A Good Place to Start
VIDEO 1: RISK FACTORS (17 min).
VIDEO 2: EVALUATION (13 min) AND TREATMENT (13 min).
The videos review the chapter and emphasize the main points. I would start with them.
The featured image shows salt harvesting from evaporation ponds.
The sea is salty and like our blood holds its salts in solution. But if you channel the sea into ponds, and balance things so the sun evaporates water faster than new water can enter, the remaining water overloads with sodium chloride. It crystallizes out of solution as sea salt. Workers collect it for us to season our food with.
Is it not an apt picture?
Our Blood is the Sea, our Kidneys Make the Pond
Mostly the Salts Stay in Solution
Our kidneys filter the salts and water of our blood into their millions of fine tubules. Like the sun they take back the water, unlike the sun they also take back much of the salts.
Mostly they are balanced, these takings back, so the final urine can dissolve its salts.
Stones Arise from Imbalances
If you ask me to say what makes stones form, I must answer that something has disturbed the balance, leaving not enough water to dissolve the salts, as in the ponds drying out under the sun.
Which salts, you might ask? After all, we are not ponds and our kidneys remove many small molecules.
Those salts, I would answer, that have made the stones.
Precisely those. Usually calcium oxalate and calcium phosphate.
The 24 Hour Urine is Our Pond
In it we measure losses of salts that can become stones, and the volume of water to dissolve them. We need the full day because things vary, with sleep and food, and all of what we do in life. Each is snapshot of our pond for one day. Which salts, how much imbalance, all this comes from our daily samples.
Abnormal Excretions Cause Stones
In our urine, excesses of calcium or oxalate excretion, or insufficiency of citrate excretion or of water are proven independent risk factors
that predict new onset of stones. Since stones cannot cause these abnormal excretions, and the abnormal excretions can cause stones, this association is equivalent to cause.
By independent I mean that the effect of each is significant when the effects of the other factors are adjusted for mathematically using common statistical techniques.
In cohorts of women (red) and men (blue) followed over decades, risk of forming stones rose smoothly with urine calcium or oxalate (upper left and upper middle panels), and fell with increasing citrate and urine volume (lower left and middle panels).
The mechanisms causing high urine calcium and urine oxalate are well known. Means for lowering them, likewise, and such lowering is known to reduce new stone formation.
Risk from low urine volume is most obvious below 1.25 liters per day (lower middle panel), a scanty volume. By 2 liters a day risk from low volume is gone.
Supersaturation is the Word for Overloading the Pond
Crystals produce kidney stones, and supersaturations produces the crystals. Modern laboratories can measure the supersaturations in 24 hour urine collections along with the key components in the urine that control the supersaturations.
As you might expect, supersaturation is a powerful predictor of whether people will become stone forming patients. The two right panels of the graph show how supersaturation with respect to calcium oxalate (top) or calcium phosphate relate to risk of stones. (Note that common supersaturation urines for calcium oxalate are 3.3 times higher than these older style supersaturation ratios. Your report will almost always use the newer units. So risk begins above 3 and rises smoothly up to 12 or more).
Given the stone crystals and the supersaturations you can gauge treatment goals from a simple maxim: In a patient who is producing new stones, urine supersaturation with respect to the crystals in the stones forming is too high.
Ideally one will lower supersaturation by improving all factors that raise it. But one must avoid a common and obvious fallacy. Water alone can lower urine supersaturation – think about rain and the pond. But water alone, without proper testing and as a sole remedy is a poor idea under all circumstances and to me anathema.
Ideal Treatment Improves All Abnormalities
Given a patient may have any one of these four abnormalities, and that they act independently, the ideal treatment strategy will attempt to improve each one to achieve synergy. It is often more practical to partly reverse multiple abnormalities than to rely on improving only one. For example, possibly extremely high urine volume might reduce stones even if urine calcium and oxalate remain high. But lesser volume would be sufficient if these two excretion rates were each moderately reduced.
When treating hypertension, as an example, one tries to achieve some weight loss, some increase in exercise, some reduction in sodium intake, and some increase in potassium intake, and then use medications as needed. The alternative, medications alone, or just exercise, would create a potential for side effects – too tired from exercise, or drug side effects in this case – which synergy would avoid.
Proper Testing Is Essential for Proper Practice
All Stone Formers Deserve Serum and 24 Hour Urine Testing
It is obvious that the only documented risk factors for stone are found in 24 hour urine, so this measurement is the bedrock of stone prevention. Systemic diseases that cause stones often alter serum chemistries, and they must be diagnosed from those alterations.
