How is absorptive hypercalciuria type I treated?

Updated: Jun 02, 2021
  • Author: Stephen W Leslie, MD, FACS; Chief Editor: Vecihi Batuman, MD, FASN  more...
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Treatment of absorptive hypercalciuria type I can be very difficult due to the severity of the intestinal calcium hyperabsorption. Therapy primarily consists of moderate dietary calcium restriction, thiazides, and orthophosphates.


Thiazides, such as trichlormethiazide (Naqua) or indapamide (Lozol), substantially reduce urinary calcium excretion, but they do not correct the primary defect, which is increased, uncontrolled intestinal calcium absorption. Thiazides may lose their hypocalciuric effect over time and cause hypokalemia, hypocitraturia, and increased uric acid levels.


Orthophosphates, such as K-Phos Neutral, Neutra-Phos K, and Uro-KP-Neutral, lower serum vitamin D3 levels and reduce urinary calcium excretion. These agents are roughly equal to thiazides in their ability to reduce urinary calcium and prevent recurrent calcium stone formation. Because of the need for frequent dosing and various gastrointestinal adverse effects, orthophosphates are not the preferred agents when thiazides alone are sufficient and well tolerated. The combination of thiazides and orthophosphates used together may be necessary in difficult or resistant cases of absorptive hypercalciuria type I.

Sodium cellulose phosphate

Sodium cellulose phosphate is an extremely potent intestinal calcium-binding agent that was previously recommended as a primary therapy for absorptive hypercalciuria type I. Concerns about creating a negative calcium balance, bone demineralization, and other adverse effects currently limit its usefulness. These risks have shifted therapy away from this agent in favor of thiazides and orthophosphates.

When sodium cellulose phosphate therapy is used, supplemental magnesium is recommended. This is because the cellulose phosphate binds intestinal magnesium as well as calcium. Supplemental magnesium, therefore, must be administered to patients on cellulose phosphate to avoid magnesium depletion.


Dietary oxalate restriction is also recommended, due to the lack of free intestinal calcium that is created with cellulose phosphate therapy. This removes the primary intestinal oxalate-binding agent (calcium) from the digestive tract and leads directly to increased free intestinal oxