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You are here: Home / Topics / Calcium Stones

Calcium Stones

June 15, 2017 by Bert Vorstman MD

About 85% of all stones contain calcium. Prevention of stone formation may be entertained when one understands the factors that may play a part in stone formation: Stone Belt People in warm climates may be prone to dehydration, resulting in increased crystalluria. Hot climates may also expose people to ultraviolet radiation, increasing Vitamin D3 production. Conversely, Afro-Americans have a decreased stone incidence because of protection from UV light.

Family History

People with a family history of renal colic have an increased incidence of stone disease.

Medications

Abuse of antacid, milk alkali (milk products and absorbable alkali) and Vitamin D supplements may predispose to calcium stones. Carbonic anhydrase inhibitors may be associated with urinary stone disease. Triamterene may be associated with stone disease also. Silica-containing antacids may predispose to silicate stones.

In general, dairy product ingestion, as long as it is done in moderation, is not associated with an increased propensity for stone disease. Similarly, increased sodium intake is probably not associated with an increased incidence of stone disease. Inhibitors of Stone Formation Citrate, magnesium and sulfates may help prevent stone disease.

Calcium Stone Components

A. Oxalate

Oxalate in combination with calcium is the most common component of calcium stones. Diet may have an impact on the amount of oxalate found in the urine, and restricting the amount of oxalate-containing foods such as rhubarb may lower the incidence of calcium oxalate stones. Vitamin C excess may also lead to hyperoxaluria. Hyperoxaluria can develop in patients with inflammatory bowel disease, after small bowel resection or in a small bowel bypass for obesity. Poisoning with antifreeze (ethylene glycol) may also lead to calcium oxalate stones. Primary hyperoxaluria presents as two possible enzyme defects, Types I and II.

B. Phosphate

Calcium phosphate stones can be found in those with the metabolic condition hyperparathyroidism.

C. Calcium

Increased calcium absorption is common in hyperparathyroidism, milk alkali syndrome, excessive Vitamin D intake, sarcoidosis, metastatic cancer to bone and multiple myeloma.

Classification and Medical Treatment of Calcium Stone Disease

A. Absorptive Hypercalciuric Nephrolithiasis

Type I. Hydrochlorothiazides.

Hydrochlorothiazides may diminish calcium excretion but may have limited long-term usefulness. Cellulose phosphate combines with calcium in the gut, preventing calcium bowel absorption and therefore normalizing urinary calcium excretion. Its use may not be appropriate in children or postmenopausal women.

Type II. Absorptive hypercalciuria.

Urinary calcium excretion can be normalized by adopting a calcium-restricted diet.

Type III. Absorptive hypercalciuria.

Absorptive hypercalciuria is uncommon and secondary to a phosphate renal leak. Treatment is through Neutra-Phos, which inhibits Vitamin D synthesis.

B. Resorptive Hypercalciuric Nephrolithiasis

This is usually due to hypercalcemia secondary to hyperparathyroidism and should be suspected in those with combined nephrocalcinosis and nephrolithiasis and especially in women with recurrent calcium stones and patients with calcium phosphate stones. Treatment requires surgical removal of the parathyroid adenoma.

C. Renal-induced Hypercalciuric Nephrolithiasis

These patients have an elevated fasting urinary calcium level and an elevated parathyroid hormone level but normal serum calcium level. Renal hypercalciuria is effectively treated with hydrochlorothiazides.

D. Hyperoxaluric Calcium Nephrolithiasis

This is due to increased urinary oxalate levels and found in those with inflammatory bowel disease or chronic diarrheal states, bringing about dehydration.

E. Enteric Hyperoxaluric Calcium Nephrolithiasis

This is treated with calcium supplementation, which binds to the oxalate in the gut, limiting its absorption.

F. Primary Hyperoxaluria

This comes in two types, I and II; and both are lethal. Type I is more common than Type II and clinically they present with nephrocalcinosis and lithiasis. Treatment involves liberal fluids, Vitamin B-6 and inorganic phosphate in divided doses.

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