Inadequate Testing Can be Dangerous
A few causes of stone disease, such as severe hyperoxaluria can destroy kidneys. Others like primary hyperparathyroidism or renal tubular acidosis can do the same. Other rare but dangerous inherited diseases lurk in any kidney stone population. They require both serum and 24 hour urine testing.
Consider that idiopathic hypercalciuria can be very severe and lead to both stones and bone disease. One cannot know without a 24 hour urine collection. Elevated serum calcium can mark for primary hyperparathyroidism, or simply benign familial hypocalciuric hypercalcemia. So one needs a 24 hour urine here as well. Low urine citrate as a cause of stones is simply unknowable without a urine collection.
Arguments Against 24 Hour Urine Testing are Specious
Cost, difficulty, and futility are all common arguments against urine testing, and none of the three convince me. Add to this that all people fear and detest surgery. Surgery is a nightmare one hopes to avoid. If testing can reduce surgery by even a small amount, testing is a virtue.
Surgical Costs Dwarf Those of Proper Testing
A common 24 hour urine with fasting blood sample costs a few hundred dollars – say three hundred for an upper end estimate. A kidney stone surgery, ureteroscopy for example, costs – about eight to ten thousand dollars, to which one must add lost work and the debilitating effects of general anaesthesia, postoperative pain, stents, infections, and postsurgical visits to physicians. Shock wave lithotripsy costs as much or more as shown in the same reference. At these rates, 30 to 40 24 hour and blood testing panels match one surgery discounting the personal losses.
Difficulty of Collection Stops Few Patients
In my decades of managing patients with kidney stones almost none have demurred to collect – pilots, surgeons, busy and successful business people, teachers. I could also point out that modern commercial vendors all provide convenient collection kits and instructions. But no one could make the case better than my partner Jill Harris did in her spirited article on this topic.
Personalized Kidney Stone Prevention
Stone Analysis is Crucial
Assuming stones are forming or have formed, everything branches off of stone analysis.
Uric Acid in Stones
Uric acid stones form mainly because an overly acid urine raises supersaturation so powerfully nothing can reliably prevent more stones but alkali to raise pH and make the urine less acid. Uric acid stone can be pure or admixed with calcium oxalate crystals. In either event, treatment must include alkali to prevent more uric acid. If your stones contain uric acid, follow this link.
Cystine in Stones
Cystine stones form only when genetic abnormalities of renal cell transporters allow a vast excess of this amino acid into the urine. Treatment is high specialized. Stones can grow very large and rapidly. Supersaturation can be measured but only in a few laboratories. Like uric acid stones, cystine stones can contain calcium phosphate crystals, but prevention of cystine crystallization is paramount and takes primary importance. If your stones contain cystine, follow this link.
Struvite in Stones
Struvite, magnesium ammonium phosphate, forms in humans only because of infection with organisms that hydrolyse urea to ammonia and carbon dioxide. Struvite can be the only stone crystal or can become part of any stone. Treatment has nothing to do with diet or the usual stone medications. Struvite stones are essentially infected foreign bodies within kidneys, and cure requires a mixture of thoughtful surgical management and use of antibiotic drugs.
The mass of patients will form calcium stones unmixed with uric acid or struvite. Out of this mass physicians – patients cannot do this
themselves -must cull the small fractions with systemic diseases that cause stones but produce illness beyond stones and require special and often very complex management.
Serum and Urine Testing
The tubule disorders are recognized from serum abnormalities, sometimes paired with specific 24 hour urine findings. Renal tubular acidosis and primary hyperparathyroidism are particularly related to stone disease. Both require both serum and 24 hour urine abnormalities for diagnosis.
Primary hyperoxaluria, and hyperoxaluria from bowel diseases, dangerous diseases that can cause kidney failure, are diagnosed from high 24 hour urine oxalate excretion and cannot be otherwise recognized. Bowel disease is recognized clinically, but 24 hour urine testing is required to assess both urine oxalate excretion and other secondary abnormalities that can cause stones and kidney disease.
Idiopathic Calcium Stones
Evaluate 24 Hour Urine and Treat Abnormal Risk Factors
High urine calcium in these patients arises from idiopathic hypercalciuria, and can be controlled with reduced diet sodium intake, avoidance of excessive diet protein intake, perhaps reduction of refined sugar intake, and, when needed, thiazide diuretic agents. Adequate diet calcium is needed to reduce risk of bone mineral loss.
Urine oxalate above 25 mg/d can be treated with adequate diet calcium, that reduces oxalate absorption, and reduction of diet oxalate intake to below 200 mg/d using lists of high oxalate foods. Of these, spinach, rhubarb, nuts, seeds, and pepper are common offenders. If diet calcium increase does not bring urine oxalate into the desired zone (<25 mg/d is ideal, <30 is acceptable), limiting diet oxalate to below 100 mg/d is a proper strategy.
