Hypercalciuria (High Calcium in Urine)

What hypercalciuria is

The kidneys filter calcium from the blood every day and reabsorb almost all of it. The rest leaves in urine. In hypercalciuria, more calcium than normal ends up in the urine. That happens when:

• The gut absorbs too much calcium from food (absorptive pattern).
• The kidneys fail to reabsorb calcium well (renal leak).
• Calcium is released from bone (resorptive pattern), as in hyperparathyroidism or immobilization.

These patterns often overlap, and most doctors no longer try to separate them, because treatment is similar.

When urine is highly concentrated with calcium, it combines with oxalate or phosphate and forms crystals that grow into stones. Between 30 and 60 percent of adults with calcium kidney stones have hypercalciuria.

Symptoms

Hypercalciuria has no symptoms by itself. People find out because of:

• Kidney stones: sudden, severe flank pain that moves to the groin, nausea and blood in the urine.
• Blood in the urine found on a routine test, especially in children.
• Urinary frequency or pain in children, sometimes with bedwetting.
• Low bone density on a scan.

Causes of hypercalciuria

Idiopathic hypercalciuria

The most common type. Blood calcium is normal and no underlying disease is found. It tends to run in families and probably involves several genes that increase gut absorption and kidney losses of calcium. A high-salt, high-animal-protein diet makes it worse.

Secondary causes

• Primary hyperparathyroidism: an overactive parathyroid gland raises blood calcium, which spills into the urine.
• Too much vitamin D, usually from high-dose supplements.
• Sarcoidosis and other granulomatous diseases, which make extra active vitamin D.
• Renal tubular acidosis (distal type) and medullary sponge kidney.
• Excess cortisol: Cushing syndrome or long-term steroid medicines.
• Overactive thyroid.
• Prolonged immobilization, which releases calcium from bone.
• Loop diuretics such as furosemide.
• Rare genetic disorders, such as Dent disease and Bartter syndrome, especially in children.
• Cancers that spread to bone.

How hypercalciuria is diagnosed

1. 24-hour urine collection: the key test. You collect all urine for 24 hours on your normal diet. The lab measures calcium, plus oxalate, citrate, uric acid, sodium, volume and creatinine (to check the collection is complete). Many specialists repeat it.
2. Spot urine calcium-to-creatinine ratio: a quick screening test, especially useful in children.
3. Blood tests: calcium, phosphate, parathyroid hormone (PTH), vitamin D, kidney function, bicarbonate and potassium.
4. Stone analysis: if you pass a stone, keep it for testing.
5. Imaging: CT or ultrasound to look for stones or calcium deposits in the kidney (nephrocalcinosis).
6. Bone density (DEXA) scan when bones may be affected.

Treatment for hypercalciuria

Hypercalciuria diet

• Drink more: enough to pass at least 2.5 liters (about 85 fl oz) of urine a day. Water is best.
• Cut salt: aim for under about 2,300 mg of sodium a day. Each extra gram of salt increases urine calcium. Processed foods, restaurant meals, bread and cured meats are the main sources.
• Keep calcium normal: about 1,000 to 1,200 mg a day from food. Cutting calcium is a common mistake: it raises oxalate absorption and stone risk and weakens bones.
• Moderate animal protein: large amounts of meat, fish and eggs increase urine calcium and lower citrate.
• Eat more fruit and vegetables, which raise urine citrate, a natural stone inhibitor.
• Avoid high-dose vitamin D and calcium supplements unless your doctor recommends them. Taking supplements with meals is better than between meals.

Medicines

• Thiazide diuretics (such as hydrochlorothiazide or chlorthalidone) lower urine calcium and reduce stone recurrence. They may also help bone density.
• Potassium citrate raises urine citrate, which blocks crystal formation, and offsets potassium loss from thiazides.
• Bisphosphonates may be used if bone density is low.

Treating the cause

Surgery to remove an overactive parathyroid gland, stopping excess vitamin D, or treating sarcoidosis or a hormone disorder often corrects secondary hypercalciuria.

Complications

• Recurrent calcium oxalate or calcium phosphate kidney stones.
• Calcium deposits in the kidney (nephrocalcinosis), which can reduce kidney function over time.
• Osteoporosis and fractures.
• In children, blood in the urine, urinary symptoms and abdominal pain.

Frequently asked questions

What is a normal amount of calcium in urine?

On a normal diet, adults usually pass less than 250 mg of calcium a day (women) or 300 mg a day (men), or less than about 4 mg per kilogram of body weight. Above these levels is called hypercalciuria. Results depend on diet, so the test should be done on your usual eating pattern.

What causes high calcium in the urine?

The most common cause is idiopathic hypercalciuria, an inherited tendency with normal blood calcium. Other causes include a high-salt diet, overactive parathyroid glands, excess vitamin D, sarcoidosis, kidney tubule disorders, steroid medicines, overactive thyroid and long periods of bed rest.

Should I avoid calcium if I have hypercalciuria?

No. Cutting dietary calcium usually backfires. Calcium in food binds oxalate in the gut, so a low-calcium diet increases oxalate in the urine and stone risk, and weakens bones. Keep a normal intake of about 1,000 to 1,200 mg a day and reduce salt instead.

Can hypercalciuria be cured?

Idiopathic hypercalciuria is usually lifelong, but it can be controlled well with fluids, salt reduction and, if needed, thiazide medicine. Secondary hypercalciuria can often be cured by treating the cause, such as removing an overactive parathyroid gland or stopping excess vitamin D.

Does hypercalciuria cause symptoms?

Not directly. Most people find out after a kidney stone, blood in the urine, or a bone density scan. Children may have urinary frequency, pain on urination or bedwetting. The main reason to treat it is to prevent stones and protect bone.