This word is commonly used to describe stone disease.

It can sound worrisome for patients.

Physicians tend to think about uncommon diseases which cause stones.

Scientists think about crystals in kidneys of humans and animals, and theorize about their causes.

But the term has become vague and blurred, we believe, and in need of sharpening. That is why we wrote this article.

Because the material is complex, we have added summaries in bold italic at the top of sections that might pose problems for the non technical reader.

Lacking such a summary, read on confidently.


The boyish face is Fuller Albright, perhaps the greatest 20th century scientist concerned with kidney stones. The lovely biography Alexander Leaf wrote in his honor for the National Academy of Sciences tells of his brilliant career and unfortunate later life illness.

Fuller Albright Made Up the Word

All scientists find their special part of the real world to study. His was the bodies and biologies of patients with kidney stones, especially those with hyperparathyroidism – a mineral disorder caused by enlargement of one or more parathyroid glands which we have not as yet discussed on this site.

In 1934, young Albright, then an Assistant Physician at the MGH and an instructor in medicine at Harvard Medical School penned a remarkable paper (this is a link to a PDF) in which he presented to the world, almost as an aside, his newly coined ‘nephrocalcinosis’ to describe calcium deposits in kidneys of patients with hyperparathyroidism. (This is the web link to the paper; Kluwer publishers makes you pay for a copy).

Who Were His Patients?

Albright described three types of kidney involvement in primary hyperparathyroidism.

Type 1 is simply formation of kidney stones.

Type 3 is an acute ‘parathyroid poisoning’ with kidney failure and, at that time, death.

Type 2 was midway between these as there were calcium deposits in the kidney tissues but kidney function, though usually reduced, was adequate.

In Type 2 cases he wrote this about the word.

First use of nephrocalcinosis

The tissues he observed and those in his references came from autopsies.

Kidneys were scarred and contracted, with calcium deposits in the cortex and medulla.

His own index case – whose tissues he did not obtain – had kidney disease.

Simple stone formers without kidney disease are our interest on this site and in this article. They do not come to autopsy very often, and he did not have tissues from them. They were his Type 1 cases.

So when albright coined the word nephrocalcinosis, he was surely referring to patients with primary hyperparathyroidism who went on to chronic kidney disease and renal failure. Their kidney calcifications were a mixture of those in common stone formation and those that occur with phosphate retention and kidney failure.

Who Are Our Patients?

We are concerned with patients whose kidneys would have been like this Type 1 cases: No obvious kidney disease, kidney stones, and – he did not and could not have known this – modest amounts of calcium deposits in their kidney tissues.

Most of our stone formers have no obvious systemic disease, like hyperparathyroidism. They are called ‘idiopathic’ stone formers, meaning caused in themselves.

Apart from recent work by us and two other research groups their kidney tissues have not been studied in detail, so the pattern of crystal deposits is newly described. Albright could not have studied their kidney tissues, and would have thought all of their calcium deposits were simply urinary tract stones.

But not all of our patients are idiopathic stone formers. Some have hyperparathyroidism, some bowel disease, some uncommon diseases like cystinuria and renal tubular acidosis and primary hyperoxaluria. But almost none would have come to autopsy, so Albright would have known little about their kidneys.

It is modern technology which has allowed us to make observations of the kidney tissue in these diverse states.

We have written this article, to summarize the deposits in common idiopathic calcium stone formers, and in stone formers with a variety of disease, and thereby make good on Albright’s neologism: Say what it is that is in the kidneys of stone formers, including his favorites – those with hyperparathyroidism.

Who Uses the Word Right Now?

Radiologists, for the most part. And what they mean is that ‘calcified’ – radio dense – material overlays the outlines of the kidneys on various kinds of imaging studies: Simple flat plates, ultrasound studies, and CT scans.

But radiographs are to the reality of tissue as in the Cave of Shadows allegory: Images projected on the wall of a cave, semblances of real objects held before the fire. And those in the cave, who can see only the shadows, theorize about what is really there and how it came to be.

Patients can be confused and alarmed by the term ‘nephrocalcinosis’. We believe clinicians and even scientists sometimes exhibit some confusions, too.

Our purposes here are to pin down what the word should mean today, and ask if it is even valuable to retain it as a diagnostic term.

What Does the Word Lead Us To?

The problem with this word today is evident if you look it up in PubMed. Try that – limit your search to humans and ask for reviews. Here it is: (“nephrocalcinosis”[MeSH Terms] OR “nephrocalcinosis”[All Fields]) AND (Review[ptyp] AND “humans”[MeSH Terms]).

There are 273 entries. The first 40 are about diseases which can entrain calcifications in kidneys. On the list are medullary sponge kidney, kidney transplant, distal renal tubular acidosis, primary hyperparathyroidism, inherited disorders of the kidney, hyperoxaluria, loop diuretics in neonates, vitamin D and A toxicity, FAM20A mutations – enamel renal syndrome – claudins, hypomagnesemic states, and hypophosphatasia.

Just to be sure, I went on to the next 20 and found much the same.

If you clear the requirement for reviews, the list lengthens. There are 1895 results. But the range of diseases is about the same.

Nowhere did we find simple, idiopathic calcium stone disease.

If you clear even humans, there are 2686 entries, and the range of diseases remains more or less the same. However, within the first 40 entries you come upon our recent work, in humans, a single center review from Italy, and the review from which this this article takes its starting point: ‘What is Nephrocalcinosis?’ by professors Shavit, Jaeger, and Unwin.

That excellent review begins, as one might expect, with a proper definition: ‘Strictly, the term ‘nephrocalcinosis’ refers to the generalized deposition of calcium oxalate (CaOx) or calcium phosphate (CaPi) in the kidney.’

What Do We Propose to Offer Here?

Where are the renal deposits of calcium that have been demonstrated to date?

What are the deposits made of?

In what diseases are deposits of a specific kind and location found?

What do they look like during stone surgery or at renal biopsy – the modern way people will see the kidney?

What should scientists, physicians, and patients think about when confronted with or when using the word ‘Nephrocalcinosis’. Should we continue to use the word?



This section names and describes the parts of the kidney and of the individual nephrons which make it up. Each normal adult kidney has about one million nephrons. It is helpful to read this section as a background and use it as a lookup for later sections.

Where Things Are

Cortex, Medulla, and Papillum


The upper 1/3 of the kidney slice, above the crescent of red and blue vessels is the cortex. In it are the filtering units that begin the nephron, the glomerulae, shown as round balls.

Below the crescent is the medulla. As the medulla narrows, its blunt end is the papilla.

Nephron Segments

Each glomerulus drains its filtrate into a squiggly – convoluted – ‘proximal’ tubule which gives way into the remaining nephron.

The portion labelled ‘Thick Descending Limb’ is actually a straight continuation of the proximal tubule. It gives way to a descending and ascending thin limb, and then an ascending thick limb which drains into a ‘Distal’ convoluted tubule’, and thence through an unmarked straight connecting segment into the collecting ducts which run from the cortex down into the medulla and thence into the papilla which contains the bottom of the long hairpin loop and the termination of the collecting duct into the urinary system.

The medulla is divided into two regions: Outer medulla, from the crescent to the bottom of the thick ascending limbs; Inner Medulla, from the bottom of the outer medulla to the papillum. There is no special anatomical divider of the papillum from the inner medulla; the papillum is basically the last few millimeters of the medulla.

The outer medullary and inner medullary collecting ducts (IMCD) differ somewhat in their cell types and appearances. Ducts of Bellini (BD) are the terminations of the IMCD and empty the final urine into the urinary collecting system through tiny holes in the lining of the papillary tip.

