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?


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


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.


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.


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.


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.


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.

88 Responses to “NEPHROCALCINOSIS”

  1. 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

    • 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

  2. 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?

    • 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

  3. 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?

    • 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

      • 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.

        • 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

          • 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

  4. Antonette de la rama

    Greetings Dr. Coe
    I am a female, 37 y.o. 5 ft.tall, 92 lbs. Asian. With solitary kidney with medullary nephrocalcinos (not passing stones)
    I just wanna clarify my recent blood works and ask for my prognosis

    Normal urinalysis, no protein no uti, no rbcs/wbcs

    Serum Creatinine june 2016: 67
    Serum creatinine sept 2016: 75
    Serum creatinine december 2016: 84
    Serum creatinine march 2017: 66

    My creatinine as well as egfr for the last 2 yrs are fine according to my nephrologist. Sept 2014: 62 as the lowest creatinine and dec 2016: 85 which is the highest.

    Pls let me know about my chances of avoiding dialysis, i mean with these level can i have a normal full life at least until age 80?


    • Fredric Coe, MD

      Hi Antonette, I assume the creatinine is in units of micromoles/liter, and therefore the range translates into 0.7 to 0.96 mg% which is common in the US. These values are not at all alarming. MSK has little known tendency to progress to kidney failure absent surgical accidents. My only suggestion is to be very careful about any surgery and if you do ever need stone surgery try to have it done by physicians who are very adept and experienced. Likewise, if you do pass a stone be vigilant about obstruction – always follow up with your physician who can be certain about such matters. Regards, Fred Coe

    • Dr Jozef Van Rens

      Dear Dr Coe, I have a question for myself. I would be very interested in your advice.

      I am 58 Years old, fit healthy,male, non smoker, non drinker, good blood pressure, BMI 23.6. Originally from the Netherlands, now working in New Zealand as a GP. I had 2x a kidney stone attack 20+ years ago. I went to the Urologist recently for review prostate and had a CT kidneys done:
      My CT kidneys. Technique helically acquired axial images of the abdomen and the pelvis with sagittal and coronal reformats. IV contrast (100 ml Omnipaque 350 IV)
      Findings: There are multiple calculi in both kidneys. In the inter polar region of the L kidney there is a large calculus measuring 15×11 mm as well as several smaller calculi in the region and one in the lower pole.
      In the Right kidney there are also at least 5 renal calculi, the largest in the upper pole measuring 4×2 mm.
      Both kidneys demonstrate multiple cortical and parapelvic cysts, some demonstrating faint wall calcification.
      There is a pre contrast hyper dense cyst arising from the upper pole of the left kidney. No enhancing solid renal lesion. No hydronephrosis. no ureteric or bladder calculi. Rest all N

      General lab: Lab: blood results Sodium 141 mmol/l (135-145), Potassium 4.0 mmol/l (3.5-5.2), Chloride 101 Mmol/l (95-110)
      Urea 4.5 mmol/l (3.2-7.7), Creatinine 79 umol/l (60-105), eGFR>90 mL/min, Urate 0.35 mmol/l (0.23-0.45) Ca 2.4 mmol/l (2.2-2.6) Phosphate 1.0 mmol/l (0.8-1.5) albumin 43 g/l (32-48)

      I had my urine tested before and after starting a Low Oxalate diet:
      Normal Oxalate full diet
      Volume 4110 ml /24 hrs secretion this period normal /24 hrs
      Oxalate 99/umol/l 407 umol H 0-310 ELEVATED
      oxalate/crea ratio 35 N 0.15

      Concentration secretion this period Normal/24 hrs
      Ca 2.0 mmol/l 8.3H 2.5-7.5 ELEVATED
      creatinine 3.0 mmol/l 12.0 mmol/d 9.0-18.0
      Na 16 64 N 100-250
      K 22 89 N 35-100
      Urate 0.9 3.6 N 1.5-4.5

      After a low oxalate, low sodium and Ca “max 1000mg through the day diet”
      24 hrs Volume 3.51 ltr
      Oxalates 0.28mmol/d (0.06-0.49) NORMAL
      Citrate 2.5
      citrate/creatinine ratio 0.4 mmol/l
      creatinine 4.2
      24 hrs creatinine 14.7/d (7.0-24)
      24 hrs Volume 3.82ltr
      Urine Ca/Creat ratio 0.83 (H) (0.00-0.60)
      Na 54 N
      K 99 N
      creatinine 3.1 11.8 N (7.0-24)
      Urate 3.4 N

      So following a low oxalate diet lowered the oxalate levels in my urine but my Ca is still to high.
      What would you advise? Stay on the low Oxalate diet even though my last kidney stone attack was more than 20 years ago.
      But I have been making stones during my last 20 years (even when not experiencing attacks) and I have partly medullary sponge kidneys.
      Start on a thiazide to reduce my calcium in the urine? what dose?

