The Diagnostic Dilemma of Medullary Sponge Kidney


Diagnosis of MSK is Increasing

Urologists and nephrologists specializing in the treatment of kidney stones seem to encounter patients with medullary sponge kidney (MSK) far more often than one would predict given the fact that this disease affects less than 0.5-1% of the general population.

One potential explanation is the high frequency of stones in such patients, nearly 70%. Stones call attention to themselves. Even so, referrals for MSK seem to be occurring at ever increasing rates, out of proportion to the prevalence of the disease.

Another explanation is that we can see more because of dramatic improvements in CT scanners and endoscopic equipment we use for stone removal.

Latest generation, thin slice CT scans can isolate tiny stones as small as a millimeter in size.  Meanwhile, modern flexible endoscopes not only visualize every crevice of the renal collecting system but are able to do so in high definition. Consequently we can identify previously unrecognized variations in the appearance of stone forming kidneys, of particular interest here nephrocalcinosis on CT and tubular plugging on endoscopy.

But diagnostic capabilities may be progressing faster than our ability to comprehend the significance of what we see. As a result, one can misclassify patients as having MSK when the correct diagnosis is another more common finding such as nephrocalcinosis or tubule plugging.

For example, a urological surgeon performing ureteroscopy with a modern high resolution digital instrument notices “hundreds of tiny stones,”, “abnormal papillary architecture” or “stones located under the urothelium” and proceeds to label the patient with MSK. Or, a patient with urologic symptoms such as renal colic, recurrent urinary tract infections, or microhematuria has a CT scan showing ‘nephrocalcinosis’ and is labeled as having MSK.

In both instances, the true likelihood of actually having MSK is, by a recent small study, only 4/15 (25%), but physicians are not generally aware of the differences between MSK, nephrocalcinosis, and tubule plugging because these are new areas of knowledge which have not been proliferated widely.

This article is one way we hope to make the diagnosis of MSK, a unique and complex disorder of renal development, clearer for physicians and their patients.

What Is MSK?

Our collective understanding regarding the development and pathophysiology of MSK is rather sparse even though G. Lenarduzzi first described it in 1939.

The Cause of MSK

The exact mechanisms that produce MSK are unknown. It is believed to be a result of abnormal renal development in utero. More specifically, scientists believe the ureteric bud – which will give rise to the ureters – interacts abnormally with the metanephric blastema tissue in the embryo which will produce much of the kidney substance.

There appears to be a genetic component to the disease. Recent evidence is that about half of patients diagnosed with MSK will have at least one relative with some degree of similar affliction. This kind of familial clustering can suggest an autosomal dominant gene expression or the actions of multiple genes giving that impression. The review of the above link is an excellent recent treatment of the matter of development and genetics which we highly recommend.

The Anatomy of MSK

MSK, as its name implies, is characterized by sponge like, cavitary regions within one or both kidneys (Figure 1).


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Figure 1 – A normal appearing kidney (left) compared to MSK kidney (right).

More specifically, the dilations occur in the inner medullary (precalyceal) collecting ducts. These collecting ducts are the terminal region of the nephrons, the individual functional units of the kidney.The inner medullary collecting ducts (IMCD) have the job of delivering urine to progressively larger ducts (ducts of Bellini) that deliver the final urine out of the renal papilla into the minor calyces (Figure 2) which connect into the renal pelvis and thence into the ureter to the bladder.

Renal Anatomy copy

One way to think of the IMCD is as a collection of streams merging and forming a river (duct of Bellini) which leads to a delta (minor calyx) and then a lake (major calyx) and ultimately an ocean (renal pelvis) (Figure 2).

Figure 2 – Anatomic depiction of kidney and collecting system

The IMCDs are not visualized in Figure 2 but if you scan down to Figure 3 just below several human nephrons which were microdissected from an MSK kidney show what is really wrong with them.

