The crystals of the common kidney stones

CoeTie4I suppose I could have made my pie chart smaller but I wanted it to shine out like some odd colored moon because the names of the stones are so important and so much of what we do depends upon knowing them. They names of kidney stones are the names of the crystals which make up the hard part of the stones: CAOX, Calcium Oxalate; CAP, Calcium phosphate; UA, Uric Acid; Cystine; Struvite. The pie wedges show their relative abundances to each other in our large population of stone forming patients. Calcium oxalate stones are the most common by a wide margin, and that has been true in every accounting of stone types I have ever seen.

The whole science of stone prevention focuses upon stone crystals. Each type of crystal creates its own unique illness and has specific details of treatment. That is why we name the stones by the names of the crystals they contain and why when stones are analysed the results are listed by these very same names. Being a bold and rather large graphic, the picture does what I intended, brings the main facts into view as, at a circus, the great animals and the small animals circle the ring by way of an introduction. Come. I will show you all the common stones, like at a fashion show, or a circus parade. You can watch as they go by and remind yourself, or wonder, which ones might have been yours. Here they are.

Which ones do you have?

Or, better put, which ones did you once have before effective treatment? I cannot help repeating myself. You might think your doctors know what kinds of stones you have formed, but don’t rely on it. People move, doctors move, health records are far from ‘all electronic’. That stone report from 4 years ago could be in a dusty filing cabinet and your new doctors unaware it exists. Worse, it could be in a dresser drawer and you forgot it you put it there. Perhaps even more worse, the stones might be in that drawer and never analysed at all.

But if there are no analyses, or they are lost, treatment remains perfectly possible; it is just less focused and therefore possibly less effective than when guided by a knowledge of the crystals. So always seek treatment. If a stone comes along the way, make every effort to get an analysis made of it.

Why should you care to know all this?

I would say an informed patient can best participate in his or her own treatment. Because stones are often chronic, their prevention depends upon a willingness to maintain treatments over long periods, treatments which ultimately work by altering urine chemistry in a direction which minimizes the risk of forming crystals. Just as the sailor who aims along a chosen track against the random, misdirecting, and confusing winds and currents maintains a constant way in proportion to that skill which comes from knowing the way of the boat, patients who aim to keep a certain kind of condition in their urine despite the demands and temptations of the world do so, I believe, in proportion to that skill which comes from knowing how their work and lives and foods affect their own bodies, and how those crystals form which they so much desire to prevent. Put another way, knowledge is power.

This post is a lot longer than most because I wanted to put all five main stone types together. There is no reason to read it all at once or even all of it. Your stones are just one part and perhaps that is all you will care to read about. It will always be on the site as a reference if you need it.

I should mention here, to save a lot of confusion, that in the real world you live in stones often contain mixtures of crystals. The pie chart refers to the most common crystals in a stone, for which the stone is usually named. Much of the time, minor crystal components are not crucial, but sometimes – to jump forward a bit – they are. Even a trace of struvite or cystine, for example, can have great diagnostic importance.

Calcium stones

Calcium Oxalate Stones.

In the great circle of stones atop this page, the calcium oxalate stone occupies a lion’s share of the space. It is the common stone, what the majority of people form. Its crystals are formed through the 152px-Oxalsäure3.svgcombining of calcium and oxalic acid. Calcium is simply an abundant urine atom. Oxalic acid, a dead end waste product that the kidneys remove, is made of two carbon and four oxygen atoms.The oxygen atoms in this simple line drawing of its structure are at the two corners where the oxygen atoms (circles) attach. The lines from the corners to the oxygen atoms are a shorthand meaning the carbon atoms, which are not marked, are bonded to the oxygen atoms in a manner that will not easily come apart. Likewise the line between the two carbon atoms means they are bonded together.

Oxalic acid is a rather strong acid and so, at the acidity of urine, it exists as a charged ion – oxalate – which has 2 negative charges. (I will write about ions later. It is the name for a solitary charged oxalic acid molecule as it exists in water and this public reference is fine for the moment). Calcium atoms carry two positive electrical charge. Broadly speaking – though my more expert colleagues may bridle at such a simplification – the calcium and oxalate combine by an attraction of their matching and opposite charges.

The stones are generally not too big, between 1 and 10 mm and most of those less than 7 mm will pass without need of surgery or lithotripsy if they move from the kidney to the ureter, the tube that connects the kidney to the bladder. The kidneys themselves are not obviously injured except when obstruction lasts too long, or something happens during surgery. The causes of calcium oxalate stones are numerous enough to command multiple chapters of a standard reference textbook and it is to their prevention that physicians turn their major attentions.

