Full Video – 19 minutes; Brief Video – 10 minutes

Unlike Zeus, or Athene, Janus did not come to Rome from Greece but from myths about a person living early in Roman history and later deified. Janus – deity – presides over beginnings and endings, gateways and doors, invariably dual in nature.

What is dual here?

Calcium stone formers are dual. A minority arise from systemic diseases we must screen for. Each systemic disease has its own universe of causes and treatment decisions. A majority are “idiopathic”, systemic causes have been excluded.

Idiopathic calcium stone formers are dual. They have no systemic cause of calcium stones. Most form calcium oxalate stones. A minority, more women than men, form calcium phosphate (CaP) stones.

Idiopathic calcium phosphate stone formers are dual. Most have hydroxyapatite (HA, like bone mineral) as their stone calcium phosphate. Some have brushite (Br, calcium monohydrogen phosphate) in their stones. These latter have more kidney damage than HA CaP stone formers, and are a special high risk group of patients.

Both kinds of CaP stone formers need special attention. That is why I have written this article for them.

Basic Facts about Phosphate Stone Formers

Phosphate Stones Damage Kidneys

Phosphate stones, HA or Br, can grow faster and larger than calcium oxalate ones. Calcium phosphate crystals invade kidney tissue – so called tubule plugs. Tissue damage is common, as is Nephrocalcinosis from plugging – often misdiagnosed as medullary sponge kidney. Kidney tissue damage is worse with Br than HA stones. Potassium citrate, a common stone prevention, may not be appropriate as a treatment because it raises urine pH.

Alkaline Urine Causes Phosphate Stones

Stone phosphate replaces oxalate when urine is too alkaline. Kidney and GI tract physiology raise urine pH, especially in women. Diet is not the cause of higher urine pH. Diet will not reliably lower the pH, and we have no specific drugs to do it, either. So although treatment uses the same tactics as for the more common calcium oxalate patient, it must follow a different strategy.

How Stone Analysis Distinguishes CaP from CaOx Stone Formers

Only CaOx and HA Present

If the average stone mineral composition of all available stones for a given patient is above 50% calcium oxalate, the patient is considered a calcium oxalate (CaOx) stone former. If the average calcium phosphate content is above 50% the patient is considered a calcium phosphate stone former.

The average must be computed using 0 – for example, given CaOx/CaP percentages of 100/0, 0/100, 40/60, the correct classification is 140/3 vs 160/3 or 46% CaOx vs 53%, and so a CaP stone former.

Uric Acid, Struvite, Cystine Also Present

If uric acid, struvite, or cystine are present we name the patient for that constituent. A patient who forms mixed stones – for example, 60% calcium phosphate/20% struvite 20% CaOx is called a struvite stone former. The reason is that these stone types have special causes and treatments. 

Any Brushite Present

Brushite is very uncommon in human kidney stones, and associates with large tubule plugs and more severe tissue damage. So when any stone contains brushite we classify the patient as a brushite stone former even though brushite is a minority of stone mineral.

Sex and Age

Single Clinic Experience

Percentages of Cases

CaptureThe table shows ‘CaP’ as cases where HA or brushite was the stone phosphate crystal (in early years we did not distinguish). CaP(b) are CaP stone formers with only HA, no brushite in any stone.

CaP predominate among females (a and b superscripts denote outsize high frequencies). Brushite does not show this difference a statistical level of significance. CaOx stone formers predominate among the total of all cases. Brushite patients are least common.

Sex vs. Percent CaP in Stones

The same study furnished this nice graph showing the sexes as the percent of stone CaP increases. The bulk of patients have very little CaP in stones (tall bars at the left of the graph). These are the common CaOx stone formers, mainly men (% female, dots, right axis about 25%). But when CaP percent is 20 – 50% in stones, women and men are nearly equal.Capture 2

This graph blurs the sex distinction because we used stone CaP% from both brushite and hydroxyapatite. Today, I would have left the brushite to one side, which would have made the female preponderance among those with high stone CaP% more marked – because the sex ratio for brushite stone formers is closer to 1.

National Laboratory Findings

The Mayo Clinic kidney stone analysis laboratory analyzed 48,446 stones in 2010, and of these 43,545 were the first submitted to the lab for that person. From these stones, they report the distribution of stone type by sex and age. I have made a graph from Table 2 of their publication.

Population Sex Ratio

stone rates and male to female stone and population ratios from Lieske

The general population contains more males than females at younger ages (blue dots). By age 30-39 the two sexes are present in equal numbers. Thereafter, as men predecease women, their blue dots slump downward.

For all ages combined, the ratio of men to women is just under 1 (last blue dot at right).

Stone Former Sex Ratio

The blue bars show male to female ratios among stone formers. Remember this is counted from the sex of the person whose stone was analyzed. A survey based on symptomatic rates of stone passage, by contrast, might give different results altogether.

In childhood, men have slightly more stones than women (blue bar is above 1.0). In the teen years and up to age 39, women predominate over men (blue bars are below 1.0). After age 40 men predominate, until at age 90 and more, in this and perhaps most things, the sexes come into a near perfect alignment. Averaged over all of life, men have more stones, which appears to be because of their midlife excesses (Height of the ‘ALL AGES’ bar above 1.0).

