IMG_2303IMG_0827Medullary sponge kidney (MSK) is more spoken about than witnessed, and more witnessed than accurately diagnosed.

This patient adds to the 12 we have described in our publication, and adds also in having a very long and evolving history with one of us (FLC).

We write for a general audience yet hope to include a level of detail that satisfies physicians and scientists. Here, we may fail of clarity to the one audience or of a sufficiency to the other because the disease is complex. But withal, the evolution of diagnosis and care for this person so educates and the surgical anatomy and histopathology so instructs we have chosen to share the experience.

What is it we are sharing?

MSK is a Unique Disease

MSK is remarkably specific in its anatomy; nothing else is really like it. The terminal nephron segments are tremendously dilated and often filled with innumerable round tiny stone particles. The papillary shapes are distorted by these filled chambers so they become round instead of conical. The masses of tiny stone particles give a radiographic picture that can resemble large collections of stones or calcified papillae, but are neither. Renal tubular acidosis, or just ‘nephrocalcinosis’ come to mind and appear on radiology reports, but neither is the right answer.

The tissue itself is specific to an exactness. The massively dilated papillary collecting ducts are lined by multiple layers of cells, whereas all other people have tubules lined by a single layer of cells. The cells in the interstitium – the spaces between the tubules and vessels – look like those found in embryonic kidneys. The scale of the duct dilation is so great one loses perspective.

MSK has Few Unique Clinical Traits

But for all that, patients with MSK present to even the most discerning clinical eye almost no distinctive traits. They can look like any calcium phosphate stone former can look – papillary calcifications, perhaps multiple stones retained in the kidneys, and little else. When intravenous pyelograms (IVP) were popular, one could diagnose MSK if the contrast agent tracked into the dilated ducts and overlaid the stones there. But obstruction from a stone can create the same ‘pyelotubular backflow’, or can seem to, so diagnosis was fraught. Almost no one does IVPs anymore, because CT scans without contrast suffice for most patient care.

Renal tubular acidosis can come to mind: Masses of renal crystals seem to provoke the idea for physicians even when the blood is normal. ‘Incomplete’ renal tubular acidosis was a name coined to describe patients who formed calcium phosphate stones and had both normal blood and a more alkaline urine pH than 6.5 that did not always fall as much as one might expect with acid loads. In 1992 this patient was so named and treated by FLC who would never use the term today, and by his fellow at the time who is now a world famous kidney stone expert.

Perhaps the most reliable clue to MSK before surgery is done, one we only recently understood, is the combination of a kind of ‘nephrocalcinosis’ with calcium oxalate stones in the absence of remarkable hyperoxaluria.

Nephrocalcinosis is a worn out term, as vague in diagnosis as it is rich in associations. It can mean small calcifications that involve all or most of the papillae, or massive calcifications that fill whole calyces. Frequently one sees the latter, masses of crystal, with calcium phosphate stones, or uric acid or struvite stones. By contrast, calcium oxalate stones usually create the pattern of multiple, bright, small calcifications on individual papillae. It is marked hyperoxaluria that can produce masses of calcium oxalate crystals.

The reason we find massive calcified deposits associated with calcium oxalate stones in MSK is that the tiny proto stones are calcium oxalate yet can bundle in huge numbers within the dilated chambers of the terminal ducts. FLC and his now famous fellow missed the diagnosis despite masses of crystal by radiograph and calcium oxalate stones because neither knew what we know today. The marginal IVP changes of MSK were dismissed because they occurred on the obstructed side.


We are writing this, but separately. FLC is the physician so he writes as ‘I’. AE is the anatomist, and he writes his sections as ‘I’. ‘We’ is reserved for the amalgam of the clinical and anatomical.

The Initial Evaluation

I saw him about about 24 years ago when he was about 25 (real ages and personal details are blurred but accurate enough). He was healthy apart from a recent kidney stone passage, and had been referred to me by a friend. The stone was 65% CaOx and 35% calcium phosphate as hydroxyapatite – no brushite. Because the stone analysis lab used optical microscopy we learned that CaP formed the inner layers of the stone and CaOx grew over it.

An IVP showed ‘bilateral nephrocalcinosis’, but the left side was the more prominent. That side showed marginal evidence of medullary sponge kidney but, being obstructed by the passing stone, prominence of the terminal collecting ducts could have been secondary to the obstruction.

