.u’s of vitamin d supplement daily, plus he is lifeguard for summer job…lot of sun)
    Result for 24 urine as follows:
    Ca urine 332
    Oxalate 45
    Uric Acid urine 939
    Citrate urine 756
    PH urine 6.1
    Total urine volume 1.57 L
    Sodium urine 247
    Sulfate urine 39
    Phosphorus urine 2222
    Magnesium urine 252
    Potassium urine 91
    Creatinine urine 2430
    Calcium oxalate 2.43
    Brushite 5.04
    Sodium Urate 6.33
    Uric acid 1.99
    As you can see, most of his urine results are abnormal and suggest kidney stones. I would so appreciate your input on his situation. We see the dr. on 7/12 and I want to make sure we proceed in best way. I am curious your thoughts on diet/medication use given his age and being endurance athlete (concerned about dehydration, loss of K) Also, how quickly once changes are made, can we expect improvement in bone strength? (concerned about stress fx’s) He has returned to running and is up to 35+ miles, is lifting several times wkly and feels good and wants to continue to progress to prepare for season. Please keep in mind he is a division 1 competitive runner. Also, safe to assume he will need an ultrasound/CT scan of kidneys to see if stones are present and how to proceed. Thank you so much in advance for your input. It is so hard to try to navigate these medical issues, especially with an otherwise healthy active young person who wants to return to his life as he knew it.

    • Fredric Coe, MD

      Hi Tracy, His results indicate idiopathic (genetic) hypercalciuria as a likely diagnosis. His urine calcium is elevated even allowing for his muscle mass. Bone mineral loss is commonplace in this condition, and things can be worsened by high sodium low calcium diets – his urine sodium is very high. Stress fractures have not been studied in this condition, but bone disease is very well established. His blood pressure seems very elevated; it is high for even an older person, and remarkably so for a young athlete. This needs to be followed up by more measurements – at home is fine. The combination of hypercalciuria and high blood pressure may point to an more complex underlying disease, so his physicians need to be thoughtful. From this distance I can of course offer only this general level of advice. regards, Fred Coe

  2. Kenny

    Hi Dr. Coe,
    Read your idea of a TUM with meals with interest. Sounds like a very practical solution.
    My oxalate output was good (30) when I was taking in about 1200 mg of calcium daily, mostly from dairy divided between breakfast and dinner. Then I had to reduce dairy for other medical reasons.
    So I switched to yogurt with breakfast, and 200 mg calcium lactate caps at the start of both lunch and dinner to begin covering all three meals and to give about 1000mg total. (I chose calcium lactate capsules to avoid unwanted antacid effects of TUMs.)
    Unfortunately my oxalate increased over 50%. Maybe calcium lactate was a poor choice. Please – Any thoughts on what went wrong or how to get back to good?

    • Fredric Coe, MD

      Hi Kenny, The problem is always timing. The dairy products have a long dwell time as they are absorbed, the Tums come in and are absorbed right away and therefore ineffective. If possible time the pills into the early 1/3 of each meal. Even then they may not match the food calcium. Regards, Fred Coe

      • Kenny

        Very helpful, thanks much!
        I could have some milk… As a rule of thumb, might say 4oz be real help with oxalate, or just a drop in the bucket?

  3. Lauren

    Lists of high and low oxalate foods contradicts each other as I am finding on the internet and from my doctor. Can you comment and send me a reputable list?

    • Fredric Coe, MD

      Hi Lauren, Here is an article on the subject with many lists. These lists have been curated by an expert (Dr Ross Holmes) and are as accurate as we can make them. Regards, Fred Coe


Leave a Reply