Low urine citrate, below 400 mg/d raises stone risk because citrate binds urine calcium in a soluble complex and directly inhibits formation and growth of calcium oxalate and calcium phosphate crystals. Five servings of fruit and veggies provides about 120 mEq/day of potassium alkali that can raise urine citrate. If needed, potassium citrate can be added as a specific treatment.
One hardly need mention that urine volume below 2 – 2.25 liters a day needs extra fluids to achieve that goal.
The Kidney Stone Diet
The elements common to the three main risk factors beside urine volume are reduced diet sodium, sugar, and protein – to permit adequate diet calcium without raising urine calcium, adequate diet calcium for bones and to block diet oxalate absorption, and fruits and veggies to provide diet potassium alkali. These are highlighted in the large upper box.
These five diet elements all correspond to present healthy diet recommendation for all US citizens, and should be advocated by all physicians for all patients unless otherwise limited by underlying diseases. Since idiopathic calcium stone formers are almost by definition free of systemic disease, it is a desired diet in general. The diet has been tested in one prospective trial and more trials are much needed.
Specific treatments, thiazide like diuretics, potassium citrate pills, and low oxalate diet are noted under their respective abnormalities. A strategy for beginning treatment with diet and adding drugs as needed is outlined here.
More is Wrong Than Just Stones
Having stones is burden enough, especially the dreaded surgery they can entail. But epidemiologists have discovered links between stone formation and risk of hypertension, bone disease, stroke, heart attack, and kidney disease including even renal failure and dialysis. The links between stone forming and these other major diseases are not as yet obvious, but the message obvious. Physicians need to treat the patient, nor just focus on preventing stones.
The kidney stone diet, being in line with best present recommendations for all US citizens, is a reasonable choice for all stone formers because aimed at reduction of risk for all of the above mentioned disorders. Even if the problems of stone formers transcend those of normal people, so that a healthy diet does not suffice, it can do no harm, and may do some element of good.
Why Not Just Lots of Water?
Consider the least threatening possible scenario, an idiopathic calcium stone former who has had only one stone – a kind of baseline kidney stone disease. Being such a common and large group why not simply treat them with lots of fluids, do a single 24 hour urine for safety, and save more refined treatment if water fails?
That Has Been Tried
Before you read what follows brush up on supersaturation.
Of ninety nine people who formed one calcium oxalate stone and drank so much they produced 2.6 liters a day of urine, 12 formed one or more new stones in five years (Group 1). Among one hundred more just like them who produced only 1 liter of urine daily 27 formed one or more new stones during the same time.
As expected water reduced supersaturations. SS CaOx was 9.9 in the low flow and 2.6 in the high flow group. SS CaP was 1.58 in the low and 0.48 in the high flow group. Excellent and predictable results.
In passing the authors note that before the trial, at baseline, patients had lower urine volumes than their non stone forming subjects. One might surmise from this that habitual low urine volume played a role in causing their stones. But that is observation, not hypothesis testing.
Water Is Not Enough
Surely water works. Stones were less with lots of it.
But why so many stones? Of one hundred random people 12 people will not make one or more new stones in five years drinking so much water as to achieve a urine volume of 2.6 liters daily. This would be 2.4 percent per year or 24 percent per decade. Even if limited to adult years this would produce stone rates approaching 75 percent in a population of high fluid drinkers.
For the controls, who drank less, the numbers essentially double.
More is wrong than water could right. Given the risk factor studies I have already presented, this is an expected outcome.
In fact, in Table 4 of the water treatment article in the link above, hypercalciuria was at least one of the reasons for higher relapse. Baseline, before anything was done, the urine calcium levels of those destined to relapse was higher than those who did not 233 vs.336 mg/d and 249 vs. 313 in the high fluid and low fluid groups, respectively; p<0.001 for those into statistics. So those destined for a bad outcome had idiopathic hypercalciuria, a well known personal risk factor.
This Was Water Under Ideal Conditions
Above all else, these patients were supervised so that water treatment was as good as it can ever be. The cost of such supervision was underwritten by the grants that supported this trial. Outside the umbra of a subsidized program, adherence to such high fluid intakes will be less ideal.
Multiple Stones Predict Higher Relapse on Treatment
This figure shows the treated patients in a number of published trials. The details can be found in the parent article.
The abbreviations refer to the treatment modalities: K Cit means potassium citrate; chlorthalidone, indapamide are thiazide like diuretics, HCTZ is hydrochlorothiazide; Multi means several medications were used together; allopurinol lowers urine and serum uric acid and proved effective in one major trial against calcium oxalate stones.
