NEPHROCALCINOSIS

Nephrocalcinosis means kidneys contain many calcium deposits. You can see them on CT scans or during surgery to remove stones. This article tells about where in kidneys the deposits reside, what they mean, and what significance we need to attach to the word.

Fuller Albright Made Up the Word Nephrocalcinosis

The boyish face of perhaps the greatest 20th century scientist concerned with kidney stones, Fuller Albright, fills the featured picture. In 1934, Albright, then an Assistant Physician at the MGH and an instructor in medicine at Harvard Medical School, used his newly coined word, nephrocalcinosis in a remarkable paper.  That paper described calcium deposits in kidneys of patients with hyperparathyroidism – a mineral disorder caused by enlargement of one or more parathyroid glands.

Who Were His Patients?

He described three types of kidney involvement in primary hyperparathyroidism. Whereas type 1 patients simply formed kidney stones, type 3 patients suffered from acute ‘parathyroid poisoning’, with kidney failure and death. Midway between these two, type 2 patients had stones and kidney tissue calcium deposits but adequate kidney function.

About these Type 2 patients he wrote this passage in which the word first appears (In text box below).

First use of nephrocalcinosisWhat Limitations Did His Patients Impose on His Understanding?    

All of his patients suffered from primary hyperparathyroidism, a disease found in only 5% or so of calcium stone formers we see today in our clinics.

Moreover, the tissues he observed came from autopsies, meaning from only his type 2 and 3 patients. His Type 1 patients, who simply formed kidney stones, rarely came to autopsy, so he did not have tissues from them.

As a result Albright coined the word nephrocalcinosis to describe the scarred, contracted kidneys of patients whose primary hyperparathyroidism had caused kidney disease. Their kidney calcifications were a mixture of those from stone formation and those that occur with kidney failure.

Who Are Our Patients?

Like Albright, some have primary hyperparathyroidism. But none have significant kidney failure. They resemble his Type l patients.

Unlike the patients for whom Albright coined nephrocalcinosis, we mainly study patients whose stones arise from no systemic disease at all. They just form stones we ascribe to excessive amounts of daily calcium or oxalate excretion, or low urine volume or citrate, or to combinations of these – so called idiopathic calcium stone formers.

So physicians today use the word nephrocalcinosis to describe very different patients than those Albright studied when he made the word up.

Who Uses the Word Nephrocalcinosis?

Radiologists

They mean many calcified – radio dense – regions overlay the outlines of the kidneys on various kinds of imaging studies: Simple flat plates, ultrasound studies, and CT scans.

But, as in the Cave of Shadows, radiographs are to the reality of tissue as shadows to real objects.

Many Others

When I looked up nephrocalcinosis in PubMed, I found 2686 entries.

Of these, most concerned diseases that calcify kidney tissues: 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.

As well, I found an excellent review from which this this article takes its starting point: ‘What is Nephrocalcinosis?’ by professors Shavit, Jaeger, and Unwin.

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

But where do they form in kidneys, and what do they signify?

Where Kidney Crystals Form

Cortex, Medulla, and Papilla

nephron-somso2

This stock web drawing depicts a slice through a kidney. The outer capsule runs along the top.

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

Below that crescent of vessels lies the medulla.

At the very bottom of the medulla lies the rounded papillum where urine drains into the renal pelvis and thence down the ureter. Urine exits through the terminal collecting ducts of Bellini – the opening of the thick long tube that runs vertically from cortex to the bottom.

Glomerulae

Each contains a tuft of capillary held within a complex web of cells. The force of the heart filters water and salts out of the capillaries into the tubule of the nephrons. Normal human kidneys contain about one million nephron units. Common measurements of ‘kidney function’ such as serum creatinine reflect the sum total of filtration through all  two million glomerulae. Obstruction from stones can reduce filtration.

Nephron Segments

Proximal Convoluted tubules

Each glomerulus drains its filtrate into a squiggly – convoluted – ‘proximal’ tubule which gives way into the remaining nephron. These tubules reabsorb much of the filtered water and salt back into the blood. They leave behind materials destined for export into the final urine.

Proximal Straight Tubules

Mislabeled thick descending limbs on the drawing, a part of the proximal tubule extends below the arc of vessels into the medulla and is called the S3 segment. I mention it only because crystals form there sometimes.

Loops of Henle

As they travels downward below the proximal convoluted tubule each nephron thins into a hairpin shaped loop. Those hairpin loops of glomerulae that lie near the outside of the kidney (look at the nephron to the left) reach down only part ways into the medulla – the portion of the kidney below the red crescent of vessels. By contrast, loops from glomerulae near the medulla – just above the crescent of vessels – reach down into the deepest parts of the medulla.