The fraction of all stones formed (red dots; scale along the right axis) for both sexes combined is highest from age 20-69, with only a small fraction in childhood or old age.

Types of Stones

sex and age vs stone type from lieske

The men are on top, women on the bottom of the picture to the left.

Stones were classified using the system I have used on this site. Uric acid in any amount meant the stones were classified as uric acid stones, and likewise for any struvite or cystine.

CaOx stones preponderate among both sexes over all ages, except in women between ages 20 – 39 stones were about half CaOx and HA. With age, HA stone frequency fell in both sexes, so that most men, and most older women (over 40) have CaOx stones.

Brushite stones, in both sexes, are very uncommon. You can see them as triangles along the bottom of both graphs.

Over age 50, uric acid stones become a significant concern in both sexes.

Struvite stones, which always arise from infection with bacteria that possess urease, are more common in women than men, a fact known for ages.

The Mystery of Brushite

Brushite stones are rare but should be rarer still. I have written a whole article on brushite because it is so important and yet so evanescent. It forms first of all crystals in human urine. If pH is not too high, oxalate steals away its calcium atoms so it vanishes. If pH is high, HA does the same, and brushite vanishes.

Why, then, are there any brushite stone formers?

I do not know nor does anyone I know of. It is an open question that seems obscure but whose answer might well lead to some new understanding of how stones form.

The Importance of Brushite

Being the first crystal to form, brushite supersaturation is crucial for stone prevention, a fact not intuitive but worthy of special emphasis. Rare in stones, vanishing in most urine, yet brushite supersaturation is foremost in importance for clinicians and patients. The goal is a supersaturation below 1, so brushite cannot form. For those who want to know more about why, please look at the parent article.

Time and Shock Wave Lithotripsy

We (left hand figure below) and others have noted an increasing percent of CaP in stones over the past 30 years. In women (black dots) CaP percent is always higher than in men, but it has risen in both. For those of a quantitative bent, the time trend of stone CaP tested by ANOVA with post hoc contrasts was significant for both sexes, and women were higher than men throughout.

In the publication, we found a relationship between CaP cappercent vs decades from parks phosphate paperpercentage and numbers of shock wave lithotripsy procedures. Use of potassium citrate, however, did not seem to increase stone CaP.

The number of shock wave procedures per patient adjusted for the number of stones and the years of stone disease rose with the percent of CaP in stones (Panel A of the figure below to the right) and the percent of CaP likewise adjusted for number of stones and duration of stones and sex rose progressively with the number of shock wave procedures (Panel B of figure to the lower right).

Not shown here, but of interest, the number of shock wave treatments was higher among BRSF than HASF suggesting a link between shock wave treatment and brushite stones.

One might infer from this set of graphs that the advent of shock wave lithotripsy caused the increase in phosphate stones, and there is nothing to contradict the idea. In fact, the very physiology of phosphate stone formation and the effects of shock waves on kidney swl and stone capfunction strongly support that idea as I shall show you.

Mechanisms of Phosphate Stone Formation

High Urine pH

As expected, percent CaP in stones (upper left panel of the figure below) rises with CaP SS. I have shown elsewhere on this site that stone crystals parallel urine supersaturations.

Because CaP SS depends powerfully on urine pH one expects and finds (upper middle panel) that urine pH tracks very closely with stone CaP percent. Urine calcium, volume, phosphate, and citrate excretions (remaining panels) had no important relationship to stone CaP percent. 

But take a look at the urine calcium excretions (Upper right panel). They are very high on average. This is because a high fraction of all calcium stone formers have genetic (idiopathic) hypercalciuria. Risk for stone forming begins at a urine calcium of 200 mg/d in both sexes.

determinants of phosphate stones sixplot

So you can think of CaP stones as a two hit model.

Genetic hypercalciuria promotes calcium stones, and urine pH controls the fraction of phosphate in the stones. High CaP SS and CaP stones require a urine pH significantly above 6 as shown in the upper middle panel.

Kidney Tissue

Plaque and Plugs

CaOx stones can be produced as overgrowths in interstitial HA deposits, called plaque.

Idiopathic CaP stone formers, and patients with stones from bowel disease, ileostomy, renal tubular acidosis, and primary hyperparathyroidism, form stones on plaque but also on plugs of HA that fill and damage the last millimeter or so of the nephron, the inner medullary collecting ducts and ducts of Bellini.

Although we are not certain, I think it is fair to say that the plugging of CaP stone formers is because more CaP crystals form in urine and can produce plugging. In a recent article I trace out how calcium phosphate actually forms, how it is a rapid process compared to calcium oxalate, and therefore more able to make plugs during the short times it takes for urine to pass out of tubules into the renal pelvis.

Distinctions Among the Three Idiopathic Calcium Stone Formers

We have table from ha br caox comparison paperpublished selected laboratory and tissue findings of CaOx, brushite and HA stone formers, in an attempt to clarify differences in how stones form, and amounts of tissue injury.