As the number of stones produced before treatment goes up, from one to 10 or more (along the horizontal axis), the percent of patients who relapse during treatment rises from 10 – 12 percent to 20 to 30 percent. More or less, the percent who relapse increases proportionally to how many stones had formed before treatment.
Results for the water trial of single stone formers and my own published observations on patients who had formed a single calcium stone are at the lower left of the graph.
Stones Form Steadily Over Time
Waiting to treat a single idiopathic calcium stone former, either by the use of relatively ineffective high fluid intake alone or, in the worst
case, doing nothing at all, will on average lead to more stones. On this graph, detailed elsewhere, time is on the vertical axis and the number of countable stone events on the horizontal axis. Squares show the rate of stones per year, a rather constant number. Circles show the inevitable consequence: more time, more stones.
So time wasted, with water as a sole remedy, or no specific treatment, will tend to increase the number of stones, and as that number increases the successfulness of even highly supervised protocol treatment as used in trials will wane.
Never Use Water Alone
I will surely not treat any patients with just water unless 24 hour and serum testing shows me that nothing at all is wrong but low urine volume. Even then I am sceptical.
The reason I am so stubborn about water and waiting is that the main force of treatment for idiopathic calcium stones – those forming in the absence of systemic diseases – is diet change. Not only that, the diet change is in the direction considered most healthy for the US population. Why would anyone force fluids on patients when much of the disordered urine chemistry can be mitigated by a healthier diet?
Analyse Every Stone
One might think that once we know someone forms, for example, calcium oxalate stones more analyses add little or even nothing to successful treatment. But obvious problems make that thought a poor one.
Every surgery poses risk of infection. As foreign bodies in the kidneys stones themselves offer lodgment to bacteria that may be passing through the urinary system. So struvite can grow over older calcium stones, or even begin on their own. The person ‘converts’ from one type of stone crystal to another. Treatment no longer stops stone growth.
Because rapidly growing, large, and laminar in appearance by x ray, struvite stones will make themselves apparent over time. But larger size means more complex surgery, and perhaps kidney injury or even sepsis from stone infection. So early detection matters.
New Uric Acid
People age, gain weight, develop diabetes and with this urine pH falls. Treatment with alkali that might have stopped uric acid production begins late, when rapid stone growth or large stone size makes uric acid come to mind. But large means harder to dissolve, perhaps impossible. That means surgery. Early detection of uric acid in stones can save future surgery.
Calcium Oxalate to Calcium Phosphate
This happens and probably matters. CaP stones most often arise over tubule plugs which means cell injury in tubules and the tissues around them. By contrast, growth over plaque, how CaOx stones form, appears less invasive. Tissues seem less injured.
My imagination tells me calcium phosphate stones may cause more long term kidney problems than calcium oxalate stones. If this hypothesis were true then mere observation of patients well characterized in stone composition should disclose differences in kidney function, or perhaps urine albumin loss. Perhaps blood pressure rises more. Perhaps someone might have such information.
Quite possibly potassium alkali that work well to prevent calcium oxalate stones do poorly for calcium phosphate stones. After all, they raise urine pH and a higher pH will foster the phosphate stone. No trial addresses this obvious question; one should.
How Good is Kidney Stone Analysis
Less than ideal
What happens if you make a rigorous analysis of stones, divide the sample up into parcels and send them to different commercial laboratories. What will they tell you?
Ideally they will tell you what you already know. But in fact they under reported struvite and calcium phosphate – as hydroxyapatite. They also failed in to identify brushite.
Not Utterly Unreliable
My own work with Joan Parks compared kidney stone content of CaP – as hydroxyapatite to urine pH and supersaturations obtained by 24 hour urine samples. Unlike work from centers that performed their own kidney stone analyses we relied on a multitude of commercial lab reports obtained over decades. Even so urine pH and CaP supersaturations tracked will with these commercial lab results.
A Reasonable Conclusion
As an inexpensive and indispensable tool, all of us need and use commercial kidney stone analysis. What we know prompts wariness about missed struvite – a most important stone diagnosis. But perhaps that argues for multiple analyses – more tries lower likelihood of missing the diagnosis.
Make Followup 24 hour and Serum Measurements
It would seem unnecessary to say, but sometimes this obvious maxum goes unfulfilled. There is no use to changing diet – or trying to – or adding medications if one does not assure that the changes lead to a betterment of stone risk. I think followup urine collections for diet change should be when a patient believes the diet has changed and is tolerable enough to be used long term. With thiazide or potassium citrate, I favor 6 weeks initially. For all patients, followup with testing and a clinical visit should be yearly at least until stones become a thing of the pasts.