These hairpin loops permit kidneys to concentrate the urine, which means extracting water from the filtrate and putting that water back into the blood. Unlike the proximal convoluted tubules that reabsorb water and salts back into the blood the loops permit reabsorption of water without the salts, so the salts destined for export are concentrated.

Names for the Segments of the Loops

As already mentioned, the ‘Thick Descending Limb‘ is actually the S3 segment of the proximal tubule.

It gives way to the descending and ascending thin limbs of the hairpin. The top of the thin ascending limb widens into the ascending thick limb. This segment reabsorbs sodium chloride back into the blood without water, leaving the ‘extra’ water – without its sodium – as a diluted fluid in its lumen. The sodium chloride collects in the medulla around these thick limbs which becomes saltier than blood.

So called Randall’s plaque, over which calcium oxalate stones may form, originates in the outer parts of the thin limbs,

Distal Convoluted Tubule

The dilute fluid drains into the ‘Distal’ convoluted tubule’. Here, the ‘extra’ water leaves, back into the blood. This segment can make the fluid more acidic, and remove calcium back into the blood.

Collecting Ducts

From there, fluid drains through the unmarked straight connecting segment and thence into the collecting ducts. Like any plumbing drains, these run from the cortex down the medulla all the way to the papilla where the final urine flows out. Along the collecting duct the ‘salty’ interstitium around the thick ascending limbs draws water – but not calcium or phosphate or oxalate back into the blood, supersaturating the fluid that remains in the tubule. Collecting duct cells make the fluid more acid, a protection against calcium phosphate crystals.

We name the portion of the collecting ducts that run alongside the medullary thick ascending limbs the outer, and the remainder the inner medullary collecting ducts.

Ducts of Bellini 

These terminate the nephron and empty the final urine into the urinary collecting system through tiny holes in the lining of the papillary tip. Because they hold the final, most supersaturated urine, crystals often form in them, creating plugs over which stones form.

Where is the Interstitium?

Envision a tall building. Pipes run from the basement to the roof – water, steam, drains, electrical conduits, elevator shafts, stairwells. Now, think about the space between the elevator shafts, stairwells, and all the pipes and conduits: That is the interstitium, what stands 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.

Mice can live in the spaces between things, but not in the pipes. Rust can plug pipes but not the spaces between them.

The Reward for Brave Hearts

To those who have read the foregoing: My regards and admiration. Like tourists who climb the ancient, winding, broken stairs up into the towers of medieval cathedrals or the battlements of long abandoned castles, panting and worried about getting back down, you now come into the reward of so much virtue and endurance. Before you lies the architecture of the nephron.

Where the Crystals Form

From what I have told you, where would you surmise crystals might form?

Surely not, you might say, in the glomerulae or proximal tubules, or in the thick ascending limbs with their excess of water. The distal tubules, perhaps, as they extract water, but – you might think – it is only the extra water.

Ah! That vast long drain, where water extraction supersaturates urine – there would crystals form.

And, those uncanny thin limbs, so deep into the medulla.

You are right.

Who Sees Them?

When radiologists spy calcium deposits in kidneys so numerous they name them nephrocalcinosis, the deposits lie – with rare exceptions – in the medulla, the papillum. Surgeons can see them in the collecting ducts and interstitium. For pathologists they lie in the thin limbs, the collecting ducts, and the interstitium – the space between the ducts.

Crystal Deposits in the Cortex

These occur in rare stone diseases. I list them for completeness only.

Glomeruli

In humans, high blood calcium can produce glomerular crystals. Hyperparathyroidism for example, when severe.

Shall I mention  intravenous dibasic phosphate in rats, Vitamin D intoxication in suckling ratscalcifications of large immune deposits? No; I demur. Not relevant to humans.

Proximal tubules

We have found calcium oxalate crystals in the proximal tubule S3 segment in primary hyperoxaluria. 2,8 dihydroxyadanine crystals due to APRT deficiency can plug proximal tubules. In transplanted kidneys we have seen scattered birefringent crystals presumably calcium oxalate.

In other words, common stone formers have no proximal tubule calcifications, only patients with rare diseases.

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.

This means, here and there, uncommonly, scattered deposits can lie in the cortex.

Cortical Interstitium

When kidneys fail and blood accumulates excesses of salts and molecules kidneys normally eliminate, crystals form in the space between tubules, the interstitium because blood itself supersaturates. The same for primary hyperoxaluria: so much oxalate is produced it can accumulate in blood and crystallize in the interstitium.