Numbers are small because each patient had been studied with intra-operative imaging of the renal papillae and papillary biopsy: 11 CaP (HASF), 25 BR (BRSF), and 30 CaOx (ICSF) stone formers.

As expected, urine pH was higher in the BRSF and HASF than in the ICSF, as was supersaturation (SS) for CaP. Incidentally, urine calcium (Ca) was also higher in both CaP groups than in the ICSF.

Mainly CaOx and BR stone formers formed plaque, and mainly CaOx SF form stones on it. About 8% and 6% of papillary surfaces were covered with plaque in ICSF and BRSF but only 0.8% among the HASF. CaOx stone formers had an average of 10 stones/patient attached to plaque, vs. only 3 plaque stones in 25 BRSF and 6 in 11 HASF stone patients: 10/ CaOx patient  vs 0.12/brushite patient and 0.54/HA patient. These are 80 and 18 fold differences, respectively!

Plugging (‘deposits’ in the table) was absent in ICSF, but common in BRSF and HASF. Plug size averaged 1.6 mm2 in BSRF but only 0.4 mm2 in HASF – a 4 fold difference. The number of plugs was 3 times higher in HA vs. Br patients: 12 vs. 3/mm3 of tissue volume. BRSF formed fewer but much bigger tubule plugs.

Calyx dilation (a abnormal finding) estimated during surgery was higher in HASF than in the other two groups, and papillary injury (papillae are the parts of kidneys inside calyces) higher in both phosphate groups than in ICSF.

In the kidney cortex, far from where stones form, many CaP stone formers had scarring (TIF, tubular interstitial fibrosis) vs. very few CaOx patients. Brushite patients had most cortical damage.

So phosphate stone formers have injury involving the papillae and cortex, whereas CaOx stone formers have almost none.

Why is Urine pH High?

Being Female

I wrote a whole article on how women raise their urine pHThey do it by absorbing from their food a higher fraction of its alkali content. No sense copying all that here, it is better to read the article. High GI alkali absorption is not easy to treat. Those alkali are nutrient – anions that cells metabolize to get energy. 

Being Young

We used a massive database of kidney stone formers to ask what happened to urine pH in men and women with age. The answer is it falls, in both sexes (women are circles, men triangles).

Why is a long story. We could exclude gain in BMI, loss of kidney function, and GI alkali as reasons, but could not find the reason itself. In fact, GI anion absorption rose with age, as if to offset the falling pH.

Here the important fact is on the graph – higher pH in women and in youth are an obvious cause of more CaP stones.

Shock Wave Lithotripsy (SWL)

No practical experiments permit us to measure effects of SWL on urine pH in humans.

For these reasons we turned to an animal model: The farm pig whose kidney is much like that of a human, and likewise is similar in size.

In these animals we could shock one kidney, and then compare the treated to control side at time intervals after the treatment, the untreated side being a perfect control as both kidneys are bathed by the same blood.

SWL Raised Urine pH.

Urine pH from the treated kidneys was 0.18 pH units higher than the control, meaning SWL had increased urine pH (first line of table under ‘Basal’).

SWL Damaged Kidney Tubule Function

There was a lot more.

Urine flow, and excretion of bicarbonate, potassium, chloride, sulfate, calcium, magnesium, sodium and oxalate all were higher from the treated side (bolded). This means that shock wave treatment affects tubule handling of multiple molecules, presumably because of injury.

table 2 from swl paperWe could find these abnormalities up to 90 days after shock wave. The control kidney reduced its losses in compensation so blood remained entirely normal.

Bicarbonate Losing Raised the pH

The higher urine pH could have been due to damage of final urine acidification in the collecting ducts or to high delivery of bicarbonate from higher up in the nephron so that acid secreted lower down was neutralized by a flood of bicarbonate.

To tell these apart we gave the pigs an acid load that lowered their blood bicarbonate and therefore filtration and downstream delivery (‘Acid load’ columns). Acid load brought urine pH and almost all other measurements to equality between the shocked and control kidneys (loss of bolding).

The tissues from the pigs showed widespread injury to the thick ascending limbs, and you can read the paper for details.

SWL Can Raise Urine pH by Damaging Kidney Tubules

The meaning of the work is clear.

After shock wave treatments the treated kidney may excrete excess calcium and produce a urine of higher pH than it would otherwise do. The effects are precisely those needed to produce calcium phosphate crystals. From the bladder urine, which mixes urine from both kidneys, one could never know this was happening.

It is possible that the advent of shockwave lithotripsy has contributed to the rise in CaP stones, and I hope that further science sorts out whether this hypothesis is false or true.

High Kidney Ammonia Production

Ammonia Production Regulates Urine pH

Kidneys excrete acid by making ammonia that can carry acid (protons) into urine without lowering urine pH. They also excrete acid by titrating urine phosphate, which does lower urine pH. If ammonia production goes down, from kidney disease, for example, urine pH has to fall so acid can be lost on phosphate.

Ammonia production relates itself to body acid load – from food and metabolism – so that the average urine pH is just around 6. But what would happen if regulation were abnormal so more ammonia than normal was made for a given bodily acid load?

Urine pH would rise.

CaP Stone Formers Make More Ammonia

The graph shows urine ammonia excretion from normals, and CaOx and CaP stone formers studied eating the exact same diet in a research center.

Fasting, all three groups are the same (left panels). Food increased urine ammonia in male CaP patients (#). Fed, the female CaP stone formers produce more ammonia than female normals (*, top right panel). So do the female CaOx stone formers. Ammonia production is governed by body acid load, which we measure as GI anion and urine sulfate – a residue of metabolic acid production. When we adjust ammonia for acid load (lower right panel) CaP stone male and female stone formers remain high compared to same sex normals.

We suspect the high urine pH that causes CaP stones arises in part from high ammonia production, perhaps an inherited trait.

Low Urine Citrate

Many articles on this site explore the powerful effects of citrate to bind calcium and inhibit calcium crystal growthIn these closely 

studied men and women we could document a uniquely low urine citrate of CaP stone formers vs. normal people.

Low Citrate in CaP Stone Formers

Food increased urine citrate is normal women and all three male groups (#). With food, CaP stone formers of both sexes have urine citrate excretions below their same sex normal counterparts (*, upper right panel) as did female CaOx stone formers.

As is well known, citrate is lower in normal men than women (compare black bars; we did not choose to compare the sexes statistically).

Adjusted for GI alkali and urine sulfate, (lower right panel) low citrate is concentrated among male CaP and female CaOx stone formers. Normal men remain below normal women.

Male CaOx stone formers have abnormally high urine citrate with and without adjustment for systemic acid balance.

Abnormal Kidney Cell Citrate Handling

Alkali loads, most famously potassium citrate, raise urine citrate and is an established stone preventionCitrate also raises urine pH, because the alkali appears in urine as bicarbonate. That is why potassium citrate is not an ideal treatment against CaP stones, and why we have for decades needed a controlled trial to see if it works or makes things worse.

But here we have a high urine pH coupled with low urine citrate, in male CaP and female CaOx and CaP stone formers. That points to something wrong with kidney cell regulation.

We measured serum citrate and glomerular filtration so we could calculate the fraction of filtered citrate excreted (FE Citrate), shown in the upper right panel of the graph at left.

FE citrate is low in female CaOx and CaP stone formers and in males with CaP stones. This means that CaP stone formers are reabsorbing abnormal amounts of citrate back from the filtrate. It is used by kidney cells to produce metabolic energy.

Adjusting for GI alkali absorption (lower right panel) removes the female abnormalities but makes the male one even more prominent.

That male CaOx stone formers have abnormally high urine citrate excretion with normal FE citrate is because their serum citrate concentration is higher, a fact for which we had no explanation.

CaP Stone Formers Have Proximal Tubule Abnormalities

Citrate reabsorption and ammonia production are linked in the proximal tubules of the kidneys as part of overall kidney regulation of bodily acid base balance. In general alkali loads raise urine pH and urine citrate, and reduce ammonia production, whereas acid loads do the opposite.

Here we have high pH and high ammonia production coupled with low urine citrate, more marked in male CaP patients but detectable among the women as well.

It is as though the cells perceive a need to produce more acid excretion (ammonia) and conserve potential alkali (citrate is metabolized to bicarbonate), but there is no need. So urine pH rises and converts calcium stones to their phosphate forms. The cause(s) of these proximal tubule abnormalities are not known.

Incomplete Distal Renal Tubular Acidosis (dRTA)

A Questionable Disorder

Some have proposed that CaP stone formers have high urine pH and low citrate as part of “Incomplete renal tubular acidosis”. In proof, when given extra acid they may not reduce urine pH as low as normal people. In my primary article on dRTA, I present contemporary evidence that acid loading creates a continuous spectrum of urine pH responses, even among normal controls, so it is not a good basis for diagnosis. It seems better to say that CaP stone formers have abnormal proximal tubule functions, and make those the focus of new science.

Heterozygotes of Familial dRTA

With one exception, hereditary dRTA arises from gene disorders of the main proton transporters or of carbonic anhydrase itself, and these disorders are in general recessive. They are recessive because you need two defective genes to knock out a transporter whereas one good gene copy will maintain function.

Of course dRTA causes massive CaP stones and kidney disease. But heterozygotes – meaning one good and one defective gene – from families with dRTA if studied in detail, may not lower urine pH normally. These might be diagnosed as ‘incomplete dRTA, because in fact that is what they are.

CaP Stone Formers are Not Like Incomplete dRTA

Unlike our CaP stone formers, urine ammonia is low in dRTA and heterozygotes from families of dRTA, when compared to their acid load – urine sulfate. Urine ammonia is never high. I suspect that some CaP stone formers have high urine pH because they are indeed heterozygotes of dRTA. Low ammonia may be a way to separate them from the high ammonia of routine CaP stone formers.

Risk of Conversion From CaOx to CaP Stones

Some patients gradually increase their stone CaP percent, often enough to alter their classification to CaP stone former. The opposite, conversion from CaP to CaOx stones must be very uncommon, as we have no cases to report. We wanted to know how to detect risk of conversion.