Crystal Deposits in the Cortex

The cortex usually has no deposits in most stone formers. This section is here because physicians and scientists who read this would expect completeness. Feel free to skip it.

The only relationships to stone diseases concern hyperoxaluric states, ileostomy, primary hyperparathyroidism, and APRT deficiency. Often, cortical calcifications reflect kidney diseases.


These rarely calcify. Intravenous dibasic phosphate in rats, rare consequence of marked hypercalcemiacalcifications of large immune deposits can occur. Vitamin D intoxication in suckling rats can cause it. Overall, it is a curiosity.

Proximal tubules.

We have provided information about proximal tubule S3 segment calcification in hyperoxaluric states with greatly reduced renal function2,8 dihydroxyadanine crystals due to APRT deficiency can plug proximal tubules. In transplanted kidneys we have seen scattered birefringent crystals presumably calcium oxalate.

Distal Convoluted Tubules and Cortical Collecting ducts.

Acute phosphate nephropathy from bowel preparation is well known. Distal convoluted tubules contain calcium phosphate deposits in cystine and primary hyperparathyroid patients and calcium oxalate in primary hyperoxaluria stone formers. In transplanted kidneys tubule and interstitial deposits are found not rarely and are said to be calcium phosphate. In primary hyperparathyroidism with stones, and ileostomy patients, deposits were found in the cortical collecting ducts.

Cortical Interstitium.

As well as in transplant kidneys, chronic kidney disease has a very high frequency of kidney cortex calcification. WIthin that rubric interstitial calcifications are common. Primary hyperoxaluria patients with reduced renal function may have cortical interstitial deposits composed of calcium oxalate at the sites of proximal tubular deposits.

What about Cortical Blood Vessels? 

To us these are in and critical to but not kidney tissue. We believe it is potentially confusing to lump vascular disease and its associated calcifications in with calcifications within the renal tubules and interstitium.

Crystal Deposits in the Medulla and Papilla – Work by Us

This is useful for everyone. The names of kidney structures are all defined in the prior section with the picture. All kinds of stone formers can have crystal deposits like this and may want to understand more about them. This is modern nephrocalcinosis.

The tissue calcifications related to kidney stones are mostly in the medulla and papilla. Biopsies have been reported by our group, and also several others. We combine here all reports to date.

As a general rule, some tissue calcium deposits are present in virtually all stone forming people. We mean by this that excluding clinical stones – the things that enter the urinary collecting system, pass, and cause pain, obstruction, bleeding, and other miseries – the tissues themselves almost always contain deposits.

These deposits are of three types: Plugs of crystals in various segments of the nephrons; calcium phosphate deposits in the interstitium; tiny micro – stones in the dilated tubules of patients with medullary sponge kidney disease.

These three types of deposits are themselves distributed variably among the eleven definable calcium stone forming phenotypes studied to date: Idiopathic calcium oxalate stone formers (ICSF); Idiopathic brushite stone formers (BR); idiopathic hydroxyapatite stone formers (HASF); distal renal tubular acidosis (dRTA); primary hyperparathyroidism (PHPT); primary hyperoxaluria type 1 (PH1); small bowel resection (SBR); ileostomy (ILEO); obesity bypass (BP); cystinuria CYS); medullary sponge kidney (MSK).

Thick ascending limbs

No deposits have been found in any stone formers to date.

Thin Loops of Henle

We have found rare hydroxyapatite deposits in ileostomy, cystinuria and primary hyperoxaluria patients with reduced renal function. These are best illustrated in Figure 4 of the ileostomy reference. No other research groups to date have reported deposits.

Outer Medullary Collecting Ducts

Patients with primary hyperparathyroidism are the only stone formers who show deposits (calcium phosphate) in this tubular segment.

Inner Medullary Collecting Ducts

Crystal intraluminal plugs have been found in all eleven stone forming phenotypes examined. The majority of these plugs are composed of hydroxyapatite.

Bypass, distal renal tubular acidosis, small bowel resection, and medullary sponge kidney stone patients possess calcium oxalate deposits.

Mixture of sodium acid urate and ammonium acid urate was admixed with biological apatite in ileostomy stone formers.

Note the above link goes to an article on this site which lists 10 phenotypes; ICSF, the 11th phenotype, did not reveal collecting duct deposits in our work but deposits of HA were found in cases of ICSF reported by Wang et al

Microliths, myriads of extremely small, round, non-adherent stones have been found only in the dilated IMCD of MSK patients. These differ from plugs in virtually all respects. Plugs adhere to IMCD lining cells and cause cell damage, and death, MSK microliths do not adhere nor cause any perceptible damage. Microliths are round, not cylindrical, and made up of concentric layers of crystal; plugs also have layers but much less regular.

Cystine plugs also differ from all other plugs in not adhering to tubule cells. They move freely and do not appear to damage the cells.

Ducts of Bellini

Crystal intraluminal plugs have been found in all stone forming phenotypes examined and in similar patterns to that described for inner medullary collecting ducts. Brushite stone formers possess intraluminal plugs of a mixture of brushite, apatite and calcium oxalate plugs while plugs in cystine patients possess only cystine. The intraluminal plugs found the ducts of Bellini are unique in that they may have an overgrowth at their distal end as it protrudes through a dilated opening of the duct.


To date, all interstitial deposits found in human kidneys have been hydroxyapatite. The primary pattern of interstitial (Randall’s) deposits seen as single multilayered spheres when located in the basement membrane of thin loops of Henle and embedded within a matrix when located in the interstitial space. Two different patterns of these deposits have been reported in apatite stone formers: the typical Randall’s plaque and NIPS (new interstitial plaque structures); both are hydroxyapatite.

What About Blood Vessels?

No evidence exists showing calcium deposits within the vasa recta within the medulla or papilla. Deposits of hydroxyapatite can be found within and involving capillaries, but this is not evidence of a primary calcification. Theoretical papers proposing vascular injury and calcification as causes of plaque have failed to advance direct evidence in support of the theory.

Crystal Deposits in the Medulla and Papilla – Work by Others

For the non technical, this can be skipped; it is our proper obeisance to the excellent work others have done.

Wang et al compared ICSF with large and small amounts of interstitial plaque. In all the cases they found plaque as we do, deposits were at the thin limbs and interstitium. Those with hypercalciuria had the heavier plaque deposits, much as we have found. They also show IMCD intraluminal deposits, which we have not shown to date. They did not analyse the crystals in the plugs

Linnes et al studied ICSF, ICSF with malabsorption, phosphate stone formers which included struvite stones, and uric acid stone formers. In 99% they found interstitial plaque with an average low abundance. It was only when they separated out hypercalciuric ICSF that they found high plaque abundances as we have. They found plugging in all stone phenotypes, in medullary collecting ducts and also by endoscopy – this latter means they say BD plugs at surgery. The patients were mostly female, and hypercalciuria was not impressive. As in the former paper, they did not analyse the crystals in the plugs.

Khan et al described a single case in which they found interstitial plaque deposits which were identical to what we have described. The clinical phenotype was not described; the patient had large calcium oxalate staghorn stones. By EDX analysis the interstitial deposits were calcium phosphate. Tubule plugs were found in the medullary collecting ducts and these were calcium oxalate. We suspect this patient had primary hyperoxaluria.

Khan et al examined biopsy tissue from 15 patients with ‘idiopathic calcium stones’ not otherwise characterized in the report. Large areas of interstitial plaque were found. Crystals were HA. No plugging was found. Stones were calcium oxalate. The main finding was intimate association of plaque with collagen, as we have also described.

Overall, these four papers more or less agree in substance that interstitial deposits are common and composed of calcium phosphate. Likewise plugging is common and plugs are variable. Only we and Khan have described the crystals in plugs to date. Because the images of the tissues from these four papers do not differ from ours, we have not added their pictures here.

