Urinary stone disease (nephrolithiasis) is a risk factor for bone disease (osteoporosis) and hip fractures. Low bone mineral density (BMD) is common in people with calcium nephrolithiasis. Calcium nephrolithiasis is described as a multisystem disease with complications of urinary stones and osteoporosis.
In one study of urinary stone patients, with average follow-up of 19 years, there was a 4X risk of having a first time vertebral fracture compared to the normal population. In another study of stone formers, 28% of men and 45% of women had fractures by their 30 year follow-up. The bone loss can be in any part of the body.
Hypercalciuria and hypocitraturia are risk factors for nephrolithiasis. Bone loss is seen in both stone formers with hypercalciuria and with normal blood calcium levels. (Hypercalciurics seem to have more severe losses of BMD.) Thiazide diuretics and alkali, such as potassium citrate (K-Cit.) help prevent urinary stone recurrence. It is not known if these treatments alter the loss of bone associated with urinary stones.
One study showed that treatment with potassium citrate for 12 months improved BMD in the vertebral spine. The benefit to the bone could have been the result of the decrease in urinary calcium and the increase of urinary citrate secondary to the alkalinizing effect of K-Cit. The dose of K-Cit. is 40 to 60 meq./day. After 44 months the vertebral bone density was increased by 3.1%.
The alkali treatment reduces the effect on the bones of a diet high in protein. High salt (NaCl) and protein consumption increase kidney stones and bone disease. This could be due to salt and protein causing a “subtle metabolic acidosis,” which has a negative effect on bones. Patients can be treated with reduced sodium diets, reduced oxylates, and reduced purines.
The pharmaceutical, thiazide, has shown a protective effect on bone mass in patients with hypercalciuric nephrolithiasis.
Forty to 60% of hypercalciuric stone formers have elevated blood levels of 1,25-dihydroxyvitamin D. In the normal process of breaking down and reforming bone cells, these patients have defective bone reformation. High levels of 1,25-dihydroxyvitamin D are associated with increased resorption of the bone and reduced synthesis of bone collagen. These patients should not be given vitamin D.
Bisphonates are not the best treatment for bone disease related to nephrolithiasis. Bisphonates suppress normal bone absorption and reformation and could make the bone problem of hypercalciuric nephrolithiasis worse.
BMD testing should be part of the lab routine for patients with urinary stone disease. The connection between nephrolithiasis and bone loss remains unexplained.
CONCLUSION: Urinary stone formation is a risk factor for osteoporotic bone disease and fractures. Treatments include K-Cit. and dietary changes. Alkalinization of the urine is important. Dietary changes may be of benefit.
Purines are high in beef, pork, bacon, lamb, seafood, alcoholic beverages, and high yeast foods, such as beer and bread. Low purine foods are asparagus, cauliflower, mushrooms, peas, spinach, whole grain breads and cereals, white poultry like chicken, duck and turkey, bidney beans and lima beans.
Oxylate stone formation can be reduced by an extract of Phyllanthus niruri. Vitamin C consumption has been shown to enhance urine oxalate excretion. High oxalate foods are sorrel, spinach, rhubarb, beets, nuts, chocolate, wheat bran, strawberries, peanuts, almonds and tea.
It is useful to check your urine with pH paper to know if you are acid or alkaline. It is good to keep your pH above 7.0. Below this is acidic.
Read about dietary suggestions for urinary stones.