I would like to add some comment about renal stones and calcium supplements in patients with osteoporosis. Now any strategies of osteoporosis treatment includes additional purpose of the calcium supplements to medication which are slowing down a bone resorption (bisphosphonates, calcitonins). Maintenance of sufficient bone density is promoted by adequate consumption of calcium with food. Foods are the best source for this important mineral. Milk, cheese, and yogurt have the highest amounts. Other foods that are high in calcium are green leafy vegetables, prunes, tofu, shellfish, Brazil nuts, sardines, and almonds. At insufficient calcium consumption with food it is necessary to accept calcium supplement in tablets (1000 mg and more) which are safe and are well tolerated. Supplements should be taken with meals and accompanied by six to eight glasses of water a day. 2500 mg daily of calcium supplement is usually the recommended amount in patients with normal renal function for prevention renal stones.

All persons with renal stones (especially if osteoporosis also present) should have Serum Ionised Calcium and PTH checked for Hyper Parathyroidism. Also check VitaminD levels. BMD is desirable to check to check response to treatment.

Hello all, i must say its a good question put forth. I am a Naturopath and a budding nutritionist working on designing a calcium rich functional food using eggshell powder. Utilizing biowaste and a natural source of calcium supplementation for osteoporotic patients. Opinions/comments welcome!

From this article it looks like you don't have to worry:

http://www.ncbi.nlm.nih.gov/pubmed/23137489 (Clin Exp Rheumatol. 2012 Nov-Dec;30(6):954-61. Epub 2012 Dec 17)

Does this help you?

The calcium level is just one of the players of the complicated urolithiasis-osteoporosis issue. An other is (beside many others) the oxalat-intake -which can be found in dark-green-leaves (spinach, kale, etc) and other plants (coffee, rhubarb, soya, etc).

The interesting thing is that if the oxalat meets the dietary calcium in the digestive tract,, they bind together and will be not absorbed from the intestine. Thus the kidney has less to eliminate - less chance to form stones. That is why less Ca-intake can lead to form stones (too much oxalate in blood) as well as too much Ca. Less or more than what? Then Oxalate. So, it's a good idea to advise the patients to take their 1200 mg daily amount of Ca in mealtime (and not just a tablet whenever a day). And, of course, Vera is correct by emphasizing the importance of the natural Ca sources and liquid apport.

Dear Zohreh

Normally the activity of osteoblasts and osteoclasts is well-balanced. Osteoclasts are regulated by several hormones and IL-6 + TNF-alpha. IL-6 is one of the factors in the osteoporosis, which is an inbalance between bone resorption and bone formation.

IL-6 is needed for the production of osteoclasts. In the postmenopause the loss of bone mass may be due to the production of new osteoclasts by IL-6. It is known that estrogen suppresses IL-6 production and testosterone also suppresses the osteoclast development.

The increased activity of osteoclasts by IL-6 leads the increased calcium level in the serum: Calcium is one component of the common type of human kidney stones.

In Multiple Myeloma the patients have osteolytic lesions and renal problems. IL-6 is a proliferative factor in this disease. High serum levels of IL-6 show a relation to the clinical symptoms.

best

Eva

Thank you for bring the discussion up the IL-6 discussions here Eva. I am a certified Nutritionist and have previously written a presentation on this aspect of women's health. Below is a section on bone heatlh for your consideration.

The principal regulators of bone health are parathyroid hormone (PTH); 1,25-hydroxycholecalciferol (1,25 DOHCC or Vit. D); calcitonin, secreted by the thyroid gland; and to a lesser extent estrogens, androgens, progesterone and thyroid hormone. Calcitonin stimulates the deposition of new bone. PTH increases when blood calcium levels are low and also causes the breakdown of bone, increases kidney absorption and excretion of calcium, and decreases kidney absorption of phosphates. Phosphates that remain in the blood bind to calcium making it inactive. DOHCC is a derivative of D3 which in the body is synthesized from cholesterol with the help of ultraviolet sunlight. D2 and D3 collectively are referred to as cholecalciferol. When PTH increases, causing calcium loss from bone, 1,25-DOHCC formation is stimulated which then stimulates increased calcium and phosphate absorption from the intestines. Therefore the hormones calcitonin, PTH, and 1,25-DOHCC all work together to maintain bone health.Estrogen stimulates the formation of calcitonin, which increases calcium uptake by the bones and inhibits the action of osteoclasts, the cells that break down old damaged bone.

Studies indicated that estrogen therapy decreased bone reabsorption and seemed to stabilize bone mass, and may be involved with a minimal increase of bone density. More recent studies show that estrogen may help prevent bone loss in the first few years around menopause, however by seven years after menopause the decline in bone mineral density was the same as for women who did not take estrogen.

Here’s the problem to consider, if estrogen slows down the action of osteoclasts whose role it is to seek out and destroy old and damaged bone, then osteoblasts which would normally fill the space with new bone are not able to build new bone because there is no space to place it in. The result would be greater amounts of old, damaged, brittle bone wouldn’t it?

Additionally, I have not seen it mentioned that along with calcium supplementation there must also be balance of magnesium intake. In fact, mineral balance is a delicate symphony and it is recommended that a balanced mineral supplement be taken rather than single minerals, to protect that balance.