His family members had no stones. He worked at a high intensity job in the entertainment industry with little time to eat or drink. Accordingly there was no breakfast, fast food for lunch, but a reasonable supper with his wife. His physical examination was normal.

Three fasting serums taken between 7 and 9 am showed normal results (not shown) including serum chloride and total CO2. Serum potassium was 4.3.

Here is my table of his lab results.

The first three rows up from the bottom (1992) were done before any treatment. Dates are partly cut off for privacy.

Urine creatinine values (Cr24) were all about the same, so the collections seem reliable.

Main urine risk factors: Volume (vol24) and citrate (Cit24) were low enough and oxalate (Ox24) high enough to confer risk. His urine calcium (Ca24) varied with urine sodium (Na24) as expected but at even the highest sodium urine calcium posed little risk. Urine uric acid, potassium, phosphate, magnesium and sulfate (UA, K, Ph, Mg and Sul, respectively) were not abnormal. We did not measure urine ammonia (NH4) or urea nitrogen (UUN) at that time.

Technically, for those who are interested, the molarity of citrate (Citmol) was far below that of calcium (Camol), so more calcium was available for crystallization, and less citrate for inhibition. Urine pH (upH) was variable and thought a bit high.

His urine creatinine was high per kg body weight (CrKg) signifying low body fat – expected for a young active man. SS for CaP was higher than usual among normal people, that for CaOx was also impressive. SS for uric acid was below 1 because the urine pH was relatively alkaline.

So, long ago, I cared for a man with a calcium oxalate / calcium phosphate stone and nephrocalcinosis whose laboratory studies showed mainly low urine volume, low urine citrate, and modestly increased urine oxalate, and whose IVP showed what might have been MSK or simply the effects of obstruction from a stone passing.

I, and my renal fellow – now a distinguished professor and director of a program – decided that the low urine citrate along with modestly high urine pH arose from renal tubular acidosis (RTA) – despite normal blood findings, and also that MSK might be the cause of RTA. We treated him accordingly, with potassium citrate 25 mEq twice daily, and fluids, and planned a follow up shortly to see if citrate would rise and CaP SS not rise overly. Likewise we hoped for a new IVP after the obstruction resolved so as to see if the ‘MSK’ was real or merely an artifact.

Looking back, I see higher urine oxalate excretion rates that I would have liked to treat, and suspect it was due to a low calcium diet. Today I would never have accepted the idea of RTA.

First Follow up Visit

In 1993, his urine volume remained low (look back at the two lab tables), citrate had not risen, but urine potassium was higher and serum potassium was 5.07 so he took the medication. Supersaturations with respect to CaOx and CaP were not at all improved. I increased the potassium citrate to 25 mEq 3 times a day and insisted on a new serum potassium a few weeks later – which was unchanged.

Laboratory Follow up Measurements

In 1994 (lab tables above) his serum potassium was 4.5, urine potassium was higher at 136 mEq/d, and urine citrate and volume higher. SS for CaOx and CaP had fallen by half or more, and I felt satisfied. There were no reported new stones since 1992.

In 1995 his serum potassium was 4.4, urine citrate and potassium had fallen, and I realized he had stopped the medication. I strongly suggested he continue it and get a new kidney radiograph to follow any changes.

I heard no more from him for ten years.

Second Follow up Visit

In 2005 I got word he was passing many more stones, and referred him to my urological colleague for management. Serum values were unchanged, urine volume was low; urine citrate and potassium were back to levels seen in 1993 even though he was not taking the potassium citrate. Urine pH was no longer noticeably high. SS with respect to CaOx was very high as was that for CaP – though this latter was below his peak in 1992 and 1993.

I saw him clinically in 2006 after the 10 year hiatus, and he explained he had stopped all treatment in 1995 as I had guessed. He had many stones in his possession and planned to send them to me for analysis. I re-instituted the potassium citrate and more fluids. My records do not indicate if he saw a urologist or what may have happened.

I heard no more from him for 10 more years. The stones were never sent, never analysed.

Third and Fourth Follow up Visits

Third Visit

In the spring of 2016 he came back because of more stones. During the 10 year interval he had passed no stones – which hiatus he ascribed to more fluids – but recently had begun to pass them again.

