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. Joy Fernandez

    Hi Dr. Coe. I am so happy to find a reliable site on MSK. I am 46 and was diagnosed with MSK in 2017. I need help and would like recommendation if you know of any doctor who can help me in Manila, Philippines or Singapore. Thank you for this site!

    • Fredric L Coe

      Hi Joy, I wish I could help. I lectured in the Philippines last fall and realized they have no organized lab testing for kidney stones. I do not know the situation ini Singapore. I am truly sorry I cannot be helpful about a consultant for you, but in general the major medical schools are best. Given the lack of even testing services in Philippines you may fare better in Singapore. Regards and regrets, Fred

      • Joy Fernandez

        Thank you for your reply Dr Coe. May I know where was your lecture in Philippines last fall and who invited/organized it? Maybe it can lead me to a doctor who can help me somehow here in Manila til I find one in SG. I am based in Manila. Thank you

  2. Elizabeth Mejia

    Hi Dr. Coe,
    Oh my gosh where does one start! First thank you so much for your in depth article as it has helped me a lot in regards to my son. My son was born with multiple medical problems and has been sick since the day he was born. He has complained of stomach pain, side and back pain ever since he was old enough to talk. He was had many bouts of hematuria throughout his life. He started having kidney stones at the age of 4 or 5. In 2005 when he was 12 he had several large stones and was hospitalized with them. He had gross amounts of blood in his urine, chronically complained of side/sides, abdominal and back pain…. In October of 2005 he was diagnosed with MSK bilaterally. Since that time MSK has been questioned as to if he really has it or not. In 2009 he had an IVP at Children’s Hospital in Seattle, WA. They told us that he did not have MSK. I questioned them at the time as by this time it had come back many times on radiology reports that it was either suggestive of MSK or due to his history of MSK and that is what he was diagnosed with. A few months after he had the IVP he was back in the ER again. I spoke with the ER Dr. as by this time they know us ): … I explained to the Dr. everything that had been going on with my son and talked with him about the IVP and the results of it. He went back and looked at the many radiology reports that they had and told me that it was in his opinion from he himself looking at and reading the reports and from all the times that my son had been to the ER and treated for the same symptoms repeatedly that he does have MSK…. Now this September that diagnosis comes into question again as I was looking for a new team of Dr.’s for my son and thought that the University of Washington would be a good place to start. He had an appointment on the 16th of this month with a possible new urologist. Very disappointed in that appointment as it wasn’t even 5 minutes long, he pulled up some recent scans and told us that he doesn’t have MSK and that he has seen this happen many times. He told us that there are no calcifications along his kidneys and that the stones that he was having surgery on in 2 days weren’t big enough for that and that he himself wouldn’t do surgery as it won’t take the pain away…. So two days later my son had surgery and his current urologist removed one 9 mm one 4-5 mm a bunch of smaller ones, what she called dust (I’m guessing this might be sand) and she also told me that he had calcifications embedded in the kidney that she had to clean out…. I talked with her about the appointment with the urologist at the university and what he said. I also told her about the other radiology reports when my son was younger and the IVP at Children’s as well as what the ER Dr. said a few months after the IVP had been done. She told me that there is a broad range for MSK and everyone presents differently. My son is tired of being in agonizing pain every day of his life and I as his mom just do not know what to do for him. He doesn’t have good pain management and his PCP/Pain Dr. is a joke which is why we are looking for a new team of Dr.’s …. we have even looked into the Renal Auto-Transplant Program at the University of Utah but I can not find any long term statistics on that? My heart aches for him, I’m tired of seeing him suffer daily, I want to help him but just don’t know where to go…. What Dr.’s really know MSK and what those patients really go through who have active symptoms of MSK. What Dr.’s will not be afraid to be proactive with pain management and not tell me that it’s in his head or that he is going to be dead in 5 or 10 years as I have been told this several times or that my son is an addict…. We live in Bremerton, Washington but I am willing to take him anywhere I need to in order to get him the help that he needs (we are not rich but if there’s a will then there’s a way). His base line pain level daily at one time was a 4 and he was able to have sort of quality of life but now his daily base line for his pain is a 7-8 and he has no quality of life what so ever and he always has pain, nausea, vomiting, headaches, the same things that everyone with MSK has. He’s in his room in the basement almost all the time. He doesn’t sleep at night time (he never has not even when he was a baby). The pain gets so bad that he vomits non stop then can’t eat, the ER thinks he’s a drug seeker and won’t give him anything….. His current urologist tells us there’s nothing she can do for him if the stones aren’t blocking. I joined the closed MSK group on FB to see what I can learn from others who suffer with this disease as my son does or at least I believe he does. I see where others write about other medical problems and can relate to my son and what he has going on and has had going on. Are these problems related to MSK because it all makes sense if they are. If you could help me at all it would be greatly appreciated. Thank you so much for your time in reading this and any help that you might be able to offer, Liz Mejia P.S. my email is, could you please respond to my email as I don’t know if I’ll be back on this group