Cortical Blood Vessels?

We believe it is potentially confusing to lump vascular disease and its associated calcifications together with calcifications within the renal tubules and interstitium.

Crystal Deposits in the Medulla and Papilla – Work by Us

Our reports comprises the bulk of human kidney tissue work to date.

Thick ascending limbs

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

Thin Loops of Henle

We have found rare hydroxyapatite deposits plugging thin limbs in ileostomy, cystinuria and primary hyperoxaluria patients with reduced renal function. These are best illustrated in Figure 4 of the ileostomy reference. As I have mentioned, plaque begins in the outer shells of the thin limbs.

Outer Medullary Collecting Ducts

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

Inner Medullary Collecting Ducts

Here is the main place for crystal formation. Are you surprised? The tubule contains supersaturated fluid progressively approximating urine itself. No wonder of it: crystals from where supersaturation is.

Hydroxyapatite crystal plugs

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

Calcium oxalate crystal plugs

Obesity bypass surgery, distal renal tubular acidosis, small bowel resection, and medullary sponge kidney stone patients form calcium oxalate deposits.

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

The Odd Microliths of MSK

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

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

We have found Bellini duct crystal plugs in all stone forming phenotypes.

This is expected as these ducts contain the final urine.

Bellini duct plugs may attract overgrowths at their distal ends that protrude through a dilated opening of the duct into the flowing final urine. These proto stones may well grow to clinically significant size. Growth on plugs is one pathway for stone production.

Interstitium

To date, all interstitial deposits found in human kidneys have been hydroxyapatite ‘Randall’s’ plaque. Growth of stones over plaque is another pathway for stone production.

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

Idiopathic calcium oxalate stone formers

Idiopathic calcium oxalate stone formers display variable amounts of interstitial plaque. Those with hypercalciuria had the heavier plaque deposits, much as we have found. Unlike our work, many patients had crystal plugs in Bellini ducts. Wang et al described much the same.

In biopsy tissue from 15 patients with ‘idiopathic calcium stones’ not otherwise characterized, Khan et al found Large areas of interstitial plaque. 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.

Mixtures of stone formers

Linnes et al studied ICSF, ICSF with malabsorption, phosphate stone formers which included struvite stones, and, also, uric acid stone formers. In 99% of patients 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. The patients were mostly female, and hypercalciuria was not impressive. They did not analyse the crystals in the plugs.

Single case report

Report of a single case describes interstitial plaque deposits identical to those we have 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.

Putting it All Together

Overall, these and our papers more or less agree. Stone former kidneys contain interstitial calcium phosphate deposits and plugs in Bellini duct and inner medullary collecting ducts. Only we and Khan have described the crystals in plugs to date. So, when we speak of multiple crystal deposits in the kidneys of stone formers, or nephrocalcinosis, we all seem to mean plaque and plugs. MSK differs altogether, because dilated ducts contain myriads of calcium oxalate microliths.

Virtually all Stone Formers Manifest Nephrocalcinosis

Virtually all Stone Formers Form Kidney Crystal Deposits

Shavit, Jaeger, and Unwin concur with Albright: ‘Strictly, the term ‘nephrocalcinosis’ refers to the generalized deposition of calcium oxalate (CaOx) or calcium phosphate (CaPi) in the kidney.’ Since virtually all stone formers deposit crystals in their kidney tissues, virtually all have nephrocalcinosis.

The Kinds of Deposits Number Three

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

The second kind 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.

Of the three, the microliths of MSK, unique to this one disease, make up the third.

The Word Means Plaque and Plugs, or MSK

In any one patient nephrocalcinosis means interstitial calcium phosphate crystals, tubule crystal plugs of diverse kinds, or both, and microliths in the dilated tubules of MSK.

Because of this specificity, I propose we restrict the word to this exact meaning: Calcifications within kidney tissues as demonstrated directly in the tissues themselves.

Radiographic Nephrocalcinosis

Because tissue calcifications and stones both brighten the confining shadows of the radiologist with similar points of light but stones do, also. Therefore, we propose the term ‘radiographic nephrocalcinosis’ define what radiologists report. I say this because radiological means cannot always distinguish masses of tissue plugs or of microliths in MSK from stones.

Surgery

Because they visualize stones, plaque, and plugging, and also the odd contours of MSK, surgeons can not only specify nephrocalcinosis but the type of calcium deposit. Therefore, they mean by nephrocalcinosis what pathologists mean. The only difference between them is in resolution. One has a microscope, the other simply an external view of the kidneys at modest magnification.