In MSK, some IMCD are dilated markedly and have outpouchings (cysts): blind sacs which begin at the IMCD lumen but go nowhere – like a hallway someone walled off at one end. It is at the ends of these hallways one finds the stones, free floating and probably trouble. Other IMCD are not dilated and do not have cystic outpouchings.

MSK NephronFigure 3 Microdissection of complete nephrons from MSK. Irregular dilation of the IMCD is present. Cystic outpouchings are present, of varying sizes. The blind ends are obvious. It is in these cysts that tiny stones are found.

Quite apart from the IMCD dilatation and cysts, the kidneys of MSK have two other abnormalities which mark it as a specific disease. Those IMCD which are not dilated nor cystic have a multilayered epithelial lining, whereas a normal undilated IMCD lining is one cell layer thick. The interstitial cells of the renal papillum – the cells between the tubules and vessels – are more numerous than in normal kidneys, and have an immature appearance much like is seen in fetal kidneys.

Why Stones Form in MSK

Elsewhere on this site we have pointed out that supersaturation is a force, a source of energy directed at forming solid phases such as stone crystals. The kinetic retardants in urine, which include citrate, stave off crystallization but can never prevent it: A supersaturated solution will eventually collapse into two phases, crystals and a residual solution precisely at the solubility point, devoid of extra free energy.

The stagnant flow as a result of the dilated MSK IMCD, and particularly the static conditions in the fluid filled blind ended cysts, are the probable reason those innumerable tiny stones form which end up packing the ‘sponges’ with masses of crystals. How MSK patients produce larger stones, big enough to block the ureter is unknown. It is not true that MSK patients have remarkably high urine supersaturations or other physiologic abnormalities such as hypercalciuria and hypocitraturia. Possibly the tiny stones somehow leave their cysts and enter the urine where they act as nucleation centers. 

Other Associations

Other common associations with MSK include urinary tract infection, microscopic and gross hematuria, and impaired renal function. Perhaps the stagnant flow in dilated IMCD and particularly in cysts, predisposes to infection. But since the papillae are abnormal in other ways it seems likely that these intrinsic abnormalities themselves must be clinically important, and more work needs to be done on the problem. 

Making the Diagnosis of MSK

Of course, when we speak of what is wrong in the MSK kidneys, and how it affects people, we base everything on knowing that a given patient has MSK. If you have a kidney from such a patient and can show the dilated IMCD, the cysts, the tri-layered IMCD epithelium, and abnormal interstitial cells, diagnosis is certain. But what can we do when we are dealing with a patient?

Radiological Studies

Intravenous Urography

Historically, the diagnosis of MSK has been made on intravenous urography (IVU). Radiographic contrast is administered and x-rays of the kidneys, ureter, and bladder are taken periodically as the contrast is absorbed and later excreted by the kidneys through the urinary tract.

The delayed phase image is essential for diagnosis. This is when contrast material fills the masses of dilated IMCD and cysts which make up the sponge.

The masses of dilated IMCD filled with contrast material produce a characteristic ‘papillary blush’ which appears like flames on the outer edges of the papillae. When particularly large it can mimic a bouquet of flowers peripheral to the collecting system.

IVP Medullary Sponge

Figure  4 – IVU image of medullary sponge kidney. The arrow designates the papillary blush in the mass of dilated IMCD space.

CT Scans and Other Imaging

Over the past 10-15 years, noncontrast CT scans have replaced IVU as the imaging method of choice for stone formers. While these scans are more sensitive in detecting small stones, the lack of contrast limits the ability to accurately diagnose MSK and has raised concerns regarding the potential for under-diagnosis of this disease.

CT does have the capability of making this diagnosis when contrast is given and CT urography is performed; though this is not used as a first line choice for stone imaging and is generally reserved for specific indications such as hematuria and concern for urinary tract injuries.

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Figure 5 – Demonstration of papillary blush (small arrows) on CT urography for patient with medullary sponge kidney.