Aids for Patients Who Have Formed Stones
I have written several articles outlining the steps to prepare for and do testing, and for obtaining the most from physician visits.
This site has a large volume of articles. This page lists all of the articles by topic.
Chapters 2 – 6 of this book give a lot of background and links to related articles.
Chapters 7 – 12 concern specific stone forming systemic diseases.
Summary of Chapter One
The miserable fragments we call kidney stones have a complex origin in the kidneys. All but one kind contain crystals without which they could not exist. The exception, protein stones, occur rarely and I do not consider them here. Stone crystals form as all crystals form, from a solution overloaded with the crystal material – supersaturated with respect to the crystal of interest.
Many Paths to Stones
Kidneys can supersaturate urine by conserving water or by increasing the amounts of insoluble salt constituents such as calcium or oxalate. They can reduce the excretion of citrate, an inhibitor or change pH. The latter can be downward, fostering uric acid or upward fostering calcium phosphate crystals.
Treatment Synergy Requires Proper Testing
Although effective and obvious, extra fluids do not reduce new stone production completely to the baseline levels of average people. Moreover, above perhaps 2 to 2.5 liters a day of urine becomes difficult to maintain. So ideal treatments employ synergies – increase of fluids and changes in calcium, oxalate, citrate, or pH of urine as indicated in any one patient. Only blood and 24 hour urine testing can tell what is indicated in any one patient, and also what treatment has accomplished.
Stone Analysis is Crucial
Since all treatments but water relate to specific crystals, prevention depends on stone analysis whenever possible. Stone crystals can change over time and I see no reason to discard stones and good reasons to analyse them. Especially, infection or uric acid stones may complicate or even replace calcium stones and be missed without analyses. Likewise for stones from drugs.
Stone Prevention is Precision Personalized Medicine
Stone prevention exemplifies the best features of precision medicine. The crystals arise from specific supersaturations we measure in simple 24 hour urine samples and can reduce with healthy diet changes and a few medications that have proven their worth in trials. No two patients are quite the same, so each needs personalized care – stone analysis and 24 urine testing along with blood tests and clinical assessment to exclude systemic diseases.
113 Responses to “Chapter One: Personalized Kidney Stone Prevention”
Hi Dr. Coe!
First off, an excellent resource of information this article is, great work. I’m a frequent stone former at 38/m, I had a 24/hr urine test back in Dec that showed a Urine citrate of 189mg/day which was well below the recommended amount. Quest results says I have “Hypocitraturia”. I’ve been looking at ways to help learn about my own issue as I’ve just learned that I have two more stones in my kidneys, 1mm and 2mm on left/right just this week respectively after having passed one in Aug 22 and two in Mar 21. (they’ve made up shop till they decide to move on to the highway that is my ureter). I’ve been dealing with this since I was 18 and I’m starting to reach the limits of my anxiety. Multiple surgeries, lasered and blasted.
I might forsee my first Lithotripsy in the future given the current homemakers.
Unfortunately, I don’t think I was provided adequate knowledge on “my diet” and recently started to eat “healthier” due to a recent “elevated cholesterol”. I’ve come to realize at least my recent run of stones may have been related to cutting dairy out and loading unknowingly high oxalate foods. With yours and Jill’s articles I’ve become more informed unbeknownst to my current healthcare provider. Unfortunately my doctor seems to just pass around a pamphlet, drink lots of water and out the door I go. I don’t really feel like I’m getting personalized care from my current doctor. Often times even feel like I have to remind them on my own history with them specifically. I’m in Sarasota, FL. Next step is a CT in April too check on things and doctor says (if I recall correctly) Potassium Citrate pills may be in the future if I keep forming stones. Mind you I’ve been going to this doctor since I was 18? I feel like I’ve already reached “the future”. See my point?
Although I don’t have the results to say otherwise, my doctor has mentioned my stones were previously calcium oxalate. I do have my most recent August stone report and it says,
Carbonate Apatite (Dahllite) 90%
Calcium Oxalate Dihydrate (Weddellite) 10%
This may seemingly contradict my supposed previous stones against “today”? Or am I still an Oxalate stoner?
I also wonder with your research/technical advice if something like LithoLyte Powder to add to my drinks is good given my scenario? I’m trying the Lemon drink scenario given my low Citrate but looking for something a bit more manageable with a busy lifestyle too mix with readily available water sources to keep up my intake.
Your thoughts and technical advice on my situation would be very much appreciated. And perhaps any recommendations for local resources to provide a more personalized and caring approach to my kidney needs. I saw you offered a search to another. You’re very kind to do so regardless!
Here are my 24/hr urine results,
STONERISK® DIAGNOSTIC PROFILE
TOTAL URINE VOLUME 2.70
Reference Range: >2.00 L/day
PH URINE 6.7
Reference Range: 5.5-7.0
CALCIUM, 24 HOUR URINE 154
Reference Range: <250.0 mg/day
OXALATE, 24 HOUR URINE 20
Reference Range: <45 mg/day
URIC ACID, 24 HOUR URINE 562
Reference Range: 320 mg/day
SODIUM, 24 HOUR URINE 103
Reference Range: <200 mEq/day
SULFATE, 24 HOUR URINE 15
Reference Range: <30 mmol/day
PHOSPHORUS, 24 HOUR URINE 694
Reference Range: 60.0 mg/day
AMMONIUM, 24 HOUR URINE 35
Reference Range: 14-62 mEq/day
POTASSIUM, 24 HOUR URINE 35
Reference Range: 19-135 mEq/day
CREATININE, 24 HOUR URINE 1219
Reference Range: 800-2000 mg/day
CALCIUM OXALATE 0.66
Reference Range: <2.00
Reference Range: <2.00
SODIUM URATE 0.73
Reference Range: <2.00
Reference Range: <75.00
URIC ACID 0.21
Reference Range: <2.00
THE PATIENT HAS:
Fredric Coe, MD
Hi Blake, Your stones (calcium phosphate) form in alkaline urine and your urine is indeed alkaline with pH of 6.7. Despite the high pH your urine citrate is low at 189. Your urine ammonia is 35 mEq/d (acid excretion) and your sulfate acid load is only 15 mEq. We see this pattern often in calcium phosphate stone formers. Possibly you are a carrier (heterozygote) for one of the gene variants that cause distal renal tubular acidosis). If so that could influence how one treated you to prevent stones. If not, treatment might take another course. Knowing nothing more than the urine labs that is all I should say. I would suggest getting the gene work which is available to you and your physicians through national vendors. If your physicians believe I could be helpful (this is an unusual situation), consultation can be arranged via telehealth. Regards, Fred Coe
Marie Torzewski Craig
I need help! I am 58 yo female, 147 lbs with Crohn’s disease/bowel resection and Randall’s plaques disease. i drink one gallon of Simply lemonade a day plus water, take 650mg of Calcium, and a magnesium/potassium/citrate supplement-Theralith XR. I am very careful about what I eat. I keep getting recurrent kidney stones-I have had two 24 hour collections that basically say I am doing the right things. My Physician is at a loss as well as I am. can you offer any help?
Fredric L Coe, MD
Hi Marie, If the 24 hour urine supersaturations for calcium oxalate and calcium phosphate are below 3 and 1, respectively, and stones are not uric acid, you may be passing old stones or experiencing within day peaks and valleys of stone risk the 24 hour urine blurs. This requires your physicians and you to review your day/diet cycle looking for problem areas. As well, one needs to keep count of stones. Regards, Fred Coe
Dr. Coe, Thank you for providing all of this information – very informative for a first time kidney stone patient. I’m a 58 year old female, 5’6″, 140 lbs with typically lower blood pressure ~101/60 with no history of kidney stones or any kidney issues nor family history. I take 7.5mg of Rosuvastatin for slightly elevated LDL, and 88 mcg of Synthroid since 1996 as a result of radio-iodine treatment of Grave’s disease. I use bio-identical compounded topical and vaginal hormones, use beginning shortly after menopause at 45 yrs. old.
Over the years I’ve had Vit. D absorption issues resulting in the need to take prescription Vit D temporarily 2x and have supplemented 5000 IU for years. On advice of my GP I decreased this to 2000IU then 1000 over the past couple of years. I’ve had low Cortisol results from saliva testing, although recent blood work shows in range. For years I’ve taken Turmeric, fish oil, CoQ10 regularly and the occasional multi-vitamin.
I had a one-time A-fib event in 2008 that was resolved (after many months of cardiac testing) by adjusting Synthroid from 100 to 88mcg. Thankfully that hasn’t happened again!
All this to say that I am completely surprised by the kidney stone that showed up last month unannounced. I consider myself fairly fit, exercising regularly and eating fairly well. I watch sugar (which has been inching up over these past several years – diabetes in the family). I don’t salt anything or cook with salt. I watch fat due to LDLs. Little red meat, not a lot of dairy and a focus on whole grains, veggies, fruit, salads. I probably don’t drink as much fluid as needed.