Sometimes these stones arise as part of a systemic disease. A common example is bowel disease. It is the job of physicians to discover systemic diseases as a cause of stones, or establish that a known disease – like bowel disease – is the actual cause of stones Patients cannot do much for themselves in this area except provide as complete a medical record as possible.

But most of the time these stones are not due to a systemic disease but to the interplay between inheritance, diet, and aspects of daily living. When changes in daily living are key parts of treatment, it is patients themselves who must create and maintain those changes even though it is physicians who discover the links between daily living and stone production, and select those changes which can prevent new stones. I believe patients can so this in proportion to how well they understand what is needed, and why.

Medications are meant to be added when changes in daily life are not enough. Several have been tested in randomized trials, the gold standard. But benefits from changes in daily living almost always add to those from medications, so in all cases patients are active therapists for their own disease.

The calcium oxalate stones come in two varieties, calcium oxalate monohydrate and calcium oxalate dihydrate. The former are harder and therefore more resistant to fragmentation by lithotripsy. LIkewise, the former appear more often when elevated levels of urine oxalate are present.

Calcium phosphate Stones.

Less common, calcium phosphate stone crystals are calcium atoms combined with phosphoric instead of oxalic acid. Phosphoric acid is simply a phosphorus atom (shown as the ‘P’ in the line drawing to the left) with 4 oxygen atoms bonded to it. One of them has two lines for its bonds; this oxygen cannot provide any charge with which to bond calcium atoms to make a crystal. The other three have ordinary bonds that are shown by a line, and a dashed and solid arrow. These two arrows mean simply that the oxygens lie above and below the plane of the paper – so if you built the molecule with sticks and balls it would have a three dimensional shape. One of the three negatively charged oxygens never has a hydrogen on it in urine but only when the solution is exceedingly acidic. A second charged oxygen is always occupied by a hydrogen atom in urine. The third oxygen is variably occupied by a hydrogen in urine so phosphate ion has one or two charged oxygens with which to bind calcium. In a urine of average normal acidity, it has mostly one, not two negative charges, so it does not readily combine with calcium by charge attraction. When the urine is abnormally alkaline, the variable oxygen becomes charged so the ion has two negative charges which can combine with calcium to make crystals. For this reason calcium phosphate stones tend to occur in people who produce a more alkaline urine than those who produce calcium oxalate stones.

phosphateLet me say here it is in fact a very complex process, this combining of charged ions, one which I will try to explicate in later posts. But for the moment what I have said is not untrue and has the advantage of a stark and simple outline. In accord with such simplicity I shall simply mention that the calcium phosphate stones are of two forms, each a different type of crystal that calcium and phosphate can make together: Brushite, which is an equal mixture of calcium and phosphate ions, and hydroxyapatite, which has more unbalanced proportions of calcium and phosphate. The latter is the mineral that makes bones hard.

Sometime I shall tell you about brushite and hydroxyapatite and their varied fates. How the one precedes the other only to be consumed. How crystals cannibalize one another in their fight to survive. How the organic molecules in urine modify their actions one to another. In other words, as time goes on I will tell you about the underlying complexity of this disease which manifests itself as common stones.

But in the mean time it is enough to say that people with calcium phosphate stones have more numerous and often larger stones than people with calcium oxalate stones. Brushite stones are very hard and do not break well with shock wave treatments. Hydroxyapatite crystals can plug the kidney tubules and injure kidney cells. For these reasons, prevention may be more urgent than for calcium oxalate stones. But I say ‘may’ as we do not as yet have evidence that this is true. Because diet and lifestyle changes are often not enough for prevention, medications are commonly needed.

Uric Acid stones.

Although about as common as calcium phosphate stones, uric acid stones are altogether different. They are made of crystals of uric acid, a breakdown product of DNA and RNA, which form when urine is too acidic. The stones can be red or orange because uric acid crystals absorb hemoglobin breakdown products that are red – orange pigments in urine. Sometimes uric acid crystals pass in urine as a red orange gravel.