Use of other imaging modalities have been investigated as well though they have proven suboptimal in their diagnostic capabilities. Ultrasound has poor sensitivity to detect dilation of the collecting ducts and MRI has the potential to delineate detailed renal anatomy but can not detect stones or calcification.

High Definition Endoscopy

State of the art high definition endoscopes have allowed investigators to make observations at the time of renal endoscopy correlating the appearance of the renal papillae and collecting system to specific types of diseases and metabolic derangements associated with stone formation. Because endoscopy is now being performed as a common and often preferred way to manage stones, this kind of detailed imaging of kidneys will be available more and more in the course of regular patient care and permit physicians to diagnose the exact kinds of disorders in the kidneys of stone formers. 

Medullary sponge kidney in particular has an entirely unique appearance unlike any other type of stone related disease, making endoscopy a particularly exacting diagnostic procedure. Detailed anatomic descriptions from twelve such patients each with evidence of MSK on biopsy were recently described by Evan et al.

The Papillary Malformations Seen Via Endoscopy

In stone formers the papillae often appear abnormal, a concept that merits its own post and which we can only briefly summarize here.


The renal Screen Shot 2015-06-11 at 9.37.45 PMpapilla is the anatomic subunit of the kidney where the IMCD merge together into the terminal Bellini ducts which empty into the minor calyx. Normally, it should have the appearance of a smooth walled mound or mountain without much if any calcification (plaque) along its surface. The link is to a detailed post about plaque by Dr Andrew Evan.

Figure 6 – Healthy appearing renal papilla with a minimal amount of Randall’s plaque (arrowhead).

Ductal Plugging

Another common abnormality identified in many papillae at the time of endoscopy are plugged ducts. The physiologic mechanisms for this process are currently unclear; Screen Shot 2015-06-07 at 9.48.55 PMhowever, we believe it is a reflection of injury that begins a potentially disastrous chain of events for stone formers.

Figure 7 – Abnormal papilla in a patient with severe ductal plugging. Yellow mineral deposits (arrows) can be seen protruding from dilated ducts of Bellini.

Our present assumptions are that once crystals begin to form within a duct, they damage the lining cells and the duct loses its ability to make acidic urine. This in turn raises the local pH level and leads to the growth of more calcium phosphate mineral deposits which are favored by high pH.

Unclear is what begins this process. Since these ducts contain fluid which is very close in composition to the final urine, we suspect it is high supersaturation with respect to calcium phosphate. This occurs in those patients with both high urine calcium excretions (hypercalciuria) and higher urine pH levels – above 6.2. Such patients often form stones high in calcium phosphate composition and plugging is strongly associated with formation of such stones.

The mineral deposits subsequently grow and we believe can even act as a nidus for stone formation. The corresponding papillae can look markedly abnormal and the dilated ducts are easily evident. Remnant dilated ducts left behind after the mineral is spit out or surgically removed (Figure 8) show dilation without the mineral plug.

Screen Shot 2015-06-07 at 9.48.20 PMFigure 8 – Evidence of abnormally dilated ducts (arrowheads) at the surface of a papilla.


The findings in MSK are comparable in some ways to ductal plugging; however, rather than the papillae having one or several abnormally dilated ducts, the entirety of the papillum is markedly abnormal.

Therefore MSK and plugging type papillae look remarkably different.

The MSK papillae are excessively round, enlarged, and billowy (Figure 9). 

MSK two plot from our MSSFigure 9 – A papillum in a patient with medullary sponge kidney. The papillae are rounded and enlarged with a billowy appearance. The papillary tips are blunted. No other kind of papillary disease is known to present this appearance which is therefore pathognomonic of MSK. Panel a shows dilated Bellini duct openings at asterisk; the arrows show yellow plaque – plugging of IMCD completely separate from the stones which fill dilated IMCD, the arrowheads show traces of white plaque. Panel b shows the billowy papillum with a blunted tip surrounded by calyceal stones.