It is not so important to us that these papers agree with our findings, but that they agree with one another and with our findings. This is helpful as it shows more or less that crystallizations in kidney tissue of stone formers are found to be about the same from multiple laboratories, and therefore we can begin to form a consensus about them.


Can We Summarize What Was Just Said About Crystals in the Kidneys?

The foregoing makes only a few main points.

In stone formers of all kinds there are only three kinds of crystal deposit.

One is plaque – calcium phosphate as hydroxyapatite – in the interstitium.

Another is plugging of the lumens of the various tubule segments, mainly the medullary and papillary collecting ducts. These plugs are usually calcium phosphate but can be calcium oxalate, cystine, or uric acid salts.

A third is the microliths of MSK, unique to this one disease.

Why Are Plugs and Microliths Not in the Cortex?

The kidneys extract water from the tubule lumens progressively, concentrating the salts – like calcium phosphate and calcium oxalate – which eventually end up in the urine. Plugs increase progressively as water is extracted.

That is why all 11 diseases have some plugging in the papillary collecting ducts.

Where is the Interstitium?

Envision a tall building. Pipes run from the basement to the roof – water, steam, drains.

Electrical conduits, the same.

Elevator shafts, and stairwells the same.

Now, think about the space between the elevator shafts, stairwells, and all the pipes and conduits: That is the interstitium.

The word means standing between.

In the kidney the long structures are the tubules and vessels; the interstitium is the space between them. That is where plaque is. There are cells in the interstitium – it is as though, as an example, insulation blocks were stuffed into the spaces between pipes in my building.

Put more bluntly, mice can live in the spaces between things in a building, but not in the pipes. Rust can plug pipes but not the spaces between them. (We know the analogy is not perfect; permit us a little room here).

Let’s return to where we started.

Albright never would have seen much of what we have shown here. He had no access to biopsies of kidney papillae, nor surgical visualizations such as have now become commonplace.

He could not have known the crystal composition of the tiny deposits.

But the deposits in the kidneys are what he meant by nephrocalcinosis: Calcium deposits in the kidney tissue: Plaque and plugs.

The excellent review by Shavit, Jaeger, and Unwin concurs with Albright: ‘Strictly, the term ‘nephrocalcinosis’ refers to the generalized deposition of calcium oxalate (CaOx) or calcium phosphate (CaPi) in the kidney.’

Given what they have said and all that we have reviewed here, nephrocalcinosis itself is, in any one patient, interstitial calcium phosphate crystals, tubule crystal plugs of diverse kinds, or both, and microliths in the dilated tubules of MSK.

That is all that has been seen in human kidneys and therefore it is the reality of nephrocalcinosis.

It is what the word meant at the beginning.

It is what the word means now.

We propose the word be restricted to this exact meaning: Calcifications within kidney tissues as demonstrated directly in the tissues themselves.


The reality of tissue plaque and plugs is inferred from how the kidneys appear on CT scans or other radiographs and during surgery. Actual biopsy such as we have reported is a research procedure. 


As in Plato’s Cave of Shadows, the true tissue calcifications, the reality of things, can appear variably in the confining shadows of the radiologist.

We propose the term ‘radiographic nephrocalcinosis’ be used to define this condition, for such a term is exact within its purview.

What matters especially is that radiological means cannot reliably distinguish masses of tissue plugs or of microliths in MSK from stones.


The post by Michael Borofsky on MSK contains excellent operative images of plugging and plaque. Likewise, one of us (AE) had provided two fully illustrated posts, on plaque and plugging. In these are multiple intraoperative views of papillae with a variety of plaque and plugging patterns.

Abundant plaque is frequently observed during routine percutaneous nephrolithotomy and ureteroscopy in idiopathic calcium oxalate stone formers, idiopathic apatite and brushite stone formers, and in patients with small bowel resection, ileostomy, and primary hyperparathyroidism. It appears as whitish, irregular areas beneath the urothelium usually near the tip of the papilla.

Stones frequently grow attached to plaque.

The papilla in distal renal tubular acidosis, cystinuria, primary hyperoxaluria and medullary sponge kidneys reveal darkish spots or shadows on the surface that represent large intratubular deposits.

Such deposits also can appear as yellow plaque – cylindrical elongate yellow tinged objects beneath the urothelium which are plugs within IMCD and BD.

Using a laser, surgeons can remove the urothelial roof covering these deposits and release the deposit. There are reasons to think this may relieve pain in patients with pain in the absence of obstructing stones. 

In some patients, mineral overgrowths protrude from the dilated openings of ducts of Bellini.

These overgrowths are attached to the distal ends of plugs located in ducts of Bellini. One can extract the overgrowth/plug complex intact for mineral analysis, but this is not presently an accepted clinical practice.

t has been suggested that the overgrowth may detach from the distal end of the plug and consequently form a stone lying freeing in the calyx. However, there is no evidence as yet to support this idea.

Ductal stones in medullary sponge kidneys are free floating in the lumens of greatly dilated inner medullary collecting ducts. The appearance of MSK is diagnostic as seen during surgery. 


On CT there is mineral in the papilla: Is it stones which can be removed, or tissue mineral that usually need not be removed? No one can tell right now until the surgery.

The primary pattern of papillary calcification that radiology can detect is intraluminal mineral deposition (tubule plugging and microliths) in diseases that produce enough of it to show up on a CT scan: Primary hyperparathyroidism, distal renal tubular acidosis, medullary sponge kidneys, and some advanced cases of idiopathic calcium phosphate stones.

CT scans cannot resolve individual tubular plugs but reveals many adjacent plugs as a field of parenchymal calcification.

Radiology cannot accurately detect plaque.

Radiology cannot reliably distinguish large plugging or microlith deposits from small stones.

Because radiology cannot accurately distinguish plugs from small stones, surgeons must examine each part of the kidney to be sure all stones are removed.

The benefits of removing tissue mineral deposits is presently unknown.


Here it is, the venerable bottom line:

Radiological ‘nephrocalcinosis’ can be stones, plugging / microliths of MSK, or some combinations of these three.

Removal of stones is an accepted and important surgical undertaking in patients with pain, bleeding, obstruction, or even recurrent infections or special risk of stone passage – eg. travel, pilots.

Removal of tissue mineral is controversial, and few surgeons will do surgery if that is all that is there.

For these reasons, high resolution ureteroscopy is the best alternative when ‘nephrocalcinosis’ is found on CT scan. Once the tissues can be seen directly, albeit from the outside not by biopsy, all stones can be found and removed. 

What to do with plugs and microliths is for future trials to determine.


68 Responses to “NEPHROCALCINOSIS”

  1. Elizabeth Tuttle

    Hi I was diagnosed at 19 with msk, dRta, medullary nephrocalcinosis, metabolic acidosis and hypokalemia. I form stones due to extreme hypocitraturia and recently have been put on sodium bicarbonate due to excess carbon dioxide. I take massive amounts of potassium citrate daily as well because I become very hypokalemic if not. I pass sandy stones very frequently and only recently had an emergent blockage that required stent placement and lithotripsy. I suffer with chronic utis as well and my latest gfr was 39 and the highest I’ve seen it get was 42. Everything I read says msk is usually a mild disease with a good prognosis so why am I at 26, living with less than half of my kidney function? On top of all this, I am suspected to have systemic sclerosis aka scleroderma, or possibly mixed connective tissue disease. Do you know if there is an association? And what do you think my prognosis might be? Also does it matter that my mom and her dad were born with unilateral renal agenesis? There has to be a connection with the kidney diseases right?

