Home kidney stones Hypercalciuria and Kidney stones: A paleo compatible solution

Hypercalciuria and Kidney stones: A paleo compatible solution


This post follows up from the previous one:

A dietician's prescription for kidney stones, what do you think?

Here is a brief outline of the solutions for the man with the high urinary calcium.

Firstly – no, he did not start eating wholegrain bread in order increase phytates to bind with calcium in his gut. He did eat a whole 30 inspired paleo diet – almost – couldn’t quite give up a little milk in his morning cup of tea. (Perhaps not a bad thing as dietary calcium bonds with oxalate in the gut and decreases urinary oxalate; many stones are made of calcium oxalate) He was however strict on everything else, cut out all grains, legumes, alcohol, processed foods, sugar and all other dairy. (As I said in the last post – he ate very little grain and no sugar or legumes anyway, so the diet changes were minimal) Good results – lost some weight and 4cm off his waist.

About those phytates: this from Wikipedia: “Phytate is not digestible to humans… Morever, it chelates and thus makes unabsorbable certain important minor minerals such as zinc and iron, and to a lesser extent, also macro minerals such as calcium and magnesium.” This study showed eating bran is effective in reducing hypercalciuria in some people, depending on the cause: Unprocessed bran and its effect on urinary calcium excretion in idiopathic hypercalciuria In my view, it doesn’t make sense to use whole grains, as the problems will outweigh the benefit. Given phytate is highly effective at decreasing calcium, the issue of it’s reduction of other minerals is not addressed / nor is it a concern of the dietician. Also magnesium is beneficial, and many people are already magnesium deficient. (This is in addition to the fact that paleo eating doesn’t include grains due to a number of gut irritants and anti-nutrients and gluten)

Protein: his protein intake was fairly high, and could be a contributor: From this Medscape  article on Hypercalciuria :

“Excessive animal protein (>1.7 g/kg of body weight) increases the body’s acid load. This additional acid load is buffered or neutralized in part by the bony skeleton, which then releases calcium into the general circulation. This extra serum calcium is eventually excreted by the kidneys into the urine, exacerbating any hypercalciuria. Acid loading also directly inhibits renal calcium reabsorption, resulting in an increase in urinary calcium excretion”.

Here is an interesting graph: Relationship between dietary protein and urinary calcium excretion in 26 studies (5 –30 ). Each point represents the mean from one of those studies. Source: Low Protein Intake: The Impact on Calcium and Bone Homeostasis in Humans

His protein intake is between 1.7 – 2.0 g/kg, i.e about 130 grams a day, so he is reducing his portion size.

Carbohydrates: his low carb, high protein diet may have also contributed, to both a higher renal acid load and constipation. Calciuric response to an acute acid load in healthy subjects and hypercalciuric calcium stone formers. And in this from Paul Jaminet: Dangers of low carb diets: Kidney stones. He is therefore increasing dietary carbohydrates from root and colourful veggies; a diet rich in alkali (vegetables, fruit) is associated with a lower risk of stone formation. Source

Sodium: Although not that high – he is reducing high sodium foods when eating out at lunch, from the same article:

Sodium intake is another significant dietary risk factor for kidney stone disease and hypercalciuria. High dietary sodium is associated with increased calcium release from bone, further contributing to any existing hypercalciuria. It also causes an increase in urinary calcium excretion through a direct effect on the kidneys and reduces or eliminates the hypocalciuric effect of thiazide therapy in hypercalciuria. Each 100-mEq increase in daily sodium intake raises urinary calcium excretion by about 50 mg/d.

Caffeine: It is also recommended he reduce caffeine, although his is not as high as this:

Caffeine intake also should be limited, because caffeine increases urinary calcium excretion. The ingestion of 34 ounces of caffeine causes a loss of 1.6 mmol of total calcium, contributing to both hypercalciuria and osteoporosis.

Alcohol: his regular habit of 300 mls or so of wine a night may also contribute:

Alcohol intake should be limited, because ethanol reduces osteoblastic activity, lowers parathyroid hormone (PTH) levels, and contributes to osteoporosis. It also indirectly accelerates osteoclastic activity, increases urinary calcium excretion, and contributes to bone loss.

Lemon juice was initially recommended by the specialist to increase urinary citrate levels – however his urinary citrate test came back showing it was quite high already. Lemon juice is a general recommendation as a treatment for kidney stones as citrate helps dissolve free calcium. It may have been high as he recently started taking magnesium citrate for constipation.