In the majority of such cases, these changes are seen diffusely throughout each kidney, though segmental sponge findings are present in a minority of patients.

The differences in appearance are well demonstrated in the post by Dr. Evan and the following video.  With ductal plugging the bulk architecture of the papilla is intact though many ductal plugs are seen.  Note the way the ductal plugs are adherent to the lumen.

In MSK on the other hand, the papillary architecture has and unique, billowy appearance with massively dilated ducts and freely mobile stones within them.  The following video is from a patient with MSK.  A duct of Bellini is massively dilated and numerous tiny stones which are free floating pass out of it during the visualization as the opening is enlarged with a laser. You can see stones bouncing within the duct because of movement of the irrigation fluid.

Clearly neither papillum is “normal” and one can imagine the tendency to misdiagnose a plugging patient as a MSK patient unless the two patterns are clearly in one’s mind.

The ductal deposits themselves are an important clue. In all plugging diseases but cystinuria ductal mineral plugs are fixed within the ducts because the crystals adhere to the lining cells and often destroy them. As the lining cells are destroyed crystals fix themselves to the basement membranes, the collagen shell on which the lining cells once grew. Inflammation follows such injury with scarring and loss of the tubule segments. Deposits therefore never float free from a dilated duct except in cystinuria and in MSK. Cystinuria is usually diagnosed directly from stone analysis and urine cystine screening.

Perhaps because the tiny stones in MSK do not attach to the epithelium of IMCD there is no evidence of cell injury or inflammation, in marked contrast to all of the plugging diseases. Even in cystinuria injury occurs, not from the free floating distal cystine plugs but from calcium phosphate plugs which form in the IMCD.

Stones may cause pain in MSK despite the lack of ureteral obstruction and inflammation and cell injury. Possibly distention of the dilated ducts by masses of tiny stones could be a factor. Consequently, laser unroofing has been postulated as a potential treatment option in both disease states: those with plugging and MSK.

The video may not make it easy for everyone to visualize the stones and cavities of MSK. The 4 still pictures below show much the same thing for clarity.

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Figure 10 (a-d) – Example of laser unroofing of sponge cavity full of freely floating stones. The massively dilated MSK bellini ducts are seen in Panel a; the white speckles at 9 o’clock are tiny stones in dilated IMCD or cysts. Panel b shows a holmium laser fiber being used to open dilated IMCD or cysts.  Panel c shows masses of tiny stones free in dilated IMCD or cysts which float out as the surface is incised with the laser. In panel d, the remnant sponge cavity can be seen now free of stones.

Nephrocalcinosis and MSK

Strictly speaking, nephrocalcinosis refers to the presence of calcium deposits in the kidney tissue. Of course, this includes ductal plugging and the masses of tiny micro – stones inside cavities produced by numerous dilated IMCD in MSK. However, the word ‘nephrocalcinosis’ is also used as a radiological diagnosis which is far less specific.

Limitations of Radiology

When radiologists speak of nephrocalcinosis they can mean large numbers of calcifications within the collecting system or kidney tissue, because they cannot differentiate reliably between tissue calcifications and stones. When urologists speak of nephrocalcinosis seen during high resolution endoscopy they can specify if it refers to tissue calcifications, stones, or both, and will reserve the term for that component arising from tissue calcifications.

MSK is one of several disease states that is commonly associated with extensive nephrocalcinosis observed by radiologists. Other common conditions are stones caused by renal tubular acidosis and primary hyperparathyroidism. Calcium phosphate stone formers without any systemic disease can also produce sufficient combinations of ductal plugging and stones that nephrocalcinosis is diagnosed radiologically.

In a recent study of 67 idiopathic calcium stone forming patients undergoing percutaneous nephrolithotomy, rates of nephrocalcinosis ranged from 18-71% depending on the type of associated stone.

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Figure 11– X-ray example of patient with MSK affecting the left kidney. Extensive nephrocalcinosis is seen.