Meaning of Nephrocalcinosis

Since all stone forming patients deposit calcium in their kidney tissues, it signifies a quantitative vs. a qualitative distinction. Unlike other patients, those with nephrocalcinosis have more tissue calcium deposits and therefore, perhaps, what one might call more disease burden.

By disease burden I mean the tissues carry more crystals in them, and therefore a greater hazard from whatever evil it is that crystals might do.

One such evil: lodgment for new stones to form on. Because stones form on plaque and the ends of plugs, more plaque and more plugs implies a greater stone production potential. Although evidence for such potential must come, eventually, from prospective observations greater tissue mineral burden seems a proper spur to greater treatment effort even now. Such greater treatment efforts mean perhaps more emphasis to patients about diet and fluid change, and earlier use of medications.

Another is tissue damage. For example, crystal plugs cause obvious tubule cell loss and inflammation in the surrounding interstitium. Although papillary, plugging may affect the cortex. Compared to patients without plugging, those with plugging have more cortical interstitial scarring that treatment might benefit. Such treatment, as opposed to stone prevention alone, would specially emphasize reduction of calcium phosphate supersaturation.

Like many stones, nephrocalcinosis quantifies stone diseases. But in a new dimension, one that complements those already in use. Because complementary, the word adds specific value, provided we use it carefully.

94 Responses to “NEPHROCALCINOSIS”

  1. Chelsea

    Hi, my name is Chelsea . I am 28 , I was diagnosed with medullary sponge kidney with major nephrocalcinosis about a year ago. I have had kidney/ flank pain on both sides for over 5years with out finding a cause. I have never had passed a kidney stone. After all testing (X-rays , ct , blood , 24 hr urine) I was informed I had two major contributors- very low citrate and very high calcium in the urine. I have been able to correct the citrate by adding lemon juice to water but can not find a natural way to fix the high calcium. I am very sensitive to all of the medications they have tried (old school blood pressure meds) and become quite ill when on them. My urine output is also kept quite high. Do you have any suggestions to help lower my urine calcium ? Thanks

    Reply
    • Fredric Coe, MD

      Hi Chelsea, As the article points out MSK cannot be reliably diagnosed except during stone surgery or by special CT scanning with contrast injection. SO you may just have multiple calcifications from stones. The high urine calcium is part of idiopathic hypercalciuria, I suspect, the low citrate is not obvious from what you have told me. Here is my best article on control of urine calcium. It is all about salt. Here is the ideal kidney stone diet – based on what trial data we have. You have kidney stones, even though none have passed, and they may well be calcium phosphate. Given the stone mass and pain, surgical approaches are a matter of present debate. Please understand that all of these remarks are in ignorance of your complete medical situation, so the best approach is to share them with your physicians who may agree or have reasons to not agree with me. Regards, Fred Coe

      Reply
      • Chelsea

        Thank you for your timely reply. I will look into the articles! I have had a ct with contrast to confirm the msk. I don’t know if this makes the mentioned articles contradictory? It’s very hard to find legitimate kidney stone / msk information and most seems under/ untested , especially for msk. I really appreciate the work you’re doing and the informative article

        Reply
        • Fredric Coe, MD

          Hi Chelsea, If you have had contrast CT and is showed MSK you have msk. take a look at the article on it. We were the only group to actually do the surgical anatomy. Treatment is complicated in that stones may form because of simple stasis of urine in the cysts. Minimal supersaturations are the best I can think of. With a lot of pain some surgeons are trying to empty out the cysts. SWL is not a good idea. Take a look. Regards, Fred Coe

          Reply
        • Amber

          Hi I am a very scared mother of five. I was told I have nephrocalinosis Msk. I have surgery to remove my stones every two months and was just told I’m a very rare case and basically there is nothing to stop my kidneys from turning into stones. Is there any truth to that?