Who We Studied

From 4767 patients in our program, we collected all CaOx stone formers who had two or more stone analyses and clinical follow up data (445 patients). From these we selected all who had a last stone CaP% at least 20% higher than that of the first stone (62 patients). Men and women were combined because we had so few cases.

Of these 62 cases, 26 had had three initial (pre-treatment) 24 hour urine studies before they passed the stone whose CaP percent was at least 20% higher than their first stone. We labeled these transformers with prior laboratory work – labs before they transformed – as ‘TP’.

the 26 converting patients with pre conversion labs TC group

For controls we chose 181 patients whose first stones were >90% CaOx and who increased their stone CaP percent <20% between the first and last stone.

This figure shows the 26 TP cases and the 181 controls.

CaP% Was High at the beginning

Even though their initial stone CaOx percent was >50%, the 26 TP cases (black circles, upper left panel) had an average stone CaP of 10% before treatment, whereas it was much lower in the controls – who never added significant CaP.

During follow-up (upper left and middle panels) the 26 TP (black circles) increased their stone CaP markedly (average 10% to 79%, top left). The controls (gray triangles) hardly changed (-0.6% for controls, 69% change, for TP, upper middle panel).

Higher Urine pH Increased CaP SS

Urine pH and CaP SS before treatment and before conversion (upper right panel and lower left panels) and during treatment (lower middle and lower right panels) were higher in TP (black circles) than controls. CaP SS rose because we used potassium citrate as part of our treatment program.

SWL May Have Played a Role

ESWL associated with conversion: 112 of the 136 total cases with no ESWL procedures were controls, whereas only 21/41 cases with >2 ESWL were controls (X2=17, p<0.001). Furthermore, a predominance of ESWL procedures preceded the final stone (not shown here but shown in the paper), meaning ESWL could have been a causal factor.

Who is at Risk?

When stone CaP is above 10%, average 24 hour pH is as high as 6.3, or CaP supersaturation is above 2 before treatment risk of increasing stone CaP may be high. More than 2 ESWL procedures likewise. Given these risk factors in a CaOx SF perhaps one is prudent to treat as if CaP stones were already forming, so as to possibly prevent further stone CaP accumulation.

Prevention of Calcium Phosphate Stones

The objective is to lower CaP SS – reported with respect to brushite – below 1.

The main modifiable factors are urine volume, and calcium and citrate excretion. Because we cannot lower urine pH, the most crucial factor, we have to use what is left to achieve our goal. Likewise, because citrate regulation is abnormal in CaP stone formers, use of potassium citrate may not raise urine citrate so much as it raises urine pH, and therefore this otherwise valuable treatment can be ineffective.


Relative calcium stone risk falls to 1 (no excess risk) at about 2.3 l/d of urine volume. Given the limitations of our treatments, I usually strive for 2.5 l/d spread out over the waking hours. This is an achievable goal if patients understand why it is important for their stone prevention.

Reduced Calcium Excretion

Genetic hypercalciuria is very common among calcium stone formers. If we understand that relative risk of stones rises above 1 at a urine calcium of 200 mg/d, both sexes, our goal is to reduce urine calcium to or below that point.

Reduced Diet Sodium

Multiple articles on this site detail the power of diet sodium to control urine calcium and bone calcium balance. The US diet recommendations for sodium are 100 mEq (2300 mg)/day as a tolerable upper limit, and 65 mEq (1500 mg)/day as ideal. These values concern blood pressure and bone rather than kidney stones. But if we achieve an ideal diet sodium it will lower urine calcium as well as defend blood pressure and bone mineral. So I have no reservations about promoting the ideal diet sodium, but also am prepared for compromise in this fast food dominated world.

Reduced Diet Sugar

As for diet sodium, I have written extensively about sugar as a factor that raises urine calcium, abruptly after the sugar load and with proven increase in supersaturations. Once again, US guidelines call for reducing sugar intake, and there is no benefit to anyone from eating refined sugar in any form. So I am shameless in my zeal to encourage patients to eat as little of it as possible.


Drugs of this class lower urine calcium about 80 to 100 mg/d below the level predicted by sodium intake. They act in part to increase proximal tubule calcium reabsorption. They are trial proven agents to reduce calcium stone recurrence. We have shown thiazide drugs lower urine pH, a possible benefit.

I have often argued to use diet as much as possible before adding thiazide to avoid drug side effects. But phosphate stones are not easy to prevent, so far as I have observed, and they damage kidney tissue. Moreover, we have no trials – none. These patients may have been in trials but are doomed to perpetual minority status unless specifically a focus.

So I am not shy about adding thiazide after perhaps only one to two efforts at diet control, should CaP supersaturation remain above 1.

Why NIH has yet to fund a calcium phosphate stone prevention trial escapes me. I cannot imagine how this has not been a priority.

Potassium Citrate  

This drug will lower urine calcium below the level predicted by diet sodium intake. It may raise urine citrate excretion. But It may also raise urine pH.

Being as it is therefore able to raise or lower CaP supersaturation, I do not so much avoid using it as view it with a cold eye.