First there was a new stone, then up to 10 or 12 more. Several of these were analysed. One was 100% CaOx the other 88% CaOx, 12% HA. His serum bicarbonate and chloride were normal, as was potassium (not shown). Urine (lab table is above) showed high volume, and the best citrate ever; the low urine calcium and high oxalate were ascribed bristol-upper-pole-posteriorto excess vitamin C and high oxalate diet along with a rather low calcium intake; SS with respect to CaOx bristol-upper-pole-stoneswas much lower at 4.5 and for CaP was below 1 mainly from the high urine volume.

Urine ammonium (NH424) and sulfate (SUL24) both in 2005 and 2016 were unremarkable. In ‘incomplete’ RTA the former is thought to be higher than normal in relation to net acid load – the sulfate. I did not comment about this in my records as the idea of RTA was no longer one I would consider.

I suggested a lower diet oxalate, continued fluids, and left out the citrate given the history of no stones for 10 years without it. I ordered a new CT.

I believed after this visit that perhaps his new spate of stones was provoked by vitamin C loading – from ‘Airborne‘ and 1000 additional units of vitamin C daily. The Airborne products contain about 1000 units of vitamin C in each pill, so with his supplement the amounts could have been quite large.

Fourth Visit

I saw him again after the CT was available.

Calcifications were only left sided but involved both the upper and lower poles. The deposits were large, and I could not tell if they were stones, calcifications in kidney tissue, or both.

Transverse views confirmed the disease limited to the left side.

Review of my drawings from 1992 showed calcifications on both sides, which was puzzling. The actual radiographs are no bristol-cross-sectionlonger available.

I was puzzled, and still am, about the conflict between my old drawing and the obvious unilateral stones, but had become convinced the present stones needed to be removed. They seemed large enough and so positioned as to obstruct flow out of calyces and gradually cause injury. Obviously they would never pass.

Lithotripsy was not a consideration nor ureteroscopy – too large. This left percutaneous nephrolithotomy (PERC) that has the advantage of offering – in potential at least – a stone free kidney, and I chose that course assuming my surgical colleague would agree.

As for his stones, I now suspected they arose from a hectic and complex work life with poor hydration and high urine oxalate. His urine oxalate had been hefty all along and there was the recent vitamin C loading. Even so, my notes expressed considerable doubt about the why of it. Of interest he made clear at this visit that he had renal pain that had been present for years and always left sided. My notes had never before recorded this fact. As for RTA the idea was foreign and unacceptable to my mind.



At PERC he had the characteristic papillary changes of MSK. The papillae in the upper pole of the left kidney contained many cavernous spaces filled with stones.

At the left of the panel to the left of this text a stone peers out from inside a dilated duct, and a larger one, in the middle of the panel, reaches out of its duct, one side of it a jagged glittering blue white.

The tissue itself is diaphanous and layered, seen well in the partition between the stones in the left and middle ducts in the image. Beneath the surface lies a maze of dilated ducts filled with stones; the openings to two of them are at about noon and 1 pm in the picture.


Imagine a family come to farm the land above the hollow shafts and tunnels of an unsuspected cave. As with time minerals in the sluggish waters consolidate into crystals and the crystals into myriad strange shapes unseen, tubule fluid in these dilated ducts – we believe –  fills with innumerable stones that appear enormous in the magnifying lens but are to the eye unaided tiny.

Seen in another papillum, at right, is the opening of such a duct and to its immediate left, facing toward the leftmost light colored stone in the tunnel – as though it were a mirror, a bulge below the shiny covering of the papilla marks another tunnel not yet opened and filled with stones.

We have shown MSK in another article, and detailed there the laciness and tunneling, and even in a movie the unroofing of some tunnels so one can peer down into them from above. Likewise we have already spoken about how ductal dilation comes about in the development of the kidney which goes awry.


A biopsy from the papillum stained with Yasue stain shows no crystals. The linings of the large collecting ducts – enormously larger than normal – are not in a single layer of cells but three layers or more. These are two of the three diagnostic traits of MSK. The third diagnostic trait is the very cellular interstitium – this is easy to see at nine o’clock where the cells become lacy looking because they have the traits of embryonic cells with many extensions off the cell bodies.

Some idea of the tremendous enlargement of papillary collecting ducts can be obtained by looking at the four or five smaller round ducts down toward 6 o’clock and ringed about the upper surface of one of the huge ducts. These are also papillary collecting ducts and even though they are much smaller than the huge ones they are still somewhat larger than normal. Even these are lined by multiple layers of cells – this is hard to see at the magnification of the slide.