    • Fredric Coe, MD

      Hi Elizabeth, I believe you were put on sodium bicarbonate because of low serum bicarbonate, but why the sodium I am not yet sure. Perhaps it is that you lose sodium in your urine and your blood pressure falls. The sandy stones are, I presume, calcium phosphate or carbonate because of high urine pH. I do not at all believe this is MSK, it is renal tubular acidosis and rather severe sounding. There are deep associations between some collagen vascular diseases and RTA, and you may well have one. As for the unilateral agenesis I am more sceptical. Your overall concern about the stones and reduced kidney function is justified and I would ask my physicians if they can provide a referral to a specialized center that is geographically reasonable for you. If that is too difficult, I would offer to review your records as a free service to them and you because this is a very complex problem and perhaps I could be helpful. Regards, Fred Coe

    • Aydin Olgun

      For Elizabeth I would like to investigate possibility of Sjögrens Syndrome which may need specific treatment besides stone prevention and other metabolic interventions. I agree that sodium in the regimen may be replaced, possibly with potassium bicarbonate. Best regards. Aydin Olgun

      • Fredric Coe, MD

        Hi Aydin, Thank you for adding your thoughtful comment – I presume you are a physician. I think she has renal tubular acidosis and Sjogren syndrome is certainly a well known cause. Warm regards, Fred

  2. Titi Akinremi

    Hi Dr. Coe,
    This is an immeasurable service that you and your team are offering to “stoners” and interested others. Thank you.
    In 2014, at 60yrs, a known idiopathic hypertensive, I was diagnosed with bilateral medullary nephrocalcinosis following primary hyperparathyroidism (2 parathyroid adenomas). 24hr stone panel showed low phosphate, sodium, magnesium, calcium and citrate rates. I was not advised as to which type of stones I was liable to form, but now there are 0.5cm calculi in both renal sinuses. Serum creatinine progressively went from 0.8 in 2013 to 1.1, 1.45 in 2014. Now 2 years post parathyroidectomy (and concomitant total thyroidectomy for hyperplasia), creatinine seems stable at 1.0-1.1. No microalbuminuria. I developed severe osteoporosis secondary to the parathyroid adenomas and now have to take risendronate and calcium/Vit D supplements.
    LDL rose from <100 to uncontrollable 140+ and I gained an intractable 20lbs in 6 months. BP is no longer well controlled on losartan/verapamil +maxide.
    I wonder if I still have a propensity to nephrocalcinosis with hyperparathyroidism over.
    And does taking calcium for osteoporosis increase my risk for particular calcium stones (female)?
    Is there anything I can do to "dissolve" the calcinosis?
    Thank you.

    • Fredric Coe, MD

      Hi Titi, I gather that you have had high blood pressure and also primary hyperparathyroidism which caused bilateral medullary calcifications. Your 24 hour urine results are confusing as urine phosphate and calcium will be high in that condition. I alsos gather that after surgical removal of two large glands you formed 0.5 cm calcifications in both kidneys in addition to the prior medullary nephrocalcinosis. This latter is not clear. How can the CT scan differentiate these stones from the prior calcifications? If you have formed more stones it is likely from residual hypercalciuria – very common after cure of PHPT; but urine studies would have shown the high urine calcium along with normal blood calcium. The bone disease of PHPT is known to heal spontaneously and bisphosphonates are not usually needed nor ideal, so perhaps your physicians are concerned about another disease. That your weight and blood pressure both went up is expected; more weight usually does that to blood pressure. The rising serum creatinine with PHPT suggests serum calcium was quite high – you do not mention it. So I am a bit uninformed about critical facts here and cannot do proper justice to your questions. Can you clarify things? Regards, Fred Coe

      • Titi Akinremi

        The message ran away before I could complete the story.
        Sir, nephrocalcinosis was diagnosed by USS only following the PHPT. No CT scan was done.
        I am just worried about the increasing abnormality in the kidneys. Is there something I need to do to reduce the negative progress and improve my GFR?
        Will drinking alkaline water help to reduce the acidity of urine? In my case, with prior osteoporosis, how important is taking Ca supplements even though there is no longer the “hungry bone syndrome?

        Thank you so much for your patience and for sharing from your wealth of knowledge.

        • Fredric Coe, MD

          Hi Titi, I understood the NC was diagnosed after PHPT but shortly after and no doubt formed from that disease. The rise in your serum creatinine appears to have occurred when you had PHPT and could well have been from the very high serum calcium at that time. As for alkaline water, I have no reason to think it helpful. As for bone renewal, it is likely and is slow. Calcium supplements – with meals! – or just a high calcium diet is important; your urine calcium seems so low – if I understand the units – there is no stone risk. The bone disease of PHPT is not osteoporosis as bone trabeculae are usually preserved and will regain mineral. Regards, Fred Coe

    • Titi Akinremi

      Thank you Dr. I am sorry for the confusing layout of information.

      07/09/14 — Initial diagnosis of PHPT followed the finding of 12.6 Ca and intact PTH 348.
      09/09/14 — Post op PTH was 20, and Ca 9.2mg/dl (ionized 1.26mmol)
      09/25/2014 — Medullary nephrocalcinosis was diagnosed on USS. No stones.
      Dexa score was -3.5 (severe osteoporosis).
      10/01/14— BUN and Creatinine were 9 and 1.1 respectively
      Postop 24hr urine panel (10/22/2014) showed low phos (0.2), magnesium (3.9) and citrate (240). Ca was just 54

      Repeat stone formation panel (01/09/15) Ca 32.4, phos 0.2, mag 3.0, citrate 324, Na <30, oxalate 17.1
      USS 07/10/15 medullary calcinosis plus 1.3×1.5cm left cyst, no stones
      USS 11/03/16 medullary calcinosis plus 2.2×2.1 & 1.6×1.1 left cysts with 0.5cm intracystic and 0.6cm sinus calculi,
      [Ca and PTH have remained normal postop. It has been difficult titrating my levothyroxine.]

      • Fredric Coe, MD

        Hi Titi, You did indeed have very marked PHPT and it was cured by surgery, although with 2 glands enlarged the possibility exists of recurrence. The medullary NC clearly occurred while you have PHPT. The urine panel after surgery looks odd; are these 4 hour excretions, and what are the units? The urine panel in 2015 also is not interpretable because the units may be millimole or mg; citrate is in mg/day, I think, magnesium in mg/day is not possibly 3. Can you clarify what these numbers are? The ultrasound studies are not very helpful in that stones are detected at about 65% efficiency vs. CT scan, so the changes may be real or technical. Regards, Fred Coe

        • Titi Akinremi

          Thank you for your calming review. I am glad to know that the bone disease of PHPT is not really osteoporosis and sort of reversible.
          The 2014/2015 24hr urine results were as follows:

          10/22/14 01/09/15 Range
          Ca 54 32.4 50-250mg/day
          Phos 0.2 0.2 0.4-1.3g/day
          Uric 270 266 250-750mg/day
          Na 72 <30 40-220mEq/day
          Oxalate 18.9 17.1 8.0-48.0mg/day
          Mg 3.9 3.0 6.0-10.0/day
          Citrate 240 324 280-1240mg/spe
          Crea 0.9 0.7 0.8-1.8g/day
          K 57 64.9 25.0-125.0mEq/day

          Should request a CT scan of the kidneys if possible? And a new 24hr urine panel?
          Best regards

          • Titi Akinremi

            I tried to paste a table to show results from 2014/2015/Lab Range. I’m sorry it is messed up.
            These are the 2015 figures alone with the range

            Ca 32.4 50-250mg/day
            Phos 0.2 0.4-1.3g/day
            Uric 266 250-750mg/day
            Na <30 40-220mEq/day
            Oxal 17.1 8.0-48.0mg/day
            Mg 3.0 6.0-10.0/day
            Citrate 324 280-1240mg/spe
            Crea 0.7 0.8-1.8g/day
            K 64.9 25.0-125.0mEq/day

            • Fredric Coe, MD

              Hi Titi, Having the units, you indeed have very low calcium and phosphate in urine, low sodium, and are small – very little creatinine. Magnesium is in mmol/day, which is 24 mg/mmol giving 72 mg a normal to high value. I think you must eat only modest amounts of animal protein given the low uric acid, and lots of veggies. The low phosphate could be part of bone remineralization and poor absorption because of calcium supplements. The low urine calcium is almost certainly bone uptake. I would just let things go, eating high amounts of high calcium foods, and retest in 6 months or so. Stone risk – supersaturations – will be very low unless you forget about the needed 2.5 liters of urine flow/day. Regards, Fred Coe

          • Fredric Coe, MD

            Hi Titi, I responded in your other note. I would ask my physician about a CT to get a reliable baseline for stone counting. Regards, Fred Coe

            • Titi

              Thank you Dr Coe. Iwill request a CT scan and a repeat urine panel since the last one was a year ago.

              I wish you a most blessed 2017.

  3. antonette de la rama

    Dr. Coe,
    i just wanna know the meaning of differential function of right and left kidney, whats the meaning if right kidney functions at 12% and left kidney at 88% does this mean total kidney function is good/ normal?
    thank you and will be waiting for your response.

    • Fredric Coe, MD

      Hi Antonette, It means that the function of your two kidneys was measured and each expressed as a percent of the total of the two. Your left kidney is contributing 88% of your total kidney function and the right kidney is contributing 12%. The total function is not stated in your question. Sometime or other the right kidney lost a majority of its function. In stone formers this is usually from obstruction with damage to the organ. Since one can live a full life with only one kidney you are quite safe but it means if your left kidney is ever obstructed you will be without much total kidney function until that obstruction is relieved. It also means that prevention of more stones is more important for you than for most other people. I am sure your physicians will want to pursue that with great vigor. Regards, Fred Coe

  4. Tracy

    I had my first kidney Stone diagnosed in 2007. It was almost an inch long and lying in the bottom pole of the left kidney. The urologist I saw said we didn’t need to do anything because that stone was not blocking any ducts and could not be causing me any pain. I went back to him a year later and told him the pain was unbearable and he finally did a lithotripsy. He did not get all the fragments out because the stone was extremely hard and he had to stop the shockwaves before he damaged my kidney. After that, though, the pain went away as well as my IBS symptoms. This lasted almost two years, but I started to have mild pain in BOTH kidneys. When it started getting really bad, I went back to that urologist. Again, I had a stone that was a little over half an inch long lying in the bottom pole of the left kidney. Again, he told me it could not be hurting me and refused to do anything. I asked him why both of my kidneys were hurting and he told me that the right kidney had no stone on x-ray. A few months later I went to a new urologist and she told me the same thing and refused to do any procedure to remove the stone. I finally went to a new urologist in 2015 (I was caring for my mother with terminal cancer in the interim). After my mother passed away I was able to go and see this new urologist who told me that of course the stone would cause pain because of the size of it and because it’s a big rock in my kidney that doesn’t belong there. He agreed to do a stone basket retrieval, which was successful, but my pain didn’t go away. He also told me that on CT without contrast he diagnosed bilateral medullary nephro calcinosis. He referred me to a nephrologist but the nephrologist told me that nephrocalcinosis doesn’t hurt. He refused to do anything about it such as further testing, such as a 24 hour urine test or another scan, to find out what was causing it and see if we could stop it’s progression and do something about the horrible pain I was experiencing along with the return of my IBS symptoms which were severely acute. Together, the pain in my kidneys and the every single day almost non-stop IBS episodes have caused me not to be able to work for the last 10 months.i cannot qualify for temp disability. I went back to the urologist and they did an ultrasound of my kidneys and of my neck to look at my parathyroid glands thinking perhaps I had hyperparathyroidism. This was at my request because my blood work for hyperparathyroidism has been borderline. The ultrasound came back showing no new stones, but also did not show the nephrocalcinosis. When I asked the doctor about that he told me that the type of nephrocalcinosis I have is not visible on ultrasound. Also the ultrasound of my neck did not show the parathyroid glands at all, they were not visible on sonogram. Could you review this and just give me your opinion on everything? I’m not really sure what to do next. Thanks so much!

    • Fredric Coe, MD

      Hi Tracy, You obviously have multiple stones in your kidneys or calcifications in kidney tissue – it is hard to tell from here – and a need to prevent more crystal build up and more stones. You do not mention stone analysis but the hardness suggests it is brushite. You need to know the stone composition. You also have pain in association with multiple small kidney calcium deposits – stones or tissue – and that is a fairly common complaint. The best treatment – surgical, for example, is still uncertain. What is certain is prevention of more crystals and stones. Take a look at this and try to see if these steps have really been followed. If so the answer to how to prevent should be reasonably clear. Let me know, Regards, Fred Coe

      • Tracy

        Thank you for your response. The stones were half calcium oxalate and half calcium phosphate. My urologist said that the tissue was calcifying. I drink at least three 32 oz glasses of water per day, sometimes fruit juice and I let myself have 2 cups of coffee per day, but always drink water afterwards. I have polyuria, urinating 20 or more times per day. I also have nocturia. I get up 4 to 5 times per night to urinate. I have to be careful with my electrolytes because I also have SVT which is currently controlled by 240mg of cardizem daily. My urologist thought about hyperparathyroidism because of all my symptoms. My serum calcium hovers around 9.9 to 10, but my vitamin D is always in the teens or lower, despite taking a supplement. I’m at a loss as to the next step.

        • Tracy

          I forgot to mention that the ultrasound showed thinning of the cortical walls bilaterally. My IBS is directly related to my kidney pain. In the ER they gave me pain meds and the IBS (obviously not constipation) stopped immediately as soon as my kidneys stopped hurting. The kidney pain is like back labor sometimes and hurts down both legs. It can be excruciating or just annoying. The constant IBS keeps me homebound, but three GI doctors have said there’s nothing they can do and insist the IBS is not related to the kidney issues.

          • Fredric Coe, MD

            Hi Tracy, Thinning of the renal cortices is important and raises the need for a diagnosis and treatment. Once again I urge an organized approach such as I offered in my link. IN the course of pursuing the needed information you and your physicians should find the right answer. Let me know. Regards, Fred Coe

        • Fredric Coe, MD

          Hi Tracy, half phosphate fits with what I would have expected – is any of the phosphate calcium monohydrogen phosphate – brushite?? I am suspicious of idiopathic hypercalciuria and I urge you follow the five steps in the article I linked to yesterday. Regards, Fred Coe

  5. Babee P Vera Cruz

    Hi Dr. Coe, I had a recent kidney ultrasound and it says that medullary calcification left kidney. Normal sonogram on the right kidney and urinary bladder. What does that mean? Can you please explain to me? Thank you!

    • Fredric Coe, MD

      Hi Babee, It means you have stones or calcium deposits in your left kidney which is most likely stones and you need to find out why you are doing this. Here is a reasonable approach. Since you do not pass stones, you cannot know what the crystals are, but you can get 24 hour urine testing and find out what about you might predispose to forming crystals and treat that, Regards, Fred Coe

  6. Lori

    I have Medullary Nephrocalnosis. The last few months I been passing many stones together 15 at once .The biggest was 6mm with spikes rest were 1 mm so 22 mm at once . This is crazy .It like I shedding stones is this a normal thing ? I use to just pass sand and 1 big one a month .what is going on with me.I feel like I have Aliens living inside me.I have pain all the time with pain control.