If thiazide is not attractive to a given patient I will try citrate and watch the effect on CaP supersaturation. CaP supersaturation is the final resultant of whatever changes it induces in urine calcium, pH, and citrate. If it indeed lowers CaP supersaturation, I am prone to use it but with appropriate 24 hour urine followup and an inextinguishable skepticism.

Reduced Diet Oxalate

I am aware that calcium oxalate in stones matters, and that even high phosphate stones often contain that crystal. If urine oxalate is high enough to confer risk – above 25 mg/d in both sexes – I make appropriate diet recommendations.

But patients cannot do everything all at once, so I generally put most emphasis on the calcium phosphate side. The exception is when urine oxalate is quite high – above 40 mg/d, for me – whereupon I do what I can with diet.

Monitoring Treatment

The objective is to lower CaP supersaturation below 1 in the 24 hour urine, and that is what I aim to achieve.

If fluids are enough, so be it. If not I add more treatments more or less as in the paragraphs above. Lacking trials, this is the best we can do. I watch supersaturation for calcium oxalate as a secondary endpoint, and if it is high enough to promote risk – above 3 – I attempt to lower it by reducing diet oxalate.

Monitoring is crucial. What we try to do may not be done because patients cannot or will not do it, so we have to know when to try another approach.

Put another way, for stone prevention, especially calcium phosphate stones, deliberation is reality.

I wish to thank Dr John Asplin for his careful reading of this article and suggestions for improvement. 



153 Responses to “CALCIUM PHOSPHATE STONES: Causes and Prevention”

  1. Majd Hawily

    My blood & urine tests show that i have high phosphorus levels of 6.4 in addition to low PTH levels of 6.6 showing that i have calcium phosphate stones. My dr told me that i need further checkups. However, upon reading further on the topic, i noticed that i can do dietary changes already. i realized that based on my test results, i need to eat more calcium concentrated products and limit animal proteins. I would love to know your suggestions, whether nutrition-based or others.

    • Fredric L Coe, MD

      Hi Majd, I cannot clearly understand your post. Serum PTH seems too low to measure, urine phosphate of 6.4 is uninterpretable as there are no units. If you can clarify matters, I would try to help. I have allowed your post as a courtesy despite what seems a linked in form I would usually block. Regards, Fred Coe

  2. Dee Henderson

    Hi, Dr. Coe… thank you for putting these wonderfully informative articles on kidney stones online. My kidneys were unremarkable until this year. I had 3 stones (5mm, 4mm, 2mm) removed last week… my first kidney surgery ever. I am a 70 y.o. Female, non-drinker, non-smoker, and my stones were 10% calcium oxalate mono hydrate and 90% calcium phosphate, hydroxy & carbonate apatite.

    My fluid intake is 2 liters a day minimum (water), sodium always less than 2000mg/day. Since I eat a low carb diet, my Protein is slightly more than your recommendation, but not excessive. However, I have minimal calcium intake due to severe lactose intolerance and calcium supplements cause GI problems.

    No doubt I need to add more calcium to my eating plan. I am adding rice milk and tums for calcium until I meet with a nephrologist in four weeks.

    However, in the meantime, i wonder if my two Prolia injections for osteoporosis a year ago may have contributed to the formation of these fast-forming stones??

    I stopped the Prolia after two treatments because I developed intense itching after injection two. The kidney stones were identified a year after the first Prolia injection. Symptoms started out of the blue with intense pain, nausea, vomiting. When I awoke, I also had other symptoms that seemed “sepsis like”: body temp of 95.2, extreme lethargy, feeling as ill as I ever felt in my life. Basically I went to sleep feeling well, and I went to the ER just after midnight.

    Stones were confirmed that morning in ER by a CT scan. Again, the kidney stone CT scan was a year after the first Prolia injection (which a bone scan showed did help my bone mass significantly).

    Your comments about Prolia and/or other osteoporosis meds in relation to calcium phosphate kidney stones would be much appreciated.

    Again, thank you for publishing this valuable kidney stone info. It’s a very complex topic, and we patients as well as our Primary Care physicians need to have a much better understanding of how various stones form… and what can be done to prevent them.

  3. Maria Carmen Johnson

    Hello Dr. Coe,
    I had my first stone two years ago with surgery and it consisted of 6.5 mm stone Calcium hydrogen phosphate (brushite 10%) CoD (Weddellite 20%), CoM (Whewellite 55%) and CaP (Apatite 15%) next stone 10mm was CoD(Weddellite 25%), CoM (Whewellite 45%) and CaP (Apatite 30%) and my last 9.8cm calcium oxalate dehydrate 40% and Calcium phosphate (hydroxy- and-carbonate-apatite 60%)
    24 hour urine collection results: Urine Volume 1.3, SS CaOx 10.23, Urine Calcium 394 Urine Oxalate Urine 22, Citrate 663, SS CaP 2.38, PH 5.84, Uric Acid 0.86 Urine Uric Acid 0.448

    All three where stent surgeries and ER visits, and I do not want anymore. If you can help, I would really appreciate it. before the 24 hour urine collection I was taking fish oil daily and before the third stone I added Calcium citrate to my diet. Of course I am drinking 50-90 oz of water too. Thank you in advance, Maria Johnson

    • Fredric L Coe, MD

      Hi Maria, you have a very high urine calcium and a very low urine volume and urine oxalate, so you are making mixed calcium oxalate calcium phosphate stones. Surely your physicians want you to nearly triple your urine volume – 2.5 liter/d would be a basic goal, and will want to help lower your urine calcium level. Given so many stones, and so much phosphate in them, I would think a few years of a thiazide would be desirable – that is their concern and responsibility. Regards, Fred Coe

  4. Helga F.

    Do non obstucting(lower left pole) kidney stones cause pain? And why is there continued sediment in urine despite a bladder washout in.a patient with kidney stones? Should these stones be removed?