So, given the enlargement of the smaller round tubules, and that the dilated ducts are perhaps 10 times larger, the overall dilation of the large ducts is perhaps 15 to 20 times normal, an immense distortion.

Fifth Visit

Looking Back

After the surgery, and with the truth of things made evident, I thought about the years behind and that I had not taken very seriously the idea of MSK first raised by an IVP long ago. In his recent CT he had one sided massive radiographic nephrocalcinosis. This itself could have been the reflection of any number of conditions – calcium phosphate stones only on one side, for example. But his stones passed were mainly calcium oxalate, a fact more evident in his recent than his first visit. Medullary sponge kidneys more often have calcium oxalate than calcium phosphate stones.

There was also the slightness of his urine abnormalities compared to the extreme amount of renal mineral deposit. If indeed stones in MSK form as in a cave, from stagnation of tubule fluid in blind end dilated ducts, then even the most normal urine chemistries are sufficient because calcium oxalate supersaturation is near universal whereas calcium phosphate supersaturation is not. I could have been, perhaps, more prescient.


Given that no trials have ever focused on this uncommon disease, and the formation of stones may well be simply spontaneous crystal formation from supersaturated tubule fluid stranded and stationary in dilated ducts, my tendencies would have been simply to lower supersaturation by any means possible. This would lead me to a 1,200 mg calcium, 1,500 – 2,300 mg sodium diet. Compared to present calcium and sodium intakes, the higher diet calcium will lower urine oxalate and the lower sodium intake will prevent a rise in urine calcium. Likewise the higher the fluid intake and urine flow the lower the supersaturation. And, given that refined sugars raise urine calcium abruptly in even normal people, I would prefer he avoid them. In other words, I would have wanted the kidney stone diet which is the modern healthy people diet for Americans. Finally I would have eschewed oxalate loading from any source.

I had at the beginning used potassium citrate for his treatment, based on a pattern of thought I would no longer be guided by. Yet he remembered it and that his stones seemed less when he used it. So at his request I added it back. He is due for a new low radiation dose CT in a while to see if his kidneys are really stone free, and I suggested he wait to use the drug until then.

This Case in Large Perspective

Our Prior Work

As against our other reported cases, this one would be as abnormal as any we have seen. The duct dilation, multilayered epithelium, and lacy aberrant interstitial cells are remarkable. Our surgeon had no difficulty in diagnosis during PERC because the dilated ducts and abnormal papillary shape were obvious.

Yet, an experienced clinician was surprised altogether, even being one of the authors of our paper.

You who practice, beware: MSK is as easily underdiagnosed as overdiagnosed, renal tubular acidosis likewise, and the lesson is clear. Radiographs are of minimal use. Only ureteroscopy can be definitive, as can PERC.

One takeaway is the combination of calcium oxalate stones and minimal urine stone risk abnormalities with massive nephrocalcinosis.

Because stones seem to form in stagnant chambers the lower the supersaturation the better. Likewise for higher urine citrate – as an inhibitor.

New Published Work

We have already commented in our paper about the probable cause of MSK as a developmental defect of the kidneys and urinary tract. But recent work since our paper suggests MSK can be associated with other genetic diseasesThis new paper reviews prior reports of linked genetic defects with MSK and adds to the list. Of 143 cases of MSK 6 – all men – had associated defects that involved the heart of brain or – on one case – was Marfan syndrome. In two cases relatives also had MSK. A prior paper from this group found an additional 7 patients with developmental disorders. This makes a total of 13 of 143 cases or nearly 10%.

My personal concern with this work is how MSK was diagnosed. In the paper, and confirmed by private email correspondence with one of the principal investigators, it is clear that contrast radiographs were always used, so one can believe that dilated ducts were directly visualized. One hopes that as URS and PERC are needed for stone management the diagnosis will be confirmed more directly and those comparisons published. This is a very important cohort and the findings of linked genetic and developmental defects of long term interest.