    • Fredric Coe, MD

      Hi Lori, I suspect these stones are calcium phosphate; is that the case? If not, let me know. Usually there are obvious abnormalities in the 24 hour urine tests; do you have such tests and so they show abnormalities?? Regards, Fred Coe

  7. Mariel

    Hi Doc,
    I am 25yr/old and diagnosed with BILATERAL RENAL MEDULARY NEPHROCALCINOSIS.
    Both of my kidneys has it. On the right it measures 10.0×5.2×3.6 cm. left kidney 10.8×3.8×4.2 cm cortical thickness of 1.2cm. both have hypoechoicparenchymal echo. there are innumerable small medullary calcificatin in both kidney. No hydronephrosis.

    creatinine= .7 mg/dL
    uric acid= 4.6
    calcium= 2.39

    My treatment as per the doctor i seen is diet modification, I have to take potassium citrate (acalka) 1tab 3x/day and drink plenty of water. I wanted to ask if this condition is reversable, or can easily be treated. What things shoul I have to do so it will not lead to some serious kidney disease (renal failure) ? will it be illiminated, its really been bothering me if my kidneys are in serius problem already. Please help me be enlightened on my condition.

  8. nicky

    Following Microscopic Haematuria, My daughter is diagnosed with Medullary Nephrocalcinosis in correlation with calcium metabolism. Also in her ultra sound scan it states ‘no Hydronephrosis of obvious calculi seen’.
    Her renal function tests state Sodium 141 mmol/L 133-146 Potassium 3.9 mmol/L 3.5-5.0 Creatinine 46 umol/L 46-70
    Can her condition be reversed or fully cured with treatment and relevant diet?

  9. Jennifer Chew

    Dear Dr Coe, I just had my health screening down. Report came back with hypertension for CASP of 148mmhg with arterial stiffness severe. Radiology report stated ‘echogenic renal pyramids seen bilaterally secondary to nephrocalcinosis and right renal septated cyst 0.8×0.5cm in mid pole of right kidney’. Blood calcium is 2.53mmol/L (within normal range). Free T4 is 14.39pmol/L and TSH 0.8157mIU/L. All other test including cholesterol & renal function screen were in the normal range. I am active in sports and has a BMI of 8.4 (just hitting the normal low range). As my BP is high, the doctor wants to put me on Norvasc 10mg. I am a little hesitant to start as I was wondering if the high BP could be due to nephrocalcinosis or any kidney conditions such as pheochromocytoma? I am reading up more on nephrocalcinosis & your posts have provided me with more insights about the condition. I am just perplexed about my hypertension & was wondering if there’s even a slight chance of nephrocalcinosis linking to hypertension, in my case, since my hypertension is idiopathic & now I know I have bilateral nephrocalcinosis & cyst. Would appreciate your advise on this. Thank you. Rdgs, Jen

    • Fredric Coe, MD

      Dear Jennifer, nephrocalcinosis itself is not known to be a direct cause of hypertension, although I would assume that in some cases it might play a role. Pheochromocytoma is an uncommon adrenal tumor and has no relationship to nephrocalcinosis, nor is there any specific evidence for it in your case that you have presented in your note. Renal cysts are their own world in that they require appropriate surveillance and interpretation by experts in reading those kinds of ultrasound and CT images. SOmetimes renal cysts can raise blood pressure if one compresses an important renal arterial branch but it is an uncommon situation. So although I like to find unitary diagnoses, you may indeed have separate ones. As for treatment of your increased blood pressure, you should certainly take whatever means your physicians suggest to lower it. Regards, Fred Coe

      • Jennifer Chew

        Dear Dr Coe,
        Thank you for taking the time to explain to me. I now understand that there may be other specific areas which I need to address wrt to hypertension. I am at least now comforted to know that nephrocalcinosis isn’t a condition which has drastic end result as I have ‘feared’. Thank you very much. Rdgs, Jen

  10. Chris Cole

    Thank you so much, My daughter has nephrocalcinosis. She is 12. She was diagnosed about 7 years ago. It is so hard to find good information on the net. They tell me that there is no reason she would have nephrocalcinosis, so they say it is hereditary. She leaks protein and calcium. Currently she is on a low sodium diet and take 2.5 mg lisinopril, Diuril and Cytra K. I am told this is managing the condition. I am also told Transplant is inevitable at some point but we are not sure when. Its frustrating that I am unsure a clear cut prognosis. At some point they thought she had Dent’s Disease, but this was not the case. Are there any more sites or helpful information? Thank you so much for your time and consideration.

  11. Melissa

    Hello and thank you for the informative site! I was just diagnosed with MSK following a renal ultrasound and CT w/o contrast showed that my pyramids were “full” of stones, mostly tiny but a few large, 4-10mm. I have no pain and haven’t passed a stone in 20 years, that I know of. The purpose of the ultrasound was to check my renal arteries (which were fine) bc of sudden hypertension. After reading this, I am unconvinced that what they saw are actually stones, but it seems as though the only way to know for sure is uteroscopy? Am I understanding that right? But if mine are in the medulla, uteroscopy can’t reach them, correct? Any insight or guidance as to how to proceed or what to ask my neph for would be greatly appreciated!

    • Fredric Coe, MD

      Hi Melissa, You ask a very important question. If you have no pain, and are not passing stones it is not clear to me why you would benefit from any urological procedure at all. I would guess many of the crystallizations are in the most distal parts of the collecting ducts and this would be seen during ureteroscopy but why see them if nothing needs to be done. The big question is why the sudden increase in blood pressure and if there is a relationship between the calcifications and the blood pressure. The obvious link is the blood calcium; primary hyperparathyroidism can produce the calcifications and raise blood pressure so it is crucial that your blood calcium be normal. Also crucial is your level of kidney function. There are conditions in which calcifications occur because of kidney problems which in turn can raise blood pressure. So there is a lot for your nephrologist to do, and little your urologist needs to do. If you have further questions please feel free to post them. All the best, Fred Coe

  12. antonette de la rama

    Dr. Coe,
    Does nephrocalcinosis caused by previous kidney infection will eventually lead to end stage kidney failure/dialysis?my nephrologist and urologist say i have a normal kidney function according to previous tests i had. My calcium, potassium, hemoglobin,uric acid are in normal range, and no protein in my right kidney is scarred and reduced in size but is working 24%, my left kidney is normal in size and shape but with nephrocalcinosis..what is the prognosis?im too scared and have pain on my kidney but my doctors tell me not to 36 y/o, female..thanks

    • Fredric Coe, MD

      Dear Antonette, nephrocalcinosis does not usually result in kidney failure. It appears that your right kidney has been damaged, but it is not clear why. Do you know why? Have you produced stones? Do others in your family have kidney disease of this kind? Is your kidney pain from infection, stones? Is your blood pressure high? I would be happy to help more but the amount of information is too slight. Regards, Fred Coe

      • Antonette de la rama

        Dr. Coe,
        I was told by my doctors that maybe i was born with my small right kidney, but i was thinking my recurrent kidney infections in the past have caused it. I have no diabetes, normal blood pressure, no kidney disease runs in my family, i never had produced a single stone and never passed one. My urologist tells me every time that my pain is not kidney related as my urine test always comes back normal but im still sick worried because it is constant though its the dull type. He tells me as well that i should not worry about having dialysis in the future as the possibility is very low.I am worried because i have only one functioning kidney but it has nephrocalcinosis and i have last creatinine reading was 68 mmol/l, i am a 36 y/o, female, small built (95 lbs, 5’0″ tall), asian descent..hope you could give me some more insights about my starting to feel so hopeless because of my pain and the endless worry i seem to have every single day..thanks