    • Fredric L Coe, MD

      Hi Helga, small stones not rarely associate with pain and research has not disclosed why. But passing crystal sediment will cause cause pain and bleeding. You need to collect this sediment and have it analyzed so you know what the crystals are – I bet they are calcium phosphate. If so, your urine is supersaturated with respect to that crystal and steps to lower the SS will stop the crystals and perhaps your pain. Regards, Fred Coe

  5. MaryAnn Roberts

    Hi Dr. Coe; I just want to thank you for all of your hard work and generous sharing of same with us kidney stone patients. My first stone, that I’m aware of, was in Feb 2012. Since that time it has been multiple stones, chronically, at great expense and loss of work, eventually disability, worst of all my time spent enjoying my grandchildren. Recently, your PTH article seemed to “jump out at me”, so I asked the PA at my urologist to please consider a blood test. I’m happy (which may sound strange) to find everything falls right into the guidelines. Along with stones, I also have high blood pressure and a very bad case is osteoporosis – to the odd extent of crumbling teeth of recent. I’ve been referred to a local endocrinologist, Priyanka C. Iyer, MD with my first consult on June 9th. My NMRIS15 test begins on June 22nd. I am So Very Excited! My osteoporosis has gone from my first dexa scan in 2012 to my recent in Feb 2021 to dropped -8.8 left fewer , 7.5 right, and 5.3 for spine and there is now IV medicine to actually re-build bone strength, sounds like a God-send to me, and with many remarks on my tests stating “supersaturation” the thought of possibly reducing the frequency of kidney stones is a miracle to me! As you can clearly tell I know little if anything regarding the medical science of this, your specialty, but it is your name I’ve enjoyed following and just cannot Thank You enough for your dedication and hard work spent helping us, those plagued with these inconvenient and expensive annoyances. Best of all, I look forward to more time spent enjoying my 2 year old granddaughter, Madilynn, something my 16 yr old granddaughter I wasn’t so fortunate to enjoy (we scarcely know one another!). My numbers aren’t too bad, PTH 78.3, Calcium 10.0 phosphorus 1.03 creatinine 1014 and magnesium 101. I have Every symptom but heart problems with my son having noticed my mental loss first and quite concerned. My GFR no-black (I’m half Japanese half Caucasian) has been up and down drastically for decades but fortunately changes each month. BUN is 61 Chloride 110. I hope I’m not boring you unnecessarily with these numbers, I clearly don’t know what they mean. But You have given me hope, that one day fairly soon I just may be clear of all this and can enjoy my senior years. Thank You Dr. Coe, sincerely and with all my heart. If you suggest a different endo you have more faith in, believe me your input is more than welcome. And if these numbers have caused you to suspect otherwise, your input is and will be greatly appreciated. (My referred to endo is due to having financial assistance. Healthcare is not cheap in the USA but I am very grateful for it and have been following your articles faithfully, despite my struggle to comprehend. I just want to thank you for the hope you’ve given me and the appreciation and gratitude to those like you who have dedicated your lives for our improved lives. My sincere and deeply felt thanks! MaryAnn Roberts My Best Wishes to you and yours Always!

    • Fredric L Coe, MD

      Hi MaryAnn, Given your bone disease and stones and estimate that stones began in midlife I would consider primary hyperparathyroidism – your single blood calcium was 10.0 which is at the border of high, your PTH is high but your kidney function is reduced which can raise PTH. I would suggest repeated fasting morning serum calcium measurements to be sure if the values are really in the 9- 10 range or generally 10 or higher. If the latter your may benefit from removal of an enlarged parathyroid gland. The other issue is your urine calcium that you did not mention – was it high? Regards, Fred Coe

  6. Soha Zouwail

    Dear Dr Coe,
    I wonder what is your plan of management for patients with hypocitraturia and Ca phosphate stones secondary to treatment with carbonic anhydrase inhibitors such as topiramate and Zonisamide. Do you tend to treat them with potassium citrate? Dose? urine pH target? how effective it could be? Many thanks

    • Fredric L Coe, MD

      Hi Dr Zouwail, I am afraid they are intractable, because they inhibit CA. The bicarbonate distal nephron delivery is perpetual because either the kidney replenishes bicarbonate losses via acid excretion, or we do with alkali supplements, so tubule fluid and urine pH are too high. Likewise citrate is a problem – I do not think the problem is systemic acidosis as citrate almost never responds to systemic alkali normally. I think it is the inhibition of NHE3 function from CA inhibition, and some imbalance of chloride to bicarbonate limiting SLC26a6 which links to the citrate transporter NADC1. So I stop the CA inhibitor and get another drug to do its job. Regards, Fred Coe

  7. Ryan

    I just received test results of:
    10% calcium oxalate (monohydrate and dihydrate), and
    90% calcium phosphate (hydroxy- and carbonate- apatite).
    INTERPRETIVE INFORMATION: Calculi (Stone) analysis
    I am trying to make sense of this before I return to the doctor tomorrow. Any help would be greatly appreciated!