  1. Diane

    Hi Dr. Coe, I was recently diagnosed with MSK, and I am relieved to find your website. Thank you so much for it. I did not think to question my diagnosis but after reading your site, I want to make sure that the diagnosis is accurate. I had a CT scan w/wo contrast and the findings are as follows: “left kidney there is a punctuate calculus in the upper pole and a punctuate calculus in the lower pole. Right kidney there are multiple small and punctuate calculi in the mid and lower kidney. Largest inferiorly measuring up to 3mm. Calculi are seen mostly at the medullary pyramid tips. Urographic images demonstrate bilateral multifocal renal tubular ectasia. There is no hydronephrosis. There is no evidence of renal mass. The urinary bladder shows no focal finding. Impression: bilateral MSK with bilateral nephrocalcinosis.” My urologist also performed a cystoscopy which was negative. Should I have a second opinion or further testing to confirm the MSK diagnosis? Also, separately, the CT scan revealed a pericardial effusion, which led to an echocardiogram. The echo found my mitral and tricuspid vales to have mild regurgitation and trace regurgitation for the pulmonary valve. I was shocked and overwhelmed by all these findings at once and the link on your site to the NCBI PubMed gave me a much needed possible explanation. I’m 50 and have always led a very healthy lifestyle. Thank you.

    • Fredric Coe, MD

      Hi Diane, I gather you had a CT with contrast and dilated terminal ducts could be seen. That is sufficient for diagnosis. Prevention is much the same as for all stone diseases and you should pursue it. I hope things go well with your cardiac issues. Regards, Fred Coe

      • Diane

        Thank you so much for your answer. Yes the CT scan was with contrast. I don’t recall having a 24 hour urine test as is recommended on this site (however the doctor did send a urine sample to a lab). Is that something I should request from my doctor? My doctor told me to drink at least 2 1/2 liters of water each day, preferably with lemon, follow a low oxalate diet (I am eliminating the big offenders), and come back in one year. Thank you again and kind regards.

        • Fredric Coe, MD

          Hi Diane, As much as I admire the diagnosis from an infusion CT I do not much believe in treatment without 24 hour testing – too random and often ineffective. The high fluids are always a good thing. The lemon is simply for taste as if one really needs the potassium and citrate lemons contain one would need a large amount of them and there are better ways to do this. Without a 24 hour urine how could you know if citrate matters at all. Regards, Fred Coe

  2. Candice Jarrett

    Hi Dr. Coe,
    I have been diagnosed with MSK (about 5 years now.) Medullary Nephrocalcinosis in both kidneys, renal pyramid calcification and scarring in the upper and lower poles of each kidney. I currently have 3 kidney stones which are named, though they are small at the moment. I have gotten a UTI once a month for the past 4 month. My Issue is pain. I don’t like taking pain medications either. I have a life to live. but I find if I don’t take something then I don’t sleep at night. I have to apply pressure to my kidneys in the form of lying on a pillow, and placing a heating pad on top of it (the heating pad really help). I have read MSK is supposed to be a “benign” disease. but I am constantly in pain. all day every day. It waxes and wanes but is always there and drs look at me like i’m some kind of drug seeker. Even though I take my potassium citrate as ordered and only take 1 pain pill at bedtime and that’s it. ibuprofen during the day. when I run out of medication, its unbearable. My questions is A.) Is this a finding that you periodically see in the setting of MSK B.) How do I explain to my Dr. what I am feeling in order to try to get some help. This is no quality of life. I recently moved. So trying to find a new Dr who understands hasn’t helped either. Thank you so much for any advice.

    • Fredric Coe, MD

      Hi Candice, You are part of a huge ‘small stone pain’ community that raises the issue of whether surgical removal would be a benefit. In your case I have some doubts about what is wrong. The polar scaring sounds more like reflux nephropathy than MSK and possibly you have infection. Your physicians may want to pursue the latter issue as infection can lead to pain. Your UTI history supports my suspicion of infection in the kidneys. Perhaps the stones are infected. The key physician you need is a very skilled stone oriented urological surgeon. Regards and hopes for getting the right person, Fred Coe

  3. Deana

    This was a fascinating article! I had an 8mm stone removed from my left ureter by ureteroscopy on Jan 11th, after having occasional agonizing pain episodes for 2 years. I found out in October that it was a stone and tried to pass it but failed. I’ve still be getting pain in my kidney and the same kind of ‘twinges’ in the left side of my abdomen that I had when the stone was still there. Is that normal for a while?