        • Fredric Coe, MD

          Hi Antonette, It sounds like the right kidney has somehow been mostly lost and your good kidney has stones in it. Your doctor is right that you should be able to live a full life without fear of dialysis. It is very important to know why you made the stones and to undertake prevention against more of them. If you have stone passage get care immediately as one obstructed kidney means transient but possibly severe loss of kidney function until it passes. I would avoid shock wave lithotripsy if possible in favor of flexible ureteroscopy if you need stone surgery. Regards, Fred Coe

  13. Patricia McClain

    Dr. Coe,
    Can you explain about the GFR and what it means? Is it possible to estimate the course of dRTA from all the lab work and 24 hour urine tests? I know my kidneys are irreversibly damaged by nephrocalcinois. Is it possible for me to make a bucket list prior to dialysis? I am going to call my nephrologist and ask him these questions… and if he could give me that information, why hasn’t he? I am only asking for general guidelines and a broad time frame. According to what I have learned, better technology might be able to offer some hope.. as you described the need for more accurate and better CT scans… and that there are doctors, and other scientists working on that right now. My other thought, may be too disturbing for this: but it is possible I could die from something else, before dialysis is necessary.

    I am not trying to scare all these other folks and say everyone with dRTA will need dialysis.. I can’t generalize my situation to all of the other kidney stoners. I know most of my stones are calcium phosphate and calcium oxalate. I also understand there are degrees of neprocalcinosis and mine is worst than most people have. I want to understand what is really going on with my disease and be told the truth, as much as possible. No doctor ever told me I would be dialysis material if I lived long enough; I went to the medical library and looked it up myself after my emergency open surgery I mentioned.

    So all that is left is to take my Urocit K, drink lots of water and moderate my salt intake.. It is very frustrating to feel like there is so little I can do.. but I want to enjoy what time I have left. I can’t begin to describe how I feel… only that I have had dRTA for almost 50 years, and I am 63 now. I don’t need sympathy and I am not trying to get attention by having other people feel sorry for me. I guess what I want is an action plan. I don’t want the other kidney stoners to think I am an expert or that there is no hope for anyone with kidney stones. I know most folks can have a better treatment plan and prognosis than I do.


    • Fredric Coe, MD

      Hi Trish,I am not so sure you are right about dialysis. The routine serum measurements you got especially if used along with 24 hour urine measurements give pretty good values for kidney function and I will bet – on sheer likelihood that your kidney function is normal or near normal. I have had a very long career experience with kidney stones including renal tubular acidosis and almost no one has even gone on to dialysis. Those few have included patients from an earlier time who lost kidneys from obstruction or from the very invasive surgical procedures that once were needed. By all means ask your nephrologist about your kidney function, however, and if it is reduced about the rate of progression. Hopefully I am right – and you are not in such danger of dialysis. Regards, Fred Coe

      • Patricia McClain

        Thank you Dr. Coe. Maybe I have misunderstood what my new urologist inferred. Also I still live in the same place with a shortage of good doctors… I got sick of how I was treated at the university and discovered that at this point in time, they offered the best doctors. It is not the doctors fault.. things are bad, due to a shortage of funding and too many patients, mainly. It is the fault of the state legislature and board of regents who mainly determine funding for the medical school/university hospital and clinics. It is a problem with the state I am in because it is largely a poor state with a population spread out in remote areas. The whole situation is a very complex political problem… how to treat all these indigent people. I saw people who appeared to be disadvantaged in ways I could never have even dreamed of. Each time I went there, I felt very fortunate.

        It is around 1500 miles to see my new urologist, round trip. The way I look at it is you only have 2 kidneys, but only one life. It is worth it to make the best of the time I have left.

        I am getting a lot out of this and trying to understand all this anatomy, physiology and chemistry. If I had known when I was younger that I would need an understanding of that so I can advocate for myself, I would have taken biology, chemistry etc. in college and not botany, geology and astronomy.


        • Fredric Coe, MD

          Thanks, Trish, for your comments as I am sure many will find them of interest and value. University hospitals do often have excellent doctors who are urged to see too many patients or have competing activities like patients and grants and research publication, or both with the result that nothing is done as well as it could be done. As for botany, geology, and astronomy, these may be better for a life lived – the small and the large plants, the world of earth, and the cosmos. All the best Fred Coe

  14. Laura Bousada

    I was diagnosed with dRTA, nephrocalcinosis, and medullary sponge kidney. Is it safe for me to assume that one or more of these diagnostic outcomes could better be diagnosed by endoscopy during surgery? I have had approx. 6 laser ureterscopies and never , what would be the advantage of one over another? Also, on this topic which procedure would be best to access the bellini? Last time my urologist accessed the caylx! Could he go further? He has been my surgeon since the start and I fully trust him, I pestered him to get to the calyx (often in the past he would do mine for a stuck stone, which happens often. I am also wondering is it the bellini that needs to be unroofed? Thank you for this article I am really liking this dialogue with you, saves us all from confusion, and I love the analogies and gives us a chance to ask instead of waiting until the next appointment with our doctors.

    • Fredric Coe, MD

      Hi Laura, During ureteroscopy your surgeon could surely determine if you do or do not have MSK. Renal tubular acidosis is diagnosed by functional testing, not surgery. The Bellini Ducts are very tiny and are not entered. Unroofing ducts to remove crystal deposits is presently an untested surgery. Some surgeons favor it when deposits are large and there is pain without obstructing stones. Surgeons remove stones from calyces so I assume your surgeon easily enters them when needed. I am glad this site and some answers are helpful. Most of all, it is your physicians who care for you, and I am sure their intention is always to prevent stones – that is the main purpose of everyone. Regards, Fred Coe

      • Laura Bousada

        I understand that my physicians are my primary source of information and care and I have good doctors. What I meant to ask and realize now that I left it out somehow, is what is the main difference between ureterscopies and percutaneous procedures? For instance why would one be benefical

        • Laura Bousada

          Over the other. When would one be used over the other.

          • Fredric Coe, MD

            Hi Laura, I believe I answered this below. The decision is specific to a particular patient and stone problem, and to the surgeon, also. Both modalities can achieve outstanding results when used properly. Being to particular it would be foolish of me to try to offer any useful generalizations. Regards, Fred Coe

          • Patricia McClain


            I also have dRTA. I can only tell you what I have learned about my specific issues and this may or may not apply to you. Often, PCNL percutaneous nephrolithotomy is done to remove large stones… usually your urologist has already tried URS and/ or ESWL, often more than one time and nothing worked. PCNL is usually the most invasive procedure urologists do to remove kidney stones, so it can be the procedure of last resort. Since, an incision is made there can be a greater risk of infection and greater chance of some other complications. Also I believe a nephrostomy tube usually may be left in… it drains urine from your kidneys but bypasses the ureters and bladder… I think this is the tube that your urologist uses to get the instruments to your kidney… the instruments used to remove the offending stones. However, when there is a need for a PCNL your situation is carefully evaluated by urologists and radiologists.. before they do anything.

            Also it is beneficial to have a nephrologist be involved… in 1983 I had emergency open surgery… after my urologist and nephrologist had an argument about releasing me from the hospital. Additional tests were performed.., an IVP which was used before CT scans were invented and a group of stones was about to move around and form a new blockage. I would have had to make another trip back to the ER room, if my nephrologist had not been there. I did not feel extremely sick but, I was in the OR within 20 minutes after the anesthesiologist came into my hospital room..( when you had an IVP, you could not eat or drink anything for a while… and or urinate.) I did make a full recovery but the normal recovery time from open surgery was about 3 months… that is why the new procedures are so important. Hospitalization time has become very short and often people can go back to work within a few days after a procedure. Many procedures are done out patient or in day surgery situations..