Acidic urine is common in obese and diabetic people, and in those with gout or kidney disease. How the urine becomes acid is known, and perhaps a topic we will cover here. How the crystals form is easy to say but brings up a new idea. The molecule of uric acid is organic, meaning it is composed of carbon atoms strung together, in this case in the shape of two linked rings. That the material is in urine, and that it leaves the urine to form crystals when the urine is acidic introduces the question of that it means for something to be in urine in the first place. And, because, after all, stone disease is about things that are in urine leaving the urine in a solid crystalline form, we might as well face the reality of those ideas now as opposed to later.

Water molecules are each a single oxygen atom (large ball) bonded with two hydrogen atoms (small balls) as in this picture from 440px-3D_model_hydrogen_bonds_in_water.svgWikipedia. The hydrogen side has a positive, the bare side of the oxygen a negative charge. So water molecules link to each other, positives to negative surfaces, to make up the clear and seemingly continuous fluid we drink, swim in, and hold up umbrellas to keep off of us when it rains. They link by charge at angles, shown by the number ‘1’ so as to make up a three dimensional macrame. To be ‘in solution’ means to have some charge to which water molecules can link up with by attraction. Calcium atoms are positive and become surrounded by a shell of water molecules facing it with their bare negative surfaces. Oxalic and phosphoric acids have negative charges and are surrounded by water molecules pointing their positive or hydrogen sides to them.

Uric acid, the molecule we are interested in here (shown to the far right), is made of carbon atoms arranged in rings (they are at the angles where lines join), with interposed nitrogen (N), oxygen (O), and hydrogen (H) atoms. There is very little charge in this molecule as it exists in normal urine except at the nitrogen at the bottom of the larger 6 sided ring on the right side of this drawing. When urine is of normal acidity, the hydrogen atom leaves the nitrogen which then has a negative charge to which water molecules can relate. Think about this; the whole huge molecule – it is so much bigger than a calcium atom, or even an oxalate molecule which has only 2 carbon atoms – and yet has only one small site that can ‘hold’ it in the water. When that site has its hydroge220px-Harnsäure_Ketoform.svgn atom on it, water has so hold on the molecule it simply leaves the water as water droplets form in the high and vaporous late afternoon clouds, and fall from the air as the warm rains of springtime.

Because there is much more uric acid in urine than there is oxalic acid, uric acid stones can become very large, even enough to fill up the entire collecting system of the kidney. Because uric acid does not have to connect itself to some other atom or molecule to make a crystal, in the way that calcium must bond with oxalate or phosphate ions to make crystals of calcium oxalate or calcium phosphate, crystals of uric acid can form very fast, in seconds, and pass as an orange gravel in the urine. If retained, such crystals can grow rapidly into large stones.

But because the whole process depends almost completely on the acidity of the urine, uric acid stones are very easy to treat. Just a modest amount of supplemental alkali will make the urine of almost any patient alkaline enough that the hydrogen atoms are removed from the one crucial charged nitrogen, and water can bond there so uric acid remains in solution. Being so simple to obtain, there is little reason to expect new stones once the stone type is known to be uric acid.

Unfortunately, however, uric acid may be only part of a stone problem, as it is commonly mixed with calcium oxalate. In this case, one needs to track down the cause of the calcium oxalate stones as well as to make the urine more alkaline in order to stop all stones from forming. It is rare to find uric acid mixed with calcium phosphate crystals, because I have already pointed out that it takes a rather alkaline urine to remove the hydrogen atoms from phosphate so it has two negative charges and can bind efficiently with calcium atoms.

Struvite stones.

Struvite crystals are made of the triple combination of magnesium, ammonium, and phosphate. The kidneys cannot themselves make such crystals; they are made by bacteria. Essentially, bacteria which are essential to the great nitrogen cycle of the planet find their way into some of us, and in doing what benefits our whole living world cause great harm in the confines of an individual urinary system.

ureaLike oxygen, nitrogen is an essential for life yet dangerous. It is integral to proteins, DNA and RNA. As these molecules are broken down and remade, some of their nitrogen slips by and can form poisonous compounds unless caught up in safe waste products. One of these is uric acid, which contains 4 nitrogen atoms (look back at the picture of it) and is excreted in the urine. The other main one is urea which contains 2 nitrogen atoms bound to a single carbon atom (‘C’ in the picture to your left). . Birds and reptiles excrete most of their nitrogen as uric acid; mammals like us excrete it mainly as urea.