          Reply
  2. Vee Smith

    Please help me understand why my eGFR is going down and what can I do to fix it. I am a 72 year old female, very active, no pain, non smoker, non Alcohol drinker, non drug user. In August 2009 eGFR 45ml, BUN 20mg, Serum Creatinine 1.4, Glucose 110, Calcium 9.8mg.
    July 2011 eGFR 34ml, BUN 30.4mg, Ser Creatinine 1.7mg, Glucose 96mg, Serum Calcium 10.6mg, PTH Intact 85pg, Alk Phos 19.9ug, Vit D 38ng. 24 hour URINE Calcium 36.6, urine volume 3325 ml, urine sodium 103 mmol/vol, urine creatinine 1.9 gm. Beta cross laps 583.
    Random urine creatinine 56mg, random urine calcium 1.1 mg, random urine sodium 31mmol/L, urine microalbumin 4.30, Albumin/Creatinine ratio 58.9. I’m taking Aspirin 81 mg and Telmisartan 80 mg tab. DEXA shows mild bone loss left hip T-1.5, US Kidney Impression – Increased cortical echogenicity likely related to medical renal disease. No hydronephrosis, contour deforming mass or renal calculi. The bladder appears unremarkable. I have seen an Endocrinologist who suggested consuming 1200 mg calcium not supplements, 2000mg vitamin D and recommended Alendronate to limit bone loss. I have also seen a Nephrologist who recommended Atorstatin 20mg daily for chronic kidney disease. He stated my calcium/creatinine clearance ratio 0.0046 may indicate a benign inherited variant, (FHH). I have not started taking these two new meds yet. I am more concerned about why my kidney function is going down. All other tests results (CBC, Lipid Panel and Comprehensive Metabolic Panel) are normal. Please help. Thank you and know that your opinion is greatly appreciated. Vee

    Reply
    • Fredric Coe, MD

      Hi Vee, This is a very complicated problem. You have a significant and progressive kidney disease with scant urine protein and a high blood calcium and PTH level. The low urine calcium is hard to assess in the presence of so much kidney function loss. I would be remiss to say anything from this distance. If your physicians and you would like a serious opinion from me and my colleagues we would need to see all of your relevant medical information and try to offer something useful. I certainly recognize this is a serious matter in an otherwise well person, and a bit unclear as to cause and possible amelioration. Regards, Fred Coe

      Reply
  3. Mark Dunstan

    Dr. Coe,
    I have been dealing with calcium oxalate stones in my right kidney since I was 12 years old. I have also had 4 lithotrypsies to break up the stones. Even on potassium citrate and Hydrochlorothyazide and drinking lots of water I seem to keep making new stones. The kidney that I am having trouble with actually has two ureters coming off of it that merge into one. It’s a hereditary thing as my father’s ureters merged into one half-way from the kidneys to the bladder. I have had a theory that because my kidney has the two ureters not enough pressure is being built up inside the kidney to help push out crystals that have formed which eventually turn into stones sitting at the bottom of the kidney. Does that make any sense at all?

    Reply
    • Fredric Coe, MD

      Hi Mark, You do not mention your 24 hour urine tests, but I imagine they are abnormal and prevention has not been complete. It is true that urinary abnormalities can promote stones but calcium phosphate would be the more common type of crystal. If you wish to put up the 24 hour labs I could take a look. Regards, Fred Coe

      Reply
  4. Kayla

    Hi, my name is Kayla. I’m 23 and was told I have nephrocalcinosis when I was 16. They ruled out everything that would cause nephrocalcinosis so they never found an underlying cause. Although a year ago I found out I have PCOS and insulin resistance so I take metformin for it. I see a nephrologist every year and he doesn’t really give me answers to my pain. He just assumes I’ve passed many stones which I don’t believe I have. I almost go daily with waves of pain in my back and constant flank pain. Is there any suggestion of treatment I could do?

    Reply
    • Fredric Coe, MD

      Hi Kayla, Given multiple calcifications I would be sure about the immediate cause – this means proper blood and 24 hour urine testing. You may have hypercalciuria. Possibly you have medullary sponge kidney. Early insulin resistance could point to possible genetic issues. Do the above testing first and be sure what is causing your crystallizations. Regards, Fred Coe

      Reply
      • Linda

        Hi Dr. Coe;
        About 3 weeks ago I went to urgent care with pain in my left side and abdomen. After a CT scan of my abdomen and pelvic area, urine with blood (moderate), the doctor said, I had a small stone in my Uterer. He sent me home with pain meds and said, it would probably pass in 4-5 days. No such luck. I just recently visited a urologist who confused me even more. She said, it may be a calcification and not a stone and I need to re-do the CT scan. What is the difference? And my pain and frequent urination is a symptom of a stone right? Very confused and worried. Linda.

        Reply
        • Fredric Coe, MD

          Hi Linda, I am afraid this is so bound up with the images themselves I have little to offer. But, frequent urination suggests the stone is at the junction of the ureter and bladder. Your urologist is right to take another look. If it is there it will pass or she can get rid of it for you. In all this, be sure about prevention. I like this article as a starter for people. Regards, Fred Coe

          Reply
          • Linda

            Thank you for getting back to me so quickly! I have been worried all weekend that is was something more serious, when she said, calcification. I have more pain then usual today and im just a worry wart. I’ll read the suggested article, thanks again. Linda

            Reply

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