            Dr. Coe may tell you some of this is erroneous, which it may be. I am not claiming to be an expert … I am only trying to explain some things I experienced.


            Before, lasers and modern techniques : cystoscopies with a stone catcher basket could be done and open surgery. Many urologists have never done open surgery… because they are young enough that URS, ESWL and PCNL existed.. these started to be used in the US around the mid 1980ies, I believe. Towards the end of the 1980ies these methods were taught in urology residency programs.

            This is my general understanding of the development of modern surgical methods… and some hospitals, medical groups etc. got the lasers and instruments for the new methods, years before smaller hospitals did. Even today, there are companies that have ESWL machines in the back of a semi truck and they travel around to various hospitals…

            I was also told that either ESWL or URS can be used in a given situation.. it is up to the your urologist to determine this, based on his skill set and experience… Some are better at one than the other… and sometimes your doctor may refer you to his partner or another urologist he believes is more skilled then he is

            • Fredric Coe, MD

              Dear Laura and Trish, No, I will not say any of what you have said is erroneous; you are valiant and capable people fathoming the complexities of a very complex branch of surgery. I will say that there are three prime modalities for surgical stone management, ESWL, PERC, and URS, and their use in a given case is a subtle choice for even the most skilled urologists. I believe all three modalities should be available for a patient, and patients should have their pros and cons explained so they can participate in the final choice. All of the urologists I know well more or less will agree with this statement. Ideally it is not so much the skill set of the surgeon as it is the best modality for a given stone situation that drives the eventual decision. If I may I would add that prevention is better than treatment, and every effort should be made to stop stones from forming. Warm Regards, Fred Coe

        • Fredric Coe, MD

          Hi Laura, ureteroscopy is via the urinary tract; an instrument is passed up the urethra into the ureter and thence the kidney. Percutaneous nephrolithotomy requires a hole be made in the back and an instrument passed into the body and through the outer cortex of the kidney into the renal pelvis. This permits use of larger instruments but is invasive. The choice of URS vs. Perc is very complex and individual to the specific patient and surgeon. Regards, Fred Coe

          • Patricia McClain

            Thank you for letting me post Dr. Coe. I do appreciate what you are doing and how you are trying to educate all of us kidney stoners. I had several urologists who explained things to me over time… for about 4 months in 2008. I also had lots of problems as the last time I had procedures, I was forced to go the university in my state. My urologist of over 20 years retired. There is one medical school here and indigent people can come from 300 miles away… besides the more local ones.

            I had many problems getting my urologist/attending to communicate with me… as the residents were in the middle of it. So I became friends with an administrative assistant for the urology department. Also the man who became my doctor, was forced to work on kidney stone patients.. for a few years. His sub specialty is not kidney stones. There is a shortage of doctors in my state and the university has a hard time recruiting new doctors… and many come and stay a couple of yeasr. I also had/have a better rapport with the urology nurse practioner… Since my urologist was so busy with other patients… who are sicker than I was/am I elected to see the nurse practioner.., I did not need the expertise of my urologist.

            Due to the fact there are really no urologists in a metro area of over 500,000 people who I feel are qualified to treat me.. I have elected to go to another state. My new doctor’s sub specialty is kidney stones and he/she is one of the best doctors in the US.


            • Fredric Coe, MD

              Dear Trish, I hope your move gets you better care. With your new doctor I hope the emphasis is on prevention of more stones. The whole secret for stone formers in getting life back together medically is prevention of new stones. That is what this site aims at, and your new doctor, too. Best, Fred Coe

  15. Linda Matuszewski

    Very interesting article.

  16. Celia Mac Donald

    I have a question Fredric. You say that blood vessels and vascular disease have nothing to do with cortical calcifications and again quote “No evidence exists showing calcium deposits within the vasa recta within the medulla or papilla. Deposits of hydroxyapatite can be found within and involving capillaries, but this is not evidence of a primary calcification” however you also refer to a study in Pubmed “What is Nephrocalcinosis?’ by professors Shavit, Jaeger, and Unwin; where they state ” . We have concluded, and hypothesized, that nephrocalcinosis is primarily a renal interstitial process, resembling metastatic calcification, and that it may have some features in common with, and pathogenic links to, vascular calcification”. Since my sister was also diagnosed in 2012 with atherosclerosis, besides MSK and nephrocalcinosis,
    I’ve read many similar studies that compare atherosclerosis or soft tissue calcifications to nephrocalcinosis, that renal arteries may also be affected, that heart disease due to atherosclerosis is associated to CKD. I’ve read that some of the systemic autoimmune disorders like lupus sjorgren’s scleroderma Wegener’s vasculitis can cause glomerularnephritis, renal vasculopathy involving renal arteries, arterioles and small blood vessels. Some of our members have been diagnosed with one of those autoimmune disorders, one or more with EDS. One of our MSK members was recently admitted to hospital following a heart attack and was diagnosed with atherosclerosis.
    Do you think in these cases, their MSK and nephrocalcinosis could have something to do with vascular disease? If not, how exactly do these systemic autoimmune diseases affect kidneys and what do they have to do with MSK and nephrocalcinosis in our members? Thank you.

    • Fredric Coe, MD

      Hi Celia. Thanks for the detailed and interesting question. Clearly I admire the review, which I chose as an introduction to my article yet do not agree with everything in it. In particular the vascular theory of plaque seems, to me at least, to lack adequate supporting data and therefore remains a theory and no more. Many confusions arise in the area of renal crystallizations because kidney disease itself appears to lead to deposits and certain kinds of renal diseases arise from vasculitis. Thus far no evidence supports the idea that interstitial plaque is part of an atherosclerosis process. Chronic kidney disease is associated with heart disease, and kidney stones are epidemiologically associated with vascular disease, but plaque and vascular disease are not associated. Sjogren syndrome causes a form of renal tubular acidosis readily identified in most cases by reduced blood bicarbonate and unduly alkaline urine. SLE renal involvement can produce a form of renal tubular acidosis. These are easily distinguished from the idiopathic stone formers, and readily diagnosed on their own terms. The vasculitides – scleroderma and Wegener’s renal involvement are very serious and usually reduce kidney function and produce multiple other abnormalities that permits their diagnosis. MSK itself is a renal developmental disease and I know of no associations with the aforementioned conditions. All of this negative commentary is not meant as a final word, but as my best immediate summary of what has supportive data and what does not. Moreover, although I am a nephrologist, I do not pretend to definitive expertise across the vast range of diseases in this paragraph. So, take this as an initial note, and over time our site will – in the course of things – try to clarify these inter-disease relationships. The site is very new, only one year old, and meant to evolve over some years. I hope this initial answer offers some ideas to consider. Regards, Fred Coe

      • Celia Mac Donald

        Thank you Fredric for your expert feedback, I appreciate that. You’re right about the different systemic autoimmune diseases that affect kidneys do cause RTA besides nephrocalcinosis, I forgot about that! I don’t have a nephrologist so have no one I can ask these questions, thanks for your help and patience!

        • Fredric Coe, MD

          I am delighted, Celia; I put up this site so people could get reliable information, from me or from other people who are experts in this field. Thanks for affording an opportunity to bring these issues into a public forum. Regards, Fred

  17. Celia Mac Donald

    I like your definition of “Interstitium” 🙂 I finally understand what it means! In not one of the articles or studies I’ve read to date that mention interstitium, do they explain where it’s found! Thanks.


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