My 4mm stone, (analysis showed calcium oxilate (80% calcium monohydrate/20% calcium dihydrate), was lodged at the distal end of the ureter at the bladder. Under general anesthesia they did a ureteroscopy and placed a stent for a week. I’m due to follow up in 6 weeks with an ultrasound & blood work. Low oxilate diet has been recommended but no talk of 24 hr. urine testing, no discussion of other possible medical issues/causes. I won’t see doc for 8 weeks post-procedure, which seems like a really long time to not discuss any of this.
I’m really stumped about this stone and how to prevent another. I welcome your thoughts and wonder if you do virtual consultations and have recommendations for Endocrinologist and Nephrologist in the Hudson Valley area of NY.
Apologies on this long-winded post but I am a worrier and have had more than my share of anxiety and fear over numerous things since mid-2019. The pandemic didn’t help. Also wonder if this has contributed to any of this. I appreciate your time and hope you can respond.
Fredric L Coe, MD
Hi Ellen, The calcium oxalate monohydrate is most compatible with oxalate excess or low urine volumes, but I would do a complete evaluation to be sure about the cause. This chapter is my best on that. New onset in mid life has special implications. I noticed the turmeric, a very high oxalate product and perhaps the culprit, but I would not count on that. I do video consultation, but perhaps your personal physicians will be able to help when you have all of your data. If not, my secretary is at 773 702 1475. Regards, Fred Coe
Thank you Dr. Coe.
I had noted that turmeric is high oxalate and I stopped taking it a month ago. Also, in reading Jill’s information and others I see that all of my “go to” snacks (peanuts, almonds, essentially most nuts) are high in oxalate, which I was eating in some form every day, multiple times per day for years now to be heart healthy and cut cholesterol. Also dark chocolate has been a regular – a small bit most days. And very likely not enough fluid intake. When you say “…have all of your data” what do you consider all the relevant data to determine a path forward?
Thank you again.
Fredric L Coe, MD
Hi Ellen, I mean 24 hour urine and blood studies, CT imaging to count stones, and a lists of all meds and supplements. Of course everyone has a different collection of medically related information – all of it can matter. Regards, Fred Coe
Hi, are there any over the counter urine tests that can help monitor low urine citrate? Or are there any over the counter tests a calcium oxalate stone former can use as a tool? It’s so frustrating to figure out the magical combination of diet, water intake, etc. with so few tools.
Fredric L Coe, MD
Hi Joe, No. But any physician in the US has access to Litholink that produces a fine set of data. I would certainly have it used for your care. You are right about many variables, and they need to be correct and all present at once. Regards, Fred Coe
Just wondering how you would treat patients with short-bowel syndrome who must drink ORS to maintain hydration. Obviously analyzing the stone would be crucial. Their diets are so limited anyway, it’s difficult to put on more restrictions. I would be inclined to have them avoid the highest oxalate foods, get calcium with meals and possibly add the K citrate regularly? Other tips or specific resources for this? Of course, these are short-bowel patients with colon attached.
Fredric L Coe, MD
Hi Merin, I suspect you are a physician, or other kind of health worker. These are very complex problems. I have found it very hard to lower urine oxalate and suspect hepatic oxalate production may be increased. Calcium additives to bind oxalate, low oxalate diet – none work well. Cholestyramine is poorly tolerated. But overall urine volume is an issue in a lot of these patients and hydration fluids are key – as you imply. I would usually try tot push that as far as possible and be guided by 24 hour supersaturation values. Regards, Fred Coe
Robin P Clarke
“I have found it very hard to lower urine oxalate and suspect hepatic oxalate production may be increased.”
Have you tried increasing vitamin B6? It’s been known (and probably forgotten again) for 60 years that B6 deficiency causes glycine to be converted to oxalate, and addition of B6 stops the oxalate formation. More at Page 184 of Adelle Davis Let’s Get Well.
However, people are recently saying that the problem of “oxalate dumping” is very non-simple, once you have oxalate deposits it doesn’t just respond like a machine you are oiling. Instead there is an effect also found in mercury poisoning detox, that there is a change from “locked down” to “let it flow out”, with the latter confusingly resulting in worse rather than better.