As the animals of the world urinate on to the soil, their urea recycles lost nitrogen to where plants have their roots, but plants cannot use urea, they cannot break it down to release the nitrogen from the carbon atom which holds them. The bacteria that make struvite crystals normally grow in soil and have an enzyme called urease which can break down urea into ammonia. which plants use as their nitrogen supply. The soil bacteria are thus essential for the nitrogen cycle of the earth. But though on the earth, our kidneys are not the earth or the soil. Urine is filled with urea, and if the soil bacteria get into the urinary tract they break it down to ammonia. The ammonia makes the urine around the bacteria extremely alkaline, and the ammonia crystallizes with magnesium and phosphate that are always in urine to make struvite.

You might wonder how soil bacteria can get into the urinary system. We eat them with foods that are not cooked, and mostly they become part of the intestinal bacterial population from an early age. So they are around us and can find they way into the urinary system, especially in women whose shorter urethra makes entry easier. No matter how skillfully used, any instrument put into the bladder can carry our personal soil bacteria with it. Because they live among molds and fungi soil bacteria easily mount resistances to antibiotics, so antibiotics given for a urinary tract infection will tend to kill sensitive bacteria and select out those that can resist them.

Soil bacteria can produce struvite stones de novo, or infect calcium stones to produce a mixed stone. Either way, struvite stones are infected by their very nature. They can become huge, and their bacteria can injure the kidneys, even enter the bloodstream and cause sepsis. Treatment is a mix of thoughtful and skilled surgery and selection of antibiotics after such surgery to kill bacteria that remain. If the stones are a mixture of struvite and calcium crystals, new calcium stones need to be prevented.

Cystine stones.

800px-Cystine-skeletalLemon yellow with a sugary coating these form only in people who have an inherited kidney disorder called cystinuria. The kidneys function well except that they permit abnormal amounts of four amino acids to enter the urine. Three do not matter that we know of. The fourth makes crystals and stones.

Cystine, as the picture on the left shows, forms through the coupling of two identical units through their sulfur atoms (‘S’ in the line drawing). Each of the two units contains two carbon atoms – as usual not shown except at the corners. Just like oxalic acid, the two carbon atoms are bonded together (shown by the single long line that connects the two corners). One carbon atom has 2 oxygens bonded to it; the other has one nitrogen (which makes it an amino – nitrogen containing – acid), a hydrogen atom, and a sulfur atom. As for phosphate, the dashed and solid arrows simply mean the hydrogens and sulfurs lie above and below the plane of the page and a stick model would have a three dimensional shape. Each unit is called ‘cysteine’; the pair is cystine.

Cysteine itself is very soluble because the sulfur atom has an appreciable negative charge. But the big, long cystine molecule has very little charge on it because the hydrogens do not come off of their oxygens in urine to any appreciable extent. The main charge is at the sulfur linkage but it is much less than when the sulfurs are not connected to each other as is the case for cysteine. So, like uric acid, cystine readily loses intimacy with water molecules and simply leaves the solution as crystals. The process is fast, and in people who lose the amino acid in their urine because of cystinuria the amount of material available to make stones is large, so stone growth can be rapid.

Like uric acid and struvite, cystine stones can become very large. Like phosphate stones their crystals often block kidney tubules and can damage their cells. Stones may begin in childhood.

Treatment is very effective but almost always requires very large amounts of fluids to dilute the urine. The few drugs that help prevent them have side effects so fluids are always the foundation of treatment.

Rare stones

I do not intend a catalog here, simply the point that here and there we find patients who are making uncommon crystals and require very special care. Uric acid, as an example, can form odd crystals such sodium or ammonium acid urate, especially in people with bowel disease and chronic diarrhea. Anti-viral drugs, especially, can crystallize in urine and form stones which are not always recognized for what they are except through stone analysis. Very rare disorders of metabolism can produce molecules which crystallize in the urine; I mention 2-8 dihydroxyadenine as an example. Stone analyses will put physicians on the right track for these special cases, although it is often a while before the right answer emerges.

The end of a very long post

That’s my parade. The common animals and the rarer animals have gone by, and you have glimpsed the main ones, big and small. The one point is what it was at the beginning. Each kind of stone crystal has its own ways, and treatment requires we know which one you have. Likewise, for whatever that one may be, it is good to know as much about it as you can know, for long term prevention of stones is hard to come by and ultimately the limit is often the patience and will and consistency of patients themselves that matters most.

If you don’t know which stones you have made, find out.

Track down old reports and pull them together.

Keep copies and send everything to the doctors who care for you.

Learn what you can about the stones you make so you can do the best for yourself over years of prevention.