    • Fredric L Coe

      Hi Elizabeth, The most brilliant stone expert near you is at UCSF – Dr Marshall Stoller. I would suggest you consult with him. The problem is very complex and he has the resources to help materially in clarifying matters and seeing a way to treatment. Regards, Fred Coe

  3. Jessica

    I also forgot to add on my first entry, that I am unaware of any passed stones. I have never actually seen or filtered a stone from my urine. Also both of my kidneys are affected and do have visible calculi within calyces or pyramids, spread throughout many locations/lower poles of both the kidneys.

  4. Jessica

    Hi, I am a 36 year old female who have recently been diagnosed with msk. I have been sick since the age of 17 with severe bouts of nausea, tremors and fatigue. These episodes come on suddenly and can last anywhere from 24 hours to a week at a time. During these episodes I am bedridden, unable to do much communicating or moving around. The extreme nausea, dizziness and sometimes rapid heartbeat, is almost too much for me to handle and I literally sleep the entire duration of these episodes. They have yet to find out the cause of the spontaneous episodes and the severity of them is just getting worse. The only other thing they have found besides the msk, is a genetic condition called MTHFR. I am homozygous for the c677t mutation. I have been severely affected by whatever medical ailment I have. I have not been able to work full time in almost 20 years and have seen more doctors and specialists than I can count. The msk was actually found on accident because I requested a CT scan of my adrenals to check for possible adrenal carcinomas because my symptoms are spot-on. My family doctor still seems to think the msk is not related to the severe episodes I am experiencing. I am from Evansville, Indiana and we do have a few kidney specialist, the one he would like me to see is not available until next year for an appointment. Obviously we cannot wait this long because of the severity of my symptoms, so I am settling for someone else who can get me in sooner. I am desperate and would like to think that msk has been the culprit this whole time, because quite frankly I am tired of searching and getting no answers. Can I ask a professional opinion? Can these severe symptoms be caused by msk? Are there any diseases or medical conditions that can be directly related to msk that could be causing these symptoms? Any thoughts or opinions would be greatly appreciated! Thanks for taking the time to read my questions.
    Sincerely, Jessica

  5. CiCi Behymer

    Diagnosed at age 24 in 1978 with MSK, I have suffered with passing and catching over 100 stones, probably same uncaught, and dozens of procedures. I am being followed by an excellent specialist, Dr. Lingeman in Indianapolis. I have been suffering intermittently for years with left sided pain and no evidence of an obstructing stone. Since April it has been constant severe pain, and ruining my life. How can I determine if the pain is due to my MSK or another reason? I am desperate for answers. Thank you for all your studies in this area and the guidance you provide. CiCi

    • Fredric L Coe

      Hi CiCi, I work with Dr Lingeman, and share patients. In fact your name is familiar, perhaps because you were in one of his studies. You need to let him know about the pain, so he can help you. He is one of the finest stone urologists in the world. Regards, Fred Coe

  6. Kay

    Hello: Assisting our son (35) in finding a specialist with expertise in MSK in the West Palm Beach area after a recent diagnosis. The pain from the stone was excruciating before it had to be removed and there are still some ongoing issues, with possibly new stone formation. After reading this helpful information, we realize that ensuring an accurate diagnosis by a skilled specialist will be crucial. Any recommendations would be helpful, thank you for this informative site.

    • Fredric L Coe

      Hi Kay, As lovely as Palm Beach may be, I know of no physicians there who are specialized in stone prevention. In Gainesville Fla, at the University, there is an outstanding stone center, and the flight should be not too much to undertake. Regards, Fred Coe

  7. Natalie Leach

    My son is diagnosed with medullary Nephrocalcinosis… His physician however so is that a possibility? Stop because he don’t know what to do about that. I also am not sure if we should be looking for why he has it, genetic disposition and where to go from here.