Fredric Coe, MD
Hi Robin, I usually do not approve posts with advertising for a commercial entity but did in this case. For readers I need to demur concerning oxalate dumping and the like. Absent kidney failure serum oxalate is in the range of 1 – 4 umol/l, so the calcium x oxalate product is an order of magnitude below that needed to form crystals. Oxalate itself is a metabolic end product. So systemic oxalate storage (deposits) is limited to renal failure and the rare primary hyperoxaluria states. Oxalate itself cannot deposit apart from calcium oxalate crystals. Regards, Fred Coe
Hi Fredric, I’m so interested in your findings. I’m making 80% phosphate (apatite) and 20% calcium oxalate monohydrate stones. I’m confused as how to prevent more. I had my parathyroidectomy as was diagnosed with Primary Hyperparathyroidism in 2014; thought that would cure me; but since then have had at least 3 episodes of 9mm blocking stones. I am at my wits end about what to do? I had shock wave lithotripsy but this made me sicker as my inflammation markers went up and my kidney function went down to 50% so they kept me in Hosp until I got better and then did the laser ureteroscopy. The urologists seemed to be arguing about my receiving the shock wave treatment as one said it was barmy to give me that? I am worried my kidneys are getting damaged as more form? I am 50 and female. Many thanks Angie
Fredric L Coe, MD
Hi Angie, Are you sure your PHPT is cured? In other words, are fasting morning serum calcium values below 10? If so, you have the problems of a routine calcium phosphate stone former, and they are significant. I would avoid ESWL as the stones will not break up easily – ureteroscopy is better. The article outlines prevention but it is tricky, and if you can consult an expert – I do not know where you live, but could try to help find you someone near – things might be simpler. There is also telemedicine. Regards, Fred Coe
Hi Fred, thank you so much for your reply; you’re so kind to respond! I live in the Uk. I have had follow up blood tests which showed my calcium was back to normal levels; but they weren’t fasting morning tests just a normal day routine one. They said I was “ok” regarding my primary hyperparathyroidism; so I accepted that as conclusive. From what you’re saying I need to ask for a morning fasting one? Is that different? I’m worried my PHPT isn’t cured then? Or that I’m just a phosphate former. Thank you for replying I am so grateful. It’s hard here in the UK to get any follow up at all sadly. We are just left alone and scared. Could you tell me what telemedicine is please? I am beginning to think I am a phosphate stone former and I feel very scared about my future.
All the best
Fredric L Coe, MD
Hi Angie, I believe I answered this (above); if not please reply for more. Fred
Thank you for your reply; much appreciated. I will ask to have a fasting serum check as not had one: only normal blood tests have been done which say normal calcium. I think I may be a phosphate former, which I’m finding very scary. What is telemedicine please? I am in the UK and our follow ups are non existent so I feel quite lost to be honest and need more investigation which I can’t seem to get here unfortunately. Do you know anyone in the UK I could get advice from ? As I’m so worried about my multiple bilateral stones.
Fredric L Coe, MD
Hi Angela, For consulting that does not require physical examination, we visit via Zoom, which is a world wide video platform. The only problem is that your insurance is via the national health service which is unlikely to pay my university in Chicago. I no longer know physicians in UK who specialize in kidney stone prevention, unfortunately. The NHS has lots of material; here is there general introduction. I imagine within your region there is an NHS group of specialists. Regards, Fred Coe
Hi Dr. Coe,
I came to your website in hope of finding a more robust answer to why thiazides prevent stones. What I found instead, was a complete treasure trove of knowledge. I am an M2 at Des Moines University in Iowa, and I am giddy knowing that this resource exists. You have written with eloquence, enthusiasm, and depth, and the interwoven references to medical history and art history captured my attention immediately. Thank you for your contributions to medicine and the medical humanities from a hopeful future educator, writer, and physician.
Fredric L Coe, MD
Hi Mikayla, Thank you for the note, and I am happy the site is a value for you. Regards, Fred
I am a 60year old petite female 110lbs. Have been diagnosed 12 years ago with osteoporosis. Which doctors have told me is a result of having kidney stones. They are calcium oxalate stones. Have had many 24 hour urines and blood tests. High calcium in urine but not blood. When I was in my 20s they told me I had something called medullary sponge kidney. Not sure exactly what that is but would this be why I have so many stones. For the past 26 years I have passed stones and have had surgery for some and lithotripsy. Every time I have a cat scan they see multiple stones in both kidneys. I am currently trying to pass a size 4 which is I can usually do but this one is taken longer than usual. My recent cat scan shows approx. 10 stones in each kidney the bigger ones averaging size 3-4. Saw your article and will try low oxalate diet. Do you know anything about medullary sponge kidney and stones?
Fredric L Coe, MD
Hi Patty Jo, Genetic hypercalciuria causes abnormal bone mineral loss when diet calcium is low or sodium intake high, or both. In general, given all of your stones, diet and meds might be a good idea. Here is my best article on what I think is your problem. Diet oxalate is usually a very minor issue. Likewise, with so many stones, be sure they are really calcium oxalate – I suspect they are calcium phosphate. As for MSK, it is unlikely, though possible. Here is my best on that. Regards, Fred Coe