Fred Coe MD

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Overview of Kidney Stone Disease






  1. Beth

    Hi Dr. Coe – I posted this in the low oxalate diet page but I wanted to post it here too as I am interested in learning about the potential connection between IBS, diarreah and dehydration. I was diagnosed with IBS (with diarreah) 30 years ago. I have without a doubt been seriously dehydrated for periods of time when suffering with bouts of IBS attacks. And then I can go months with no incident. Ironically I’ve actually noticed an improvement in my IBS since learning of my kidney stone and increasing my water intake – which doesn’t really make much sense to me and maybe it is a coincidence. I’ve mentioned my IBS and a connection to the kidney stone to my Gastroenterologist as well as to my Urologist but neither seemed too convinced. I’m posting the rest of my story here – in case anyone has any comment.

    Hi – I am a 50-year-old healthy female (5’7, 120 pounds) who experienced what I believe to be kidney stone pain on June 23. I had pain in my left flank that radiated to the front and down into my groin area. I got up for work and the pain was very intense so I drove myself to the ER. As soon as I walked in to ER and showed them where my pain was – the nurses and ER doc all said kidney stone. They did a catscan and found no hyronephrosis or ureteral dilatation. But did find a 7mm non-obstructing calculus in the midportion of the left kidney, (“probably in an upper pole infundibulum). No other renal, ureteral, or urinary bladder calculi identified. I had microscopic hematuria and was sent for an ultrasound of abdomen which found nothing. I was loaded up with IV fluids, Dilaudid (which after the first dose made me extremely nauseated) and Toradol. A Urologist examined me and said your pain is not coming from the stone. They kept me for observation and sent me home following day. From start of the intense pain to finish I’d say it lasted about 48 hours or so. It would come in waves and was like nothing I’ve ever felt before. I will also mention that many years ago a former doctor ran a catscan on me (I forget why) and saw a tiny stone, he said I’d likely pass it without ever knowing. That is my only history with a stone. My older brother had a uric acid stone 20 years ago, he is now 55.

    I saw a Urologist after I was discharged from hospital (2 days later) and the blood in my urine continued. He also believed the 7mm stone was not the issue but discussed the small possibility that I had passed a tiny stone without it being picked up on catscan by the ER. He ordered an xray and the report said “a 7 mm calcification overlies the medial aspect of the left renal outline. A questionable tiny calcification overlies the lower portion of the left renal outline, no calcifications are noted overlying the right renal outline.” Based on the blood in the urine I had a Cystoscopy performed 2 weeks later – and nothing was found, though he did have to dilate my urethra (I was sedated) as he could not get the scope in. Next we did a 24-hour urine collection via Litholink with the following results:

    Urine volume: 2.70

    SS CAOx: 1.50

    Urine Calcium: 109
    Urine Oxalate: 17
    Urine Citrate: 782
    SS CaP: 0.58
    24 Hour Urine pH: 6.751
    SS Uric Acid: 0.08
    Urine Uric Acid: 0.520

    Interpretation: High urine ph. High urine pH can promote calcium phosphate stones. When coupled with low urine citrate consider distal renal tubular acidosis. When using alkali supplements (citrate or bicarbonate) manage urine volume and urine calcium to maintain SS CaP less than 2.0.

    Stone Risk Factors/Cystine Screening – Negative
    Dietary Factors:
    Na24: 147
    K 24: 53
    Mg: 59
    P 24: 0.555
    Nh4 24: 20
    CI 24: 141
    Sul 24: 23
    UUN 24: 7.04
    PCR: 1.0

    Normalized Values:
    CR 24: 1210
    Cr 24/kg: 21.9
    Ca 24/kg: 2.0
    Ca 24/ Cr 24:

    I returned to my Urologist who was not concerned about the mention of distal renal tubular acidosis. He’s had me order a supplement called Theracran (cranberry supplement) to take twice day for a few months to try to acidify my urine. And I will take another 24-hour urine test end of October.

    Lastly – I had an ultrasound done of my kidneys last week as I was asked to fly/travel for work and I’m concerned about the stone moving. The results are confusing though! It says “There is no hyronephrosis bilaterally. There is a small right extra renal pelvis measuring 1.5cm AP dimension. There is a small echogenic focus in the lower pole of the left kidney measuring 5 mm. Demonstrates variable shadowing. Impression: Suspected small calculus lower pole left kidney. Suggest CT or KUB imagining for conformation if not performed previously.