    • Fredric L Coe

      Hi natalie, I am not sure what the diagnosis is; if he/she means multiple calcifications it may be a form of kidney stone disease. Common causes are indeed MSK or calcium phosphate deposits. If your physician does not know what to do you need a referral to a center to help with the problem. If you write back where you live I can try to help identify a possible source. Regards, Fred Coe


        Dear Dr. Coe,
        I apologize for the haphazard email I had a faulty keyboard. My son, 20, has Medullary Nephrocalcinosis. He has substantial pain with it. So much so when he gets a bad flare up he throws up uncontrollably and we usually have to go to the ER for meds. This last visit he had high Liver levels as well and creatine kinase was 1008! We live in Atlanta and I really need some help with this. Any information is greatly welcomed.
        Thank you,
        Natalie Leach

  8. Marie

    Hi Dr. Coe,
    I am a healthy 62 year old woman who was diagnosed in my 30’s with MSK. At the time I had multiple calcium oxalate stones, 75%, that were removed using lithotripsy. My urologist at the time prescribed Miacalcin or Calcitonin Salmon nasal spray which I have taken since. A recent study has indicated that these meds may have a slightly higher cancer rate
    (2.9-4.1%). At this point I wonder if I really do have MSK and if I need this medication (your opinion). I realize that I should be taking calcium along with my Vit. D. My stone formation has been kept in check for the most part. Occasionally I feel kidney stone pain and increase water consumption and even use a slant board. I do not have UTI’s which are connected to MSK. I drink about 80 oz. of water daily and follow the oxalate diet. Due to acid reflux, I am careful about consuming too much acidic foods. Over the years I have had several GP’s and none of them address MSK. A recent lower middle back pain prompted me to search for a qualified urologist in southern NH or Mass. who can test to determine if stones have been forming and where I should go from here. Any recommendations? Your site has been a great resource and I thank you!

    • Frederic L Coe

      Hi Marie, I would not personally want someone on calcitonin so long term, and I do not know that it has a role in stone prevention. The longer article on MSK makes clear that stones probably form because of stagnation, so the hormone would have little role. MSK is much over diagnosed, and you may have it or not. If a urologist wants to do anything about stones in your kidneys I would advise ureteroscopy that permits direct visualization. Given little pain, is surgery even important to you? Perhaps a new CT – if none for some years. As for local physicians, Boston is the one place I know of. Dr Gary Curhan at MGH is very skilled, and he would be a good choice. Regards, Fred Coe

  9. Jupiter Ranger

    Thankful for your information and grateful for your time xo
    I have msk kidneys and am as I type passing a 3 mm stone from my left and waiting for , another surgery, on the right 6.3 mm (first surgery did not work ..)… having it removed from the back…both kidneys are active with stone movement…
    If I could say one thing to any fellow friends it would be … try getting a license for weed and smoke every 4 hours … when needed … it’s not for everyone but nor is morphine.
    The pain with this condition is real , with or without active stones… it is my personal goal to change the paragraph written in the text books here in Canada for future students…
    I am in search of a specialist in London Ontario Canada that you might know or heard of that I can work with…who is msk kidney knowledgeable xo
    I am reaching as far out as I possibly can ,I thank you from my heart

    • Frederic L Coe

      Hi Jupiter, A very large number of patients who have considerable numbers of stones in their kidneys have pain without stone passage, as you do. You need not have MSK for this, as a majority do not. If your surgeons have seen inside your kidneys via ureteroscopy or percutaneous nephrolithotomy and have seen the sponges, then you have it. Otherwise, radiographic diagnosis can be quite wrong. This does not matter to your main issue which is pain even without stone passage. This latter – or last – can be from passage of crystals. You can tell if it feels like stone passage but there is no stone. Sometimes the crystals can be seen in the urine under a microscope. Sometimes the urine appears milky. In others, there are no crystals and the pain is of unknown cause. Also unknown is whether surgery will help, no trials have been done. As for a referral, I am afraid I am not very worldly and do not know who might be there. Regards, Fred Coe

    • Jocey

      Jupiter…please look up Dr. John Denstedt from London Health Sciences Centre…he has been around a very long time, he did lithotripsy on me 30 yrs ago and still follows my brother for his stones.

  10. Jennifer

    Hi Fred. Thank you for the excellent article. I was diagnosed with MSK in 2014 and was just told to increase fluids. Since that time, I have been pain-free, but have felt increasingly “acidic” which has caused dry, cracked, bleeding hands and feet, only relieved by drinking sodium bicarbonate upon arising each morning. I live in northern NJ and I’m having trouble finding a nephrologist with good knowledge of MSK. Can you recommend a physician in the northern NJ-NY metro area? Thank you.

    • Fredric Coe, MD

      Hi Jennifer, Dr David Goldfarb at NYU is outstanding and I would recommend him. Regards, Fred

    • Barbara

      Hello. I too was just diagnosed with MSK in northern NJ. I have been having stones for the passed one year. I have had 2 ESWL and 4 ureteroscopies but have never passed a stone! I was hospitalized for sepsis twice. I am just trying educate myself and trying to prevent stones from forming as I get some work up done.


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