Hypercalciuria is a common metabolic condition defined by the excessive excretion of calcium into the urine. This occurs when the kidneys release too much calcium over a 24-hour period, stemming from various points in the body’s calcium regulation system. While often asymptomatic, hypercalciuria is strongly associated with the formation of painful kidney stones and can impact bone health. Understanding the causes and management of this disorder is important for preventing long-term complications.
How Hypercalcuria is Identified
The standard method for identifying hypercalciuria is the 24-hour urine collection test. This test requires a patient to collect all urine produced over a full day, allowing for the precise measurement of the total calcium excreted. Hypercalciuria is typically diagnosed when daily urinary calcium excretion exceeds 250 milligrams (mg) for women or 275 to 300 mg for men, especially when the patient is on a regular, unrestricted diet.
The 24-hour urine collection is the most reliable diagnostic tool, as random urine samples can be misleading. Blood tests are often performed concurrently to help determine the underlying cause of the excessive calcium loss. These evaluations check levels of parathyroid hormone (PTH) and Vitamin D, which are key regulators of calcium metabolism. The results from both the urine and blood tests allow a medical professional to categorize the specific mechanism driving the hypercalciuria.
The Root Causes of High Urinary Calcium
The excessive loss of calcium into the urine is classified into three main physiological mechanisms, which determine the appropriate treatment strategy. Absorptive hypercalciuria, the most common type, is characterized by the digestive system absorbing too much calcium from the diet. This excess calcium enters the bloodstream and is filtered out by the kidneys, leading to high urinary excretion.
Resorptive hypercalciuria is nearly always caused by an endocrine issue such as primary hyperparathyroidism. In this scenario, an overactive parathyroid gland releases too much PTH, which signals the bones to release calcium into the blood. This constant mobilization of calcium results in an increased calcium load that the kidneys must excrete.
The third mechanism is renal leak hypercalciuria, where the problem lies directly with the kidneys’ ability to conserve calcium. The renal tubules have an impaired capacity to reabsorb calcium back into the blood, causing an obligatory loss into the urine. This loss can trigger a compensatory increase in PTH to maintain normal blood calcium levels, which in turn can stimulate intestinal calcium absorption.
Health Consequences and Physical Symptoms
While hypercalciuria itself rarely causes immediate physical symptoms, its long-term consequences are significant and often prompt a diagnosis. The primary health consequence is the formation of calcium-based kidney stones, known as nephrolithiasis. The persistently high concentration of calcium in the urine makes it easier for calcium oxalate or calcium phosphate crystals to form and aggregate.
The passage of these hardened mineral deposits can cause intense pain in the flank or abdomen, often referred to as renal colic. Hypercalciuria is the most common identifiable metabolic risk factor for calcium stone disease, accounting for nearly 50% of cases. Another serious consequence is the gradual loss of bone mineral density, leading to osteopenia and osteoporosis.
When the body consistently loses calcium through the urine, it may draw calcium from the bones to maintain stable blood levels. Individuals with hypercalciuria who form stones may have bone mineral density measurements 5% to 15% lower than their peers. This continuous bone resorption weakens the skeletal structure over time, increasing the risk of fractures.
Lifestyle and Medical Management
The management of hypercalciuria is tailored to the underlying cause but begins with lifestyle adjustments. Increasing fluid intake is foundational; drinking at least 2.5 liters of water daily helps dilute the calcium concentration in the urine, making crystal formation less likely. Dietary modifications include reducing sodium intake to less than 2,300 mg per day, since high sodium promotes urinary calcium excretion.
Limiting animal protein intake is also advised because it can increase the body’s acid load, causing calcium to be released from the bone and lost in the urine. Maintaining a moderate, rather than restricted, calcium intake is often recommended, typically between 1,000 to 1,200 mg daily, to allow calcium to bind to oxalate in the gut. Excessive Vitamin D supplementation should be avoided, as it increases intestinal calcium absorption.
For patients who do not respond adequately to dietary changes, pharmacological treatment is introduced, with thiazide diuretics being the primary medical therapy. Medications like hydrochlorothiazide or chlorthalidone enhance calcium reabsorption in the distal renal tubules, effectively reducing the amount of calcium excreted. For patients with certain types of stones, potassium citrate may also be prescribed to increase urinary citrate, which inhibits stone formation.