      Kind Regards Nga Mihi (with respect as the Maori say)

      Dr van Rens

      • Fredric Coe, MD

        Hi Doctor, Your urine oxalate was a bit high, urine calcium more so. Diet – less oxalate and I gather 1000 mg calcium lowered the oxalate but the calcium remains high. I suspect you have idiopathic hypercalciuria, and even so low a sodium intake of 54 mEq/day does not lower it fully. I think this article is my best on the low sodium high diet calcium as a treatment. It has links to a deeper article on the science supporting this kind of diet. You obviously formed stones but with your new data, are your supersaturations now lower than they were? They are key as guides to overall stone risk. If not available, and given the numbers of stones that appear to have formed, you might add a low dose of chlorthalidone – 12.5 mg/day or the equivalent of Indapamide 1.25 mg/day to the low sodium high calcium diet. Regards, Fred

  5. Monday Mercer

    I am a 66 year old woman who was put on Telmisartan (80 MG) and Hydrochlorothiazide (12.5 MG) for high blood pressure in February 2016. Since I have been placed on these drugs, I have had kidney stones 3 times and never before taking these drugs. I had to have surgery to blast very large kidney stones in July 2016, had kidney stone again in December 2016 and now in March 2017. What do you recommend I take for high blood pressure that would not cause kidney stones. I now believe it is the Telmisartan causing this problem. I have no other side effects from this drug and it has stabilized my blood pressure but having kidney stones 3 times since starting this drug a little over a year is not good. Can you explain why this is happening and what I can do about it? Thank you!

  6. Kim

    I wish i had a doctor, like yourself, that could explain to me my diagnoses of MSK and Nephrocalcinosis. I was told 4 years ago that i had these but no real exsplaination of what it is or what will be my future. All i really know is from articals and sites like yours and that i live in almost some level of constant flank pain and nausea. I get recurring kidney infections that last months due to wrong antibiotics and/or not a long enough course to remove entire infection. 8 times out of 10, when pain and nausea are at their worst and i do go to the ER, im told that because they cannot see an obstruction thru ct w/o contrast that the pain im feeling and following nausea is in my head. That without obstructions there should be no pain. Since im normally, upto the last few years at least, was active person, involed with my childrens school and a boy scout leader and now have to struggle to get out of bed most days, id like to hear your opinion before i book myself a rubber room.
    Tired of being branded a drug seeker without history of drug use.
    Lost in southern indiana, kim

    • Fredric Coe, MD

      Hi Kim, I am very sorry to hear about all this. Perhaps you might benefit from evaluation and treatment in a center devoted to stone management, Given you live in Indiana, you might want to consult with Dr James Lingeman at Indiana University, Indianapolis. Small stones with pain are well known to him, and he may well be able to help. Regards, Fred Coe

  7. 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

  8. 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.

          • Kristen

            Dear Dr Coe
            I would like to know if there is any way of getting rid of a Calcium mass in my right kidney? I also have a lot of small stones caught in the meat of the kidney. The kidney measures 13cms. My other kidney is not affected and measures 9 cams. After having my first child I was in Intensive care after passing blood an vomiting. I was diagnosed with a Medallary Sponge Kidney at the age of 22 in 1972.
            I do felel intermittent pain in my kidney that passes.
            I would like to know if there is anyway to dissolve the Calcium in my kidney?
            I have recently been diagnosed with Osteoporosis and I am now taking a natural supplement from BoCeuricals called AdvaCal Forte with K2 and D3 it does contain Calcium etc
            I have always led a healthy outdoor life and have a mainly organic vegetarian diet.
            I look forward to hearing from you

            • Fredric Coe, MD

              Hi Kristin, Without seeing the actual images I cannot say anything useful about the calcifications. You may indeed have MSK involving one kidney. If you do not have pain, bleeding, infection or obstruction, surgery would be a poor option. Your bone disease with kidney stones maybe part of idiopathic hypercalciuria, and that would require careful management. But most of all, I sense a lack of purposful evaluation and prevention. Take a look at this article and see if it applies to you. Be sure you have been tested properly and know what is wrong, then get it treated. Remedies like advacal are essentially useless without clear reason to take them. They can cause disease if not used in the proper setting. Regards, Fred Coe

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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.

  14. 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?

  15. 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

  16. 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.

  17. 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

  18. 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

  19. 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

  20. 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

  21. Linda Matuszewski

    Very interesting article.

  22. 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

  23. 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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