Because radiographs cannot reliably distinguish tissue calcifications from stones adjacent to tissues, the very word ‘nephrocalcinosis’ needs to be re-defined. 

In particular, the situation with respect to diagnosis of MSK has worsened as radiological techniques have changes. When IVU was the first line imaging modality for stones, contrast enhanced urographic phase imaging gave additional clues to MSK – the papillary blush illustrated in a prior section.

Nowadays since a single non-contrast CT series is all that is typically performed, the papillary blush effect cannot be seen, and diagnosis of MSK must rely more on the presence and pattern of nephrocalcinosis itself, which is not very specific to MSK. This means that the diagnosis of MSK by radiology has become unreliable.

The Power of Endoscopy

Differentiation of Nephrocalcinosis from Stones

During endoscopic procedures, stones and tissue calcifications can be directly identified and told apart. For example, in the images below, some of the calcifications were identified as stones. Others were tissue calcium deposits such as plugging or extensive plaque.

This has led to the notion that kidneys should only be labeled as having nephrocalcinosis once confirmed visually on endoscopy.

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Figure 12 (A-C) – Evidence of increasing degrees of nephrocalcinosis confirmed visually at the time of percutaneous nephrolithotomy. In each image a nephrostomy tube (not calcification) is depicted by an arrow. The remainder of the images have increasing degrees of calcification (bright white) within the kidney. Ignoring the nephrostomy tube, one can clearly appreciate a minimal but very present degree of accessory brightness (calcification) in panel A, a moderate amount in panel B and a severe amount in panel C.

Diagnosis of MSK

Of course, all of the problems of nephrocalcinosis are compounded when it comes to MSK. Stones and tissue mineral are easily mistaken for one another in CT scans, and ‘MSK’ affixed as a label to patients who do not have it. Endoscopy will easily identify the remarkably abnormal papillary shapes and dilated sponges, so MSK patients are properly diagnosed.

Tips for diagnosing MSK

1) Confirmation with flexible renal endoscopy can make a definitive diagnosis in patients suspected to have MSK and can be diagnostic as well as potentially therapeutic in terms of stone removal.

2) Consider urographic phase imaging either with IVU or CTU to confirm MSK suspicion in cases where renal endoscopy is not clinically indicated.

3) MSK should not be confused with ductal plugging as these are distinct clinical entities.

4) Nephrocalcinosis is more common than previously appreciated and does not necessarily indicate systemic disease or the specific developmental disorder of MSK.

A Final Word on Treatment

MSK is a true disease and deserves more attention and research efforts to help clarify its etiology and optimize treatment strategies. Because diagnosis by CT scanning is unreliable, the condition is easily overdiagnosed, a problem which leads to many kinds of confusion, clinical and research.

Alternative diagnoses to MSK, such as severe ductal plugging, are not benign and require their own treatment in order to prevent progression. Very often patients with plugging have multiple and severe abnormalities of urine chemistry which can be treated with diet and medications. Proper classification of patients is therefore especially important as different disease states may require unique treatment strategies.

In the event that an accurate MSK diagnosis is made, the tendency to give up on treatment and surrender to the inherent challenges of the disease should be avoided. In fact, these are the patients where metabolic evaluations and attempts at stone prevention are most critical.

Moreover, just because many of these patients tend to have extensive nephrocalcinosis on imaging does not mean they can’t form symptomatic stones in the collecting system as well. In fact, for such patients the clinical history is especially important as visualizing new stones in the setting of extensive nephrocalcinosis can be quite challenging.

Oftentimes when there is a high index of suspicion based on clinical factors, the optimal approach is ureteroscopy as this can be both diagnostic and therapeutic.

That being said, realistic surgical goals should be established. Clearing all stones from such kidneys is rarely feasible, though unroofing those pockets closest to the collecting system or largest on CT imaging offers a good place to start.