  8. John Espy, Ph.D.

    Dear Dr. Coe, In 2018 I had cystolitholapaxy and in 2019 had 2 of the same procedure. In 2020 I had an open procedure to remove 1.5 lbs of bladder stones and for a simple prostatectomy to core out a 170 gm prostate. Three months later (Jan. 2021) I had another cystolitholapaxy to remove a small stone fragment that was left in a bladder diverticuli. This is was suppose to be the ‘final’ stone related event. Approximate 2 weeks ago I passed two small grainy stones in two separate events. The initial analysis of the stones in 2018 were “80% calcium phosphate (brushite) and 20% calcium phosphate (apatite)”. The current urologist has recommended another cystoscopy to evaluate for any stone recurrence. I have not been on Thiazide but have in the past, on the recommendation of the previous surgeon taken potassium citrate (800 mg, BID). I am inquiring as to find out if there are any dietary recommendations or clinical suggestions for future testing, evaluations, etc. My sodium intake is very low but my sugar intake in moderate. I do not smoke (never have), do not drink (have never had a taste for ETOH), age = 68, height = 6′, weight = 167. Do not eat red meat, drink green tea regularly. I “Thank you” for your time and would be happy to pay for your comments. John Espy…

    • Fredric L Coe, MD

      Hi John, Brushite is an uncommon stone type and often recurrent. Most people have high urine calcium and pH>6.3 on a 24 hour basis. Brushite itself is a probable starting crystal for all calcium stones. I would take a careful look at the 24 hour urine studies and blood to be sure all causes of stone were being controlled via diet and meds – of especial importance brushite supersaturation below 1. Potassium citrate raises urine pH and may or may not be ideal for brushite stones, no trial data exist. Regards, Fred Coe

      • John Espy, Ph.D.

        Dear Dr. Coe, If I may I would like to add one aspect that I left out. Do to the number of the bladder stones and the time they were in my bladder I have also developed numerous bladder diverticuli. Part of the current thinking is that even though I have had a simple prostatectomy that I am still not fully emptying my bladder and therefore urine is collecting in the pockets and producing stones. Again, I thank you and appreciate the value of your time. My best, John

        • John Espy

          Thank you again…

        • john espy, Ph.D.

          May I ask if you see the bladder diverticuli as being problematic with regard to my previous posts. Thank you, John Espy

          • Fredric L Coe, MD

            Ho John, Diverticulae can harbor crystals till they grow to worrisome size that normally are swept away as particles too small to recognize. Regards, Fred Coe

            • John Espy

              Thank you again for your willingness to take the time to answer questions regarding these difficult medical situations. Please forgive my bad manners in taking so long to say, “Thank you…”

  9. Carol

    Dr. Coe,
    1) My 24 hour urine does not show Ammonium. Can that be ordered as a separate urine test?
    2) What is the test to measure GI Anion Gap, is that the same blood test that is in the routine chemistry with the result range of about 4 mEq/L – 14 mEq/L?
    3) In regards to Urine Anion Gap, is that suppose to be in a 24 hour urine or is that a separate urine test or called something different?
    4) Lastly, How do you measure Bicarbonate? I see that a lot in articles, is this the same as CO2 in the complete blood count?
    Thank you for your time.

    • Fredric L Coe, MD

      Hi Carol, It is always best to get 24 hour urines for kidney stones from a vendor that specializes in it. Litholink is the best of breed, but most large labs have kidney stone 24 hour urine packages that include it. The GI anion is calculated: urine sodium + potassium + 2*calcium +2* magnesium -(1.8* urine phosphate + urine chloride). Calcium, magnesium, and phosphate have to be calculated in millimoles, the others are already reported that way. The factors of 2 and 1.8 convert to their charged form. No present vendors calculate this – it is just emerging into clinical practice, mainly because of our publications. Serum TCO2 is measured in blood and is presented in all routine blood panels – it is CO2 in the label. Regards, Fred Coe

  10. Stephen J Knohl

    Dr. Coe,

    Given that potassium can have an effect on glutamine metabolism, whereby potassium depletion augments its metabolism to ammonium and bicarbonate, I wonder whether the alalkaluria, hypocitraturia, and increased urine ammonium could be a response to real or “inappropriate sensed” potassium deficiency? And I say potassium deficiency as opposed to hypokalemia as we know that serum potassium measurements are not a true reflection of total potassium content. Thanks.

    • Fredric L Coe, MD

      Hi Steve, You are a mind reader – I have had the same thought. I wonder if KCl would lower HH4 production and urine pH. Fred


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