    • Fredric Coe, MD

      Hi Deana, The pain may be from ureteric irritation and should abate. If it does not let your surgeon know who will figure out the problem. Regards, Fred Coe

  4. Jody Sulesky

    I had 5 golf ball stones removed in April, 2016 from my left kidney. Stent placed for 30 some days. I had emergency surgery a week later because my stent became blocked. In Sept. 2016 I had ESWL with no stent. I passed a few stones. I started in August on HCTZ (fluid pill). X-Ray in late October showed 1 small stone in each kidney. October thru December 2016 I passed 19 large stones on my own (10 to 13mm). 8 of the stones were tested in November came back as being 80% Calcium Phosphate. I have changed my diet, low sodium, low protein for the last 3 months. Should I be taking another supplement along with the fluid pill and do these kinds of stones for quickly?

    • Fredric Coe, MD

      Hi Jody, I doubt you have MSK even though you reference your comment to that article. Given such vast amounts of CaP stones (I presume the 20% is calcium oxalate and that brushite is not named) I would do low sodium and high fluids and a thiazide type diuretic – this last does nothing to urine volume, it lowers urine calcium excretion by a direct effect on the kidneys and only works well when salt intake is low. I favor chlorthalidone 12.5 mg daily and check if urine calcium is low; if not 25 mg daily. Low protein means normal, 0.8 to 1 gm/kg/day, there is no purpose to restricting below the normal requirements. Calcium intake is important for bones, and when high and with meals reduced urine oxalate. Take a look at the right article for you. Regards, Fred Coe

  5. Victoria O'Neal

    Dr. Coe, I was told by a Urologist that I have MSK in my left kidney (25 years ago). It has never been mentioned since. I do not recall ever having a completely clear CT in the past thirty years, although I may have had ONE a month after lithotripsy. The largest stone that I have had to my knowledge was 9mm x 5mm x 3mm and I passed it at home–I had four small children and there was no time for an ER visit or surgery!. Although I have had many stones, they are small. Some of them causing me A LOT of pain and eventually needing some help getting them out.Most I have passed. I am usually very active but find this current battle with stones has left me discouraged and exhausted. The 5mm stone and 6mm stone that landed me in the doctors office in early December were gone December 29. However there are three “new” tiny stones. Is it possible MSK is causing the pain? Or movement of the stones.? I am about to get a “million dollar” work up because the doctor insists these stones are not causing my pain and nausea. I am baffled and frustrated. The nausea and pain are real and thankfully not due to a neoplasm-workup so far unremarkable. My blood calcium is low right now. (anorexia due to nausea?) I was on a low calcium diet for 16 years, (late 80’s – 2002) then the doctor put me on low oxalate due to my age with the risks of osteoporosis outweighing the benefits of the diet. It didn’t seem to change the number of stones I am making. The only thing that seemed to help was HCTZ and increased water. Could MSK be the issue? Thank you for all of your wisdom. I just discovered your site yesterday and am reading as much as possible.!

    • Fredric Coe, MD

      Hi Victoria, Firstly I am always sceptical of MSK diagnosed by CT alone; usually all that is seen is numbers of tiny stones that could be from any number of causes. One clue is that the stones are indeed calcium oxalate and that the calcifications involve more than the tips of the papillae – subtle enough distinction. Whatever about MSK you are forming stones and have pain and it is very hard to say stones are not the cause of pain when present. Usually prevention of stones will gradually obliterate the pain. Take a look at these two approaches to prevention, and be sure they have been done right and abnormalities treated. From your note I am not sure. Putting it altogether Stepwise approach to stone evaluation and treatment Regards, Fred Coe

  6. Celia Grace

    Hi Fredric, I notice Heather commented above, Heather is one of our group members who has been suffering from chronic MSK pain for years, like so many others, including my sister Laura. I’ve been told that pain becomes chronic when it lasts or continues for more than 3 months. Heather, my sister and so many other group members have been suffering from this same chronic pain for years!
    We’ve all been wondering for so long, what causes this chronic pain in their MSK (Nephrocalcinosis RTA stones pluggings pyelonephritis chronic uti’s). We’re not scientists, anatomists nor world renown researchers but we’re still hoping you experts can figure it out, and let us know. If not a treatment or even cure, this information would help our MSK group members afront and deal with ER Drs and nurses who continue to ignore and underestimate their pain, have the nerve to ridicule them and send them back home with no medical assistance, even in emergency cases of urinary tract obstruction, active stones and pyelonephritis with risk of sepsis! All because they’ve never heard of this MSK!
    We know you’re following our group, we know you care and are trying to help with stone prevention, we trust in you for bettter MSK awareness in the medical community.