MSK is a complex and poorly understood disease that can manifest uniquely from patient to patient. In that respect what works for one person may not be appropriate for another and treatment strategies should thus be organized on a patient to patient basis.

343 Responses to “The Diagnostic Dilemma of Medullary Sponge Kidney”

  1. A Razak

    was diagnosed with MSK 15 years ago, have had over 21 RIRS to remove stones blocking my ureter from both kidneys. I am on Urocit as prevention,
    what is the long term solution? i’ve had so many CTs i am worried it is hurting me

  2. Kelly Rick

    I’m 54. Disgnosed with MSK on IVP at age 29. Have had only two stones that caused pain five years ago. I’ve never had any treatment or tests done. The last few years my urine has smelled bad and my sweat is so salty it can be seen on my clothes. Are these symptoms I need to be concerned about?

    • Fredric L Coe

      Hi Kelly, when sweat is salty, it means diet sodium is very high. I would consider a more moderate diet. As for the smell, if it is like ammonia I would mention it to your physician who would want to look for the common cause of it – colonization with urease possessing bacteria. Regards, Fred Coe

  3. Jennifer C.

    Hi I’m 35 years old and was diagnosis with MSK in both kidneys almost a year ago. My urologist did remove as many stones as possible from both kidneys but was unable to remove them all due to where they were located. I make calcium oxalate and calcium phosphate stones and I have been told my right kidney is becoming calcified. My question is do you know the percentage of patients that have parathyroid problems that relate to calcium oxalate and calcium phosphate plus nephrocalcinosis? My parathyroid level was 38 pg/ml on during my last lab work.
    Thank you.

  4. Tania

    Very interesting read. I’ve been diagnosed 10 years ago. It started with flank pain, blood in urine and UTIs. Later on I had to have my ureter rebuilt due to extensive damage from stones passing (formed scar tissue making my ureter close up). I stopped breathing as a baby 2/3 times. They later on found out it was due to a serious kidney infection. Had one more time in middle school where I fainted when I had to go pee. Otherwise I only started showing symptoms 12 years ago. Pregnancy went well, just had a UTI towards the end but I have a reflux ureter post surgery in 2013. They tested when diagnosed – both kidneys show renal calculi – calcium oxalate. My brother have been diagnosed with same this year. My specialist is however almost 2000kms away from me, and I had a real struggle to find a GP that trusts me (for example, it is known to not have pain if not passing a stone, where MSK patients have contra indicated that). I’m not on any treatment, but I’m doing quite alright.

    • Frederic L Coe

      Hi Tania, I gather you have MSK with infections and ureteric scarring as well as reflux, with many stones seen on radiographs – thence the MSK diagnosis. What seems unfortunate is that you have no physician expert close enough to you to provide ongoing care. Thanks for sharing your experience. As you pose no specific question, I presume you wrote to share – a gracious act. Regards, Fred Coe

      • Beau Freeman

        I really enjoy the in depth articles you are providing.

        I have recently done some more 24hr urine tests after undertaking a low sodium diet.

        I have been told I have MSK and have analytics done of several stone and they have shown to be calcium oxalate stones. I have passed around twenty stone of various sizes generally increasing over the years. I am currently 31 and started getting them at 18. They were tiny at 18 but the last one I passed was 3&5mm.

        Before going on a low sodium and low processed sugar diet my readings were as follows

        Urine output 2.6ltrs
        Urine creatinine 6
        Calcium 4.9
        Calcium 24hrs 14.1
        Ca/creatinine ratio 0.82
        Sodium 95
        Sodium 24hrs 285
        Potassium 46
        Potassium 24hrs 138
        Creatinine 24hrs 18

        Then with the diet it was
        Urine output 3.345
        Urine creatinine 4.9
        Calcium 2.5
        Calcium 24hrs 8.4
        Ca/creatinine ratio 0.51
        Sodium 13(L)
        Sodium 24hrs 43
        Potassium 32
        Potassium 24hrs 107
        Creatinine 24hrs 16.4

        So my question is there anything else you would suggest that might help with my diet? And would a fasting 24hr urine and blood test tell me anything more accurately?
        I have been told I have MSK based on about 20+ calcifications on each of my kidneys. Most of them are quite small (1mm) but are obviously growing. When I was 18 there was no signs of it.
        Your help would be appreciated.

        • Frederic L Coe

          Hi Beau, With the fall in urine sodium, urine calcium fell remarkably – as expected – but remains high enough to produce considerable stone risk. Fasting urine would tell you nothing useful. I presume your serum calcium is normal. As for MSK, just having multiple stones on a CT says nothing, and I suspect you have more commonplace stones. You might mention to your physician adding a low dose of chlorthalidone 12.5 mg daily to your low sodium diet, to lower urine calcium more. Alternatively, given the stones are not calcium phosphate, you might add potassium citrate 10 mEq twice daily, which may lower urine calcium without the side effects of the drug. Regards, Fred Coe

          • Beau

            Thank you, yes serum calcium was normal. Initially the specialists wanted me to go on a drug, I imagine the one you mentioned, but when he mentioned the side effects I said was still quite young and that I’m sure my diet had something to do with it. I went about researching(thanks to your website) I was able to adjust my diet to achieve better results but he is still pushing me towards the tablet (which I’m not against) I just want to do all I can first. It is not my wish to be on a tablet the rest of my life if I can help it. He also mentioned the tablet diuretic/ thiazide also looses its effectiveness over time and would have to be increased the longer I use it, is this correct? Are there any other levels that I can monitor, as in vitamin D, phosphate ect that will effect calcium urine?
            Thanks again beau

            • Frederic L Coe

              Hi Beau, This article gives a sequence of steps culminating in a drug. It is reduced sodium, high diet calcium, moderated diet protein, reduced refined sugars, high fluids all together. This diet mimics the ideal US diet. I add the drug to the diet, so the dose can be very low and indeed it can work life long. But see how far the diet can take you, and read the rationale in the article. Regards, Fred Coe

    • Lori R

      Very interesting article. I was diagnosed with MSK in 2006. My stones have tested as composed of calcium oxalate. Thankfully my stones have remained somewhat unchanged over the last few years without extensive need for surgeries as others have commented. My question is I am currently dealing with elevated parathyroid hormone levels while my calcium remains within normal limits and my Vitamin D levels have dropped below 10. Referral to endocrinologist has me taking a large vitamin D supplement but I question the relation to my MSK diagnosis. Any correlation between MSK and PTH/ Vitamin D issues that you are aware of?

      • Frederic L Coe

        Hi Lori, High PTH with normal serum calcium arises from low vitamin D stores (as you have) and also from low calcium diet. The latter is very bad for bone health and probably for kidney stones as well. This so called secondary hyperparathyroidism is very well known, and should respond to vitamin D and a high calcium diet. Stone prevention should shun low calcium diet, and rather use low diet sodium to control urine calcium while providing for bone. High diet calcium also lowers urine oxalate. The whole package is the correct kidney stone diet – here is a good review of its parts. Regards, Fred Coe

  5. Katie

    Thank you for this article. Like many who have replied, I’ve suffered since early childhood with UTIs, abdominal pain and flank pain. My pregnancies were difficult with excessive fluid gain and high blood pressure. It was only by a fluke CT scan that my PCP discovered I had MSK in both kidneys. Since that time every ultrasound tech or doctor comments on how “interesting” my kidneys look and how they are so full of little stones. I now take diuretics for higher than normal calcium levels in my urine, however that doesn’t really help with the pain and frequent UTIs. In fact, my doctors are resistant each time I reach out for antibiotics saying my urine looks ok – despite high PH levels, high squamous cells, and other slightly out of range results. The general response is that it is a benign condition and I should just get on with it. It’s really frustrating to have professionals discuss drinking lots of water, hygiene and cranberry juice when I’ve been dealing with this for over 40 years. So my question is this…where are the specialists who actually take this condition seriously and what are the “treatment strategies” because I haven’t found them. Most Urologists seem focused on prostates and Nephrologists with more advanced disease. Any recommendations in Boston? Thank you for drawing attention to this disease. It has impacted my life in a very real way. It would be nice if more MSK research and education was available for physicians. I feel I’ve been under-treated and doubted for many years and fear a “cry wolf” situation each time I seek help.