    My questions are: Due to my low urine oxalate content, should I still be vigilent about low oxalate foods all the time? Is my urine oxalate level only indicative of what I ate in the past 24 hours or is more cumulative?? I’ve increased my water intake – which is obvious due to my test results. I never watched my salt previously but had no reason to and rarely salt my food – nonetheless I have cut back on salt. I am not a big red meat eater, eat small portions of animal protein. My doctor really hasn’t advised me on any main dietary factor to prevent stones – and doesn’t even recommend removing the stone.

    But the latest ultrasound concerns me. I know they are not as accurate as catscan – but is it possible I now have a 5mm stone in my lower kidney and they did not pick up the 7 mm stone in the upper pole? Or is it possible the 7mm stone dropped and the size reading is off?

    I’m so concerned about having a kidney stone attack. And I swear I always have this lingering dull ache in my lower flank and sometimes I get a sharp pain. Docs say it can’t be the non-obstructing stone. I’m seeking a 2nd opinion at the end of the month. I want to consider lithotripsy – but if the 7mm stone is now in the lower pole – I have read that can be more of a challenge to blast and then pass the fragments?

    I am told it is unlikely I can pass stone of that size – so I just wait for it to cause me all this excruciating pain people talk about? That isn’t really something I think I can do. But the other concern for me is do I now have TWO stones? I really don’t want the radiation of another catscan. Can MRI pick up on the stone just as well? Do I get a KUB?

    I’d appreciate any feedback you can provide.

    • Fredric Coe, MD

      Hi Beth, I imagine you passes a small stone and have at least one more in your kidney. The CT is far more sensitive than the ultrasound so I would use the former as my guide. Your 24 hour labs are normal, so I imagine you have it about right. Your formed stones during episodic dehydration and that is not presently a problem but will be when your GI disorder becomes active again. You have no oxalate problem, and as for the urine pH it is not important. I and John Asplin wrote the litholink algorithms, so I understand why it says what it does but I also understand to ignore it for you. Your issue is to avoid dehydration as you can form stones – many people do you despite dehydration. Be sure and analyse the stone if it passes or is removed. MRI does not visualize stones. As for surgery, I would think I might wait – surgery is also a problem. If the stone comes part way own the ureter is an easier target for the surgeon – marginally so with modern instruments. Regards, Fred Coe

      • Beth

        i Dr Coe, thanks so much for responding. Regarding my 24-hour collection results, don’t you think it would be wise to test it again once or twice since one collection only – might not show any other variables? Regarding opting out of ESWL — do you think it might not be successful or just not worth potential complications/pain as its easier to remove once it starts to pass? Aren’t there others like me who fear the pain of such an episode of a stuck kidney stone in the ureter as well as the potential of it happening during an inconvenient time such as while traveling etc? Every time I have a pain in my back I fear it’s the stone.

        Why do you think the cat scan did not show a stone passing while I was in hospital with the pain? Was it too small to see possibly? Would there have been other indications of the passing stone such as inflammation? I still have microscopic blood in my urine, is that likely from the stone I still have?

        Lastly the cat scan in June said stone was in mid to upper pole. But last weeks ultrasound says lower pole. It’s possible the stone dropped right?? My doc said the ultrasound was more reliable than cat scan and that this was same stone but now moved. That didn’t make much sense to me as I thought the CAT scan was much more accurate than an ultrasound based on all the reading I’ve done. How often should I monitor a 7mm stone – as I’d assume if it got much bigger it should come out?

        Thank you again for your time, it is sincerely appreciated!

        • Fredric Coe, MD

          Hi Beth, Repetition is always prudent. Stones in the kidney that are not doing anything – obstructing, causing pain or bleeding or infection – it is unclear to me why one would undertake a preemptive surgery on their behalf. Surgery is itself burdensome. But if anxiety overcomes you, go ahead. Be rid of it, so long as your physician believes that is a reasonable and safe undertaking. As for the mysterious attack I think it might have been a tiny stone or a lot of crystals. Either way be sure you have a good prevention program in hand. Regards, Fred Coe

  2. Rod Martin

    Dr. Coe,
    I have a total of 12 stones that have been deposited over the years from both kidneys. I have read most of the comments but have seen none with my concentration of stone make-up. 90% WHEWELLITE 10% WEDDELLITE. Why is the Calcium Oxalate Monohydrate so high and what causes it to be so?