Increased fluid intake: although this does not reduce calcium, it dilutes urine and lowers urinary calcium concentrations. He is already at a high – 4 litres / day intake, so more is not necessary.

Vitamin D intake: the specialist thinks the vitamin D may be the cause and this has scared him off vitamin D supplements. So he has stopped taking them to bring his vitamin D storage levels down. One test not done is his serum active vitamin D level. It is possible that this might be high despite the 50ng/ml storage vitamin D.

There are a number of paleo researchers who do not recommend the high levels other vitamin D advocates do.

Chris Kresser, Supplement Wisely

Contrary to what some researchers and doctors have recommended, there’s no evidence that raising blood levels of 25D above 50 ng/mL is beneficial, and there’s some evidence that it may cause harm. Studies show that bone mineral density peaks at 45 ng/mL and then falls again as 25D levels rise above 45. Other studies have shown that the risk of kidney stones and CVD increase with high 25D levels, due to elevated serum calcium levels that accompany excess vitamin D.

Chris Masterjohn, Are some people pushing their vitamin D levels too high?

Has science proven that the minimal acceptable blood level of vitamin D, in the form of 25(OH)D, is above 50 ng/mL (125 nmol/L)?  No.  If you’ve been trying to maintain your levels this high because you thought this was the case, I’m sorry to break the news.  There is, on the contrary, good evidence that 25(OH)D levels should be at least 30-35 ng/mL (75-88 nmol/L).  Much higher levels may be better, or they could start causing harm, especially in the absence of adequate vitamins A and K2.   Once we leave the land of 30-35 ng/mL, however, we enter the land of speculation.

Paul Jaminet, Perfect Health diet

We believe that high dose supplementation with vitamin D3 to drive 25OHD levels above (40 – 45 ng/ml) this stable level are undesirable… Adjust to 25OHD level of 40 ng/ml (whites/Asians), 30 ng/ml (blacks)

He sites this study that shows lifeguards in Israel have kidney stones 20 times more often than the general population.

March 2012: Vitamin D supplementation and it’s effect on calcium kidney stones. Those with low Vit D levels may be able to supplement safely depending on their response. If supplementation is required again, careful monitouring of urinary calcium would be wise. Effect of Vitamin D Repletion on Urinary Calcium Excretion among Kidney Stone Formers.

As mentioned by Chris Masterjohn – an inadequate intake of vitamin K2 and A may have been part of the problem – in fact K2 deficiency may be the main issue

Vitamin K2. Vitamin K2 is often deficient. It is a fat soluble vitamin which comes in two forms, MK4 and MK7. MK7 is produced by bacteria, and MK4 is from foods like liver, dairy fats and eggs. Vitamin K2 makes sure calcium goes to the right place – that is in bones and teeth and not in arterial walls. He has added LEF Super K2 with Advanced K2 complex

2 articles of note: Vitamin D and Vitamin K Team Up to Lower CVD Risk: Part II

Vitamin K2: Optimal Levels Essential for the Prevention of Age-Associated Chronic Disease

Vitamin A is also recommended as it protects against vitamin D toxicity. Vitamin A is found in codliver oil and liver.

Vitamin C, Ascorbic acid can be turned into oxalate by the body. The dietician recommended cutting this out because of this. But as Paul Jaminet notes a low carb diet, insufficient antioxidants, excess PUFA (e.g. a high omega 3 intake), and infection can increase vitamin C degradation. Therefore increasing carbohydrates to 100 grams or more a day, and increasing anti-oxidants are recommended:

  • Glutathione and precursors such as N-acetylcysteine;
  • Selenium for glutathione peroxidase;
  • Zinc and copper for superoxide dismutase;
  • Coenzyme Q10 for lipid protection;
  • Alpha lipoid acid;
  • Colorful vegetables and berries.

However this study shows it depends on the type of vitamin C supplemented. (Note Ester C is the form he takes)

“This randomized, double-blind, crossover study examined the effects of two different vitamin C formulations and found that vitamin C with metabolites (Ester-C) significantly reduced urine oxalate levels compared to ascorbic acid.”

Magnesium: Low magnesium levels might exacerbate hypocalciuria and is associated with the constipation. In this study magnesium supplementation is beneficial.

The results of this study indicate that the oral supplementation of magnesium in patients with hyperabsorptive hypercalciuria and renal calcium stone disease is favorable because it decreases calcium absorption and increases magnesium absorption. Both factors may reduce risk factors for renal calcium stone formation.

And this study: Effects of magnesium hydroxide in renal stone disease, showed magensium supplementation decreased calcium stone formation:

Magnesium is a known inhibitor of the formation of calcium oxalate crystals in the urine and was proposed for prophylactic treatment in renal stone disease as early as the 17th and 18th centuries. We have treated 55 patients with recurrent renal calcium stone disease without signs of magnesium deficiency (normal serum magnesium, urinary magnesium, intracellular magnesium in muscle biopsies, gastrointestinal absorption of 28Mg, and magnesium loading test) from our outpatient stone clinic for up to four years with 500 mg Mg2+, in the form of Mg(OH)2, daily. The mean stone episode rate before therapy was 0.8 stones/year/patient. Forty-three recurrent renal calcium stone-formers without medical therapy served as controls. Serum magnesium increased initially but after one year returned to the pretreatment level. Urinary magnesium excretion increased promptly and remained elevated during the follow-up period. The urinary calcium excretion remained unchanged. The magnesium/calcium ratio in the urine increased and approached a value earlier found in healthy subjects without stone disease. Urinary citrate increased on therapy when analysed after three years of treatment. The mean stone episode rate decreased from 0.8 to 0.08 stones/year on treatment and 85% of the patients remained free of recurrence during follow-up, whereas 59% of the patients in the control group continued their stone formation. Side effects were few. Magnesium treatment in renal calcium stone disease is effective with few side effects. No clinical signs of magnesium excess were observed.

He started taking magnesium citrate, as this is form is great for constipation. An interesting conversation happened on twitter, where a Stabby noted on PaleoHacks –  Magnesium citrate sapping my joy . Curious – this man found too that he was waking up feeling our of sorts. He switched to magnesium malate recommended by Dr Kruse, and like Stabby and RNikoley found – he is feeling much better.

Potassium Bicarbonate may be useful, shown to decrease urinary calcium in two studies (llok down the page in this review) Idiopathic Hypercalciuria: The Contribution of Dr. Jacob Lemann, Jr.  and Long-Term Persistence of the Urine Calcium-Lowering Effect of Potassium Bicarbonate in Postmenopausal Women

Carbonated water: A maybe contributor “Excessive urinary phosphate excretion is also a cause and can be seen with high carbonated beverage intake or high phosphate levels in urine” This is more of an issue with soft drinks due to the phosphates added than it is to sparkling or carbonated water. (see comments) He was drinking around 2 litres sparkling water a day – he’s cutting this out in the meantime.

Well that is about it, I’ll be updating progress in a couple of months, this person is already feeling a lot better, no more headaches, and constipation is resolved.

Oxalate Kidney Stones, although not a factor in this case is a problem for many (see comments) – Cut down or cut out on high oxalate foods: http://www.nal.usda.gov/fnic/foodcomp/Data/Other/oxalic.html

Thanks to Paul Jaminet, Dr Kruse and That Paleo Guy for their contributions


  1. It’s misleading to generalize the problem to “carbonated water.” Carbonation does not introduce phosphates. It’s not the carbonation but that phosphates are commonly added by bottlers of fizzy drinks as flavoring. Your warning should focus on the added phosphates, not on carbonated water. Drinking water is a good thing. Carbonation increases palatability for many people so they more readily drink water. Anyone who wants fizzy water without phosphates can read labels to identify unadulterated beverages or make his own seltzer.

  2. I have been a chronic kidney stone sufferer in the past. I have made all of the adjustments you talk about above, but I also find I must stay on a low oxalate diet, also. I am confident that I won’t have another stone after these adjustments and have been stone-free for several years now. I can tell if I have too many oxalates when my urine splatters and feels constrained instead of just flowing like out of a non-constricted hose.

    • Thanks for your comment – great to hear these strategies worked.

      Oxalate is not an issue in this man’s case (normal oxalate urinary levels) otherwise the advice would be as you have found, to eat a low oxalate diet.
      The foods that contain large amounts of oxalates are spinach, rhubarb, beetroot, chocolate, nuts, legumes, soy beans, tofu, soy ‘meat’ substitutes, wheat-bran and starfruit.

      Are there other oxalate foods you avoid Renee Ann?

  3. I have to be pretty strict with oxalates. I use white pepper instead of black and have to avoid many vegetables. This is a good site with a good food list: http://www.lowoxalate.info/index.html

    I can’t eat anything on the high list except small amounts of chocolate because you really don’t eat cocoa by the cup full. I can only eat from the medium list in moderation. I have found that I can eat cashews if I prepare them like this: http://www.thenourishinggourmet.com/2008/07/soaking-nuts.html

    Soaking removes oxalates along with phytic acid.

Leave a Reply