    • Fredric Coe, MD

      Hi Katie, Frankly I doubt MSK and suspect you have stones from the high urine calcium. One clue is stone type. MSK is usually calcium oxalate, other kinds of nephrocalcinosis are usually calcium phosphate stones with tubule plugging. Idiopathic hypercalciuria may be why your urine calcium is high, and treatment is more than a diuretic. Pain from small stones is a major US issue right now, incidentally and we need surgical trials to see if removing them helps. Dr Gary Curhan at MGH is an excellent kidney stone expert who might be helpful to you. Regards, Fred Coe

  6. Erica scarbrough

    I am 38 yrs old. Been passing dozens of stones for 15 years now. They say it msk. I have had every test, chemical wise, nothing abnormal.i have had lithotripsy 5x. Stints endless uti. Pregnancy is miserable they multiply and are 10x worse. I wish there was a solution.

    • Fredric Coe, MD

      Hi Erica, I doubt it is MSK as most such diagnoses are incorrect being based on mere CT scans. Perhaps you form calcium phosphate stones and have myriad tubule plugging. I frankly doubt your 24 hour urine and fasting morning serum values all are normal, and suspect you have too high a urine pH and calcium excretion. I would be sure about all this with your personal physicians. There may indeed be many solutions to such extreme stone disease. Regards, Fred Coe

  7. Gee

    I am 53 and was accidentally diagnosed with MSK last year. As a teen and young adult I was plagued with UTI and finally thru and IVP Doctors said that there was a nerve where the ureter connected to the kidney that was causing a blockage and they needed to do surgery immediately to repair this birth defect and get the urine flowing again. So at 27 I was cut from my belly button all the way around to the middle of my back on the left side of my body. At 47 they found a stone in the same kidney (my left) the told me it was attached to a suture and they needed to go in through my back to take it out as I wasn’t a candidate for lithotripsy because of the previous surgery and the scarring it may have caused, so they went in through my back took the stone out and I walked around with an 18″ tube hanging out my back for a week then they pulled the tube out and I had pee splashing/;running out my back for about 4 days then it healed. The incidental diagnosis came during a trip out of the Country. I went to the ER in east Africa with severe stomach pain and I have a very high tolerance for pain, when I came out of both surgeries mentioned above and 2 C-sections, I refused all pain meds as I hate the way they make me feel. Anyway, this pain was radiating around my waste and was severe and I was vomiting, they hydrated me and did an CT scan which showed that I had a stone in my right kidney. So I went to South Africa and the urologist there order her own CT scans and found that a case of pancreatitis caused the pain but she diagnosed with MSK and said that my case was classic as my kidneys glowed on CT scan, both kidneys are affected. I was 52 and I have only had two stones in my life or that I am aware of and both of them (well one now) were high in the kidneys. However this did explain my frequent UTI’s (one time I was on preventive antibiotics for a year), and the bright red blood that was frequently in my urine which always seemed to alarm the nurses but not me because it was par for the course for me. I came back to the US and is seeing a nephrologist that put me on 25mg chlorthalidone as he says it should reduce the number of stones I produce, but I’ve only produced 2 in my life?! He also put me on allopurinol because I have high uric acid levels, but no gout, yet. My concern is now that I know that I have MSK what do I do with that diagnosis? Not many Doctors know anything about it…when I tell a PCP they just stare at me…helpless in Georgia


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