  3. Lisa

    Dr. Coe,
    I have a long history of kidney stones. I read an article many years ago about apatite having significance and you mention it here briefly. Can you explain it in more detail please. I have seen that element in a few reports. For example I passed a 5mm stone–not so easy!– and the composition was reported:
    50% hydroxy and/or carbonate apatite
    40% calcium oxalate mono hydrate
    10% calcium oxalate dehydrate
    I was diagnosed with osteoporosis at 44yrs old and have felt my kidney stones and bone loss are correlated. Can you offer any insight based on the composition of this one stone? Thanks

  4. Bethany

    Hello Dr. Coe! Nice article great info! Ive had a history of stones going back 9 years. Both times it started with pregnancy. The first incident i had a couple lithotripsys done and i finally got rid of them. But now Ive had stones in both kidneys for 6 years, they havent been too bothersome until recently. My major concern is frequent uti’s but also just a general discomfort…bloating, nausea, irregular urination. So i have a procedure scheduled for the Dr to go in and get a sample of the stone. Based on your article it sounds like its struvite or mixed, i dont know. I was wondering what i can do in the meantime to help with discomfort, i feel as if they prescribe me antibiotics for a uti, an i feel better while im taking it, but as soon as i stop i feel like the uti is right back?

  5. Lois

    My daughter (20 yo) had stones consisting of Ammonium Hydrogen Urate 90% and Uric Acid 10%. What causes this type of stone and what can she do to minimize chances of future stones?

    • Fredric Coe, MD

      Hi Lois, This is a very interesting and important question. Such stones require the combination of a modestly high urine pH and very high urine ammonium ion, and that usually occurs because of diarrhea, either from bowel disease or laxative use. It can also occur with potassium depletion. Here is a case where 24 hour urine testing is absolutely necessary for understanding. Let me know. Regards, Fred Coe

      • Lois

        She does have IBS, so that part makes sense. The doctor didn’t mention 24 hour urine testing, so I’ll tell my daughter about that. I have IBS and never had stone, so why does she have them and what can she do?

        • Fredric Coe, MD

          Hi Lois, Stool electrolyte losses are the key, and these can vary a lot. 24 Hour urine testing and serum as well are crucial to see what is going on. Often serum potassium will be slightly low, as well. That you have what she has may be a matter of degree – the worse the losses the higher the risk of these special kinds of stones. Regards, Fred Coe

  6. Rebecca F

    Good Morning Dr. Coe,
    On May 30, 2016 I was diagnosed with a 1.4cm stone cluster in my rt kidney, and kidney infection (after an ER visit for extreme rt lower back pain). During that visit, thanks to a CT of my abdomen, I also found out that I had aortic valve stenosis (1.3 opening) from calcium build up. After many tests and procedures to obtain a cardiac clearance, I finally had lithotrypsy and a stent placed in my right kidney. As previously stated, the cluster was 1.4cm, a month later it was seen on KUB to be a 1 cm cluster, and subsequently seen on a CTA Runoff 2 weeks after to be a 1.5 cm solid stone. The lithtrypsy was successful. The stone report just came back and the stone was 15% Whewellite (calcium oxylate monohydrate) and 85% Dahllite (carbonate apatite). I am a 37 yr old female with no previous hx of kidney stones but have a maternal family hx of CKD at a young age. I do not take any supplements including nothing with calcium. When I asked my urologist what I can do to prevent them, he had nothing to offer (which was extremely disheartening). Can you help me understand what this type of stone is from and how I can try to prevent further stones. Thank you so much for your help.

  7. gloria

    Hi Dr. Coe,
    In 2007 I had the wave surgery to remove kidneys stones a month ago I had passed a stone and kept it for the doctor all they said was “compostion, calculus, infrared spectroscopy hydroxyl apatite with moderate portion of calcium oxalate”. What does that mean?
    I was in a lot of pain when they were in the verge of passing and now realize I have had a number of them pass through the years without realizing what it was.


  8. Michelle Negron

    Dear Dr Coe,
    My kidney stone analysis resulted in Calcium Oxalate Monohydrate (Whewellite) 60% and Calcium Oxalate Dihydrate (Weddellite) 40%. Can you explain this to me? It is the first time I have ever experienced kidney stones. I had my gallbladder removed in 2003. I developed a boutique of H. Pylori and, as a result, I suffer from IBS. Any information would be helpful. Thank You.