I should add that I have been hypothyroid for 18 years and my experience with calcium supplementation recommended by a Naturopathic doctor I was seeing resulted in some excruciating episodes of renal stones. I was told that the Synthroid medication for hypothyroidism blocked the absorption of calcium which resulted in the formation of renal stones. What research do you all have that would support this?

Dear Moira

Osteoblasts produce RANKL. This is a member of the TNF-family and it is a key factor in the differentation of the osteoclasts. The overproduction of RANKL is be found in degenerative bone diseases.

Estrogen is a natural inhibitor of RANKL. The inhibitor effect of the estrogen in the menopause (postmenopause) is dependent on the dosage of estrogen and the beginning of the therapy. The start with estrogen is the best in the perimenopause.

with best wishes

Eva

Dear Sydney

You can tell your opinion really: We are living in a democracy..

I do not like mouse-models in the medical research. The life expectancy of a mouse is 1.5-2 years , mine is above 80 years. It is not allowed to transfer the findings to the humans automatically.

best

Eva

I should report a case of hyperparathyroidism with recurrent production of renal stones. The therapy was surgical parathyroid removal. I think that a study of parathyroid function is an important option for patients with recurrent renal stones.

Dear Enzo

Parathormone (PTH) is secreted by the cells of the parathyroid glands; It increases the concentration of calcium in the blood. It enhances the release of calcium from the large reservoir contained in the bones. Bone resorption is indirectly stimulated by PTH.

(1) It binds to osteoblasts leading to increased expression of RANKL and to reduced expression of Osteoprotegerin.

(2) It enhances the absorption of calcium in the intestine.

(3) It enhances active reabsorption of calcium from the distal tubules of kidney.

with kind regards

Eva

Dear Eva,

thank you very much for your interesting lesson to a Gastroenterologist. However, I am unable to understand whether a parathyroid dysfunction may be involved in recurrent production of renal stones as well as the interaction between parathyroid hormones may be more relevat than the single action of PTH. If you are interested, I can retrieve the complete history of the patient, I did not observe as a specialist, but only as a familial. My best

Enzo

Dear Enzo

PTH releases the Calcium from the bones.

The constant filtering of large amount of Calcium causes the collection of Calcium within the renal tubules leading to renal stones.

It is known the a high Calcium level in the serum is associated with a high PTH level due to hyperparathyroidism.

Conversely Teriparatide (a recombinant PTH) is effective in the treatment of women with postmenopausal osteoporosis due to low serum levels of PTH (hypoparathyroidism).

I would be interested for the history of the patient. You can send it to my email address [email protected]

Thanks and with best

Eva

Dear Eva,

the patient had a long term history of renal stones development with many urological treatments for this problem. Finally an hyperparthyroidism was diagnosed due to an adenoma of parathyroids. Surgical operation was the final solution of the problem. This short history was derived from my efforts to remember as many details as I could. I am trying to find the phone number of the patient for further details (he does not live in my town and I do not have news by him from the time of the operation, i. e. two years ago). Do you think believable this clinical reconstruction?

My best

Enzo

Hello, I am doctor in endocrinology and osteology. We look patients. All people with kidney stones should be studied with serum calcium, fosforo, and Parathormone , and uriary Ca, P, uric ac, magnesium, citrato and oxalato. If the patient has renal hypercalciuria it is more probable that bone mineral density (BMD) is lower than expected for age. If he has absortive hypercalciuria habitually BMD is normal. Obviously, BMD should be studied.

Thank you to Eva and José for confirming my primary hypothesis in a field which is outside of the topics of my specific interest. The message for a practitioner could be: in a patient with recurrent renal stones, parathyroids could be involved and, then, investigated.

Hello. I add: all patients with stones must be studied. Most has not high PTH and serum calcium, and the diagnosis is idiopatic hypercalciuria, that can be renal or absortive (it depends on calciuria without dairy products). Less people has high PTH. We must measure urinary calcium, oxalato and uric because high levels produces more chance of litiasis, and magnesium and citrato because low levels produce the same!

Dear Jose

Your opinion is absolutely correct.

I have a new project: Preventive Medicine/Osteoporosis). I will measure the following parameters regarding calcium metabolism: Calcium in serum and in urine, PTH and Calcitonin and Vitamin-D in serum.

Thanks and with kind regards

Eva

Hi,

I've found a high prevalence of osteoporosis (documented by BMD) and pathologic fractures in patients with idiopathic hypercalciuria and recurrent calcium stone disease . The prevalence and severity of osteoporosis was higher among men than women. These results were mainly observed in individuals with hypercalciuria secondary to bone reabsorption, but also in some patients with hypercalciuria and intestinal calcium hyperabsorptium to whom a very restrictive calcium diet had been prescribed for several years. These results were published in a book about idiopathic calcium stone disease edited by BIAL foundation (unfortunately it's in Portuguese).

Because there is some overlap between different phenothypes of hypercalciuria, I believe BMD should be part of the initial investigation of all individuals with idiopathic hypercalciuria and recurrent calcium stones. This information may be useful for treatment planning.