    • Fredric Coe, MD

      Dear Celia, Of course we do not know. Partly it may be inflammation, from stones, from surgeries, from infections. A huge question is whether surgical removal of plugs or unroofing of cysts will improve pain or not. Such a trial would be invaluable in planning for treatment. Prevention is my main theme and I see no reason why it should not be pursued with vigor for and by every patient. Many are frustrated by what appears to be inconsistent results, but I believe that much of those inconsistencies can be remedied. I am especially interested in what patients can do for themselves to bring that about. Regards, Fred

  7. Michelle

    Does exercise help prevent stones? Is walking a helpful way to prevent stones? Thank you for your time.

  8. Heather Murphy

    Dr. Coe, I, too, was properly diagnosed with MSK and nephrocalcinosis after my urologist did a lithothripsy to remove a 7x14mm stone, blocking my ureter. She noted that my kidney was full of Randall’s plaques and embedded stones …

    As with this patient, I have severe flank pain, even thought I am not able to pass my very large stones. What is your takeaway as to stones that remain lodged in the kidneys; is it possible to the kidneys to feel pain? I have a very rough time with flank pain (I have bilateral MSK) when I do even the simplest chores around my home or grocery shopping, or even walking around for too long. Unfortunately, many medical professions believe that flank pain is ‘muscular’ unless there is an active infection or blockage.

    I greatly appreciate you posting this article, as well as your expertise and continued research on MSK.

    • Fredric Coe, MD

      Hi Heather, Embedded stones and plaque are not so characteristic of MSK as they are of brushite stones. Be sure about what was found in you. MSK creates large cavitary cysts filled with tiny stones, and these can be unroofed. Plugged tubules can, too, but with more hazard and restraint. Plaque is not part of MSK and is rather modest in such patients. Stones are calcium oxalate in MSK for the most part. As for pain, small stones do seem to cause it, but surgical treatment has not been proven effective thus far. Pain that worsens appreciably with movement or exertion may well be muscular, because renal pain tends to be interior and not much influenced by motion – as a rule. Regards, Fred Coe

  9. Cecile Behymer

    I was diagnosed with MSK in 1978 by an IVP at age 24. My life has been filled with a tremendous amount of stones and suffering and am fortunate to be under the care of a terrific urologist in Indianapolis, whom you know. Thank you for your dedication towards kidney stones and particularly MSK. I was very interested in your reference to genetics, as my daughter was born with Gitelman Syndrome, and I have always thought it was strange with both of us having such bizarre abnormalities of our kidneys. Have you come across this genetic kidney defect before in your studies of MSK?
    Thanks again.

    • Fredric Coe, MD

      Hi Cecile, No, I have not encountered this linkage but it is now on the site with the case so everyone can make the connection. As for your terrific urologist, he is. Regards, Fred Coe

  10. Celia

    Very interesting Fredric, I see you are reconsidering an old case, this is a good sign, it means there’s still hope for our MSK members, all diagnosed with MSK, most make ca-ox stones, but many CaP (my sister Laura) most suffer from chronic renal colic, many of chronic uti’s/pyelonephritis, most diagnosed with nephrocalcinosis, recurrent stones, RTA, hypocitraturia, high urine Ph, hyperoxaluria but not only, many other coexisting disorders like autoimmune EDS, lupus, RA MS Raynaud’s, Sjorgren’s, Diabetes, IBS, Crohn’s, not to mention hematuria, RLS, edema and emotional disorders, depression, confusion, anxiety, etc etc, the list is much longer, our MSK is very complex.

    • Fredric Coe, MD

      Hi Celia, I did not so much reconsider him so much as his surgical findings reconsidered me. I am glad you have appended this list of associations to the case report; the article reviews new genetic associations from Professor Gambaro’s group as well. Warm regards, Fred

  11. Jenelle Huntington

    I have been diagnosed with MSK, RTA, and nephrocalciphonisos. I am a 33 year old female. I have chronic renal colic and it’s over taking my life. I follow a calcium oxalate diet and drink a lot of water but the pain is always present. I hate taking pain meds as I have three children and have a husband to care for. I have 1-2 surgeries a year to clean me out. What else can I do to make my quality of life better. I want to work. I hate not working but with the pain and low energy it’s impossible.


Leave a Reply