  9. Mary

    Hello Dr. Coe,
    Three wks ago had pcnl for a 2.3 cm staghorn stone that had been within the kidney for 6 years. I have had multiple complications since surgery including hemorrhage, infections and fever. The physician was expecting struvite and I have had Proteus mirabilis pyelonephritis. The stone analysis, however, showed:
    Brown portion of calculi composed of calcium oxalate monohydrate.
    Tan portion of calculi composed primarily of 80% calcium oxalate dihydrate and 20% calcium phosphate (hydroxy- and carbonate- apatite).
    Can you give me any insight on this type of stone. I certainly want to avoid going through this again if I can!
    Thank you for your time.

    • Fredric Coe, MD

      Hi Mary, these constituents are from calcium and oxalate disorders and you would want a standard evaluation for them. Try this general approach. But the proteus and the size makes me suspicious that some struvite was in the stone and either the fragments in the stone that were analysed did not happen to have those crystals or the lab was not accurate. Struvite is the least accurate analysis in labs. I would have hoped the stone was cultured, and also that the PCNL left you free of all fragments. If there are any residual fragments your physician might want to consider a few month course of acetohydroxamic acid – a blocker of the urease enzyme that permits proteus to produce struvite, so permit dissolution of any residual struvite. As this drug has lots of side effects and significant hazard he/she may not want to use it, understandably. But overall I am very suspicious there was some struvite there. In any event prevention is to be directed against the calcium oxalate stones as in the Five Steps article. Regards, Fred Coe

  10. John

    Dear Dr Coe,
    Have a great day. Great article about Kidney Stones. My kidney stone analyses resulted in Ammonium Hydrogen Urate 50% and Carbonate Apatite (Dahllite) 50%. Can you explain me? Thank You.

    • Fredric Coe, MD

      Hi John, AMmonium acid urate occurs in settings of potassium depletion and bowel disease. It is otherwise unusual. Do you have bowel disease or a cause of diarrhea or potassium depletion? Regards, Fred Coe

      • John

        Hi Dr. Coe,
        So far I know I don’t have any bowel disease or cause any diarrhea or have any pain in my stomach I’m overweight 235Lb but never feel I have problems to going bathroom or any weird color of my feces very normal for the color. My story in the last year since November 2015 I been almost sedentary, ate junk food and a lot of cola and sugar. In June 10, 2016 I thought I had UTI infections for the symptoms cloudy urine, smelly and pain in the tip of the penis but I took home remedies to cure myself I never went the doctor because the symptoms I was feeling better and gone but In June 30 I was in ER because I had a great flank pain right side kidney, the doctors found I had a massive UTI in the kidney and bladder infection plus 4mm stock in the uretra right side took 30 hours to passing the stone when I was in the hospital they give antibiotics for UTI, Morphine 2mg and 4mg, flomax and I took pills to going the bathroom for going to number 2. The doctors told me I have pre-diabetes, B12 deficiency and 2mm kidney stone left side. After I was discharged I had 2 fallow ups one July 13 with primary doctor and July 16 an Urologist.
        I had a fallow up with a primary doctors July 13 and I got the urine test showed Ketones 15mg the doctor told me if I’m drinking enough water I told her I’m drinking 8 to 12 Oz of water every day plus oatmeal with water 1Lt, she felt might something wrong going with my kidney isn’t process the water.
        I spoke with an urologist in July 16 I had an appointment he showed the CAT when ER took it, my right kidney was 2.5 bigger than the normal size he said was very much inflammation pushing everything inside. When I got the results of the kidney stone 3 days ago July 21 he told if I had problems of diarrhea because I was drinking medicine to going the bathrooms for the constipation, I told when I was in ER the doctors give pills to going to number 2 because I was stock. Also I told him I been almost sedentary, ate junk food and a lot of cola and sugar since Nov 2015. The urologist told me July 16 in the coming week I will get a 24 hour urine test and in July 7, I will have an Ultra Sound to see my kidneys are working correctly and how is going on with the stone of 2mm.
        Dr. Coe I feel nervous about my situation right now my symptoms are having trouble with memory, in some nights not every night I have very little pain when I going to pee in the tip of penis, some pain in the left side kidney when I walk more of 30 min, my eyes hurt me, my leg shin/calf part hurts me in the night and I feel thirsty.
        I told the urologist this he says this will be pass no worry but will take time and he don’t know when.
        Thanks for following up my case, appreciate it any advice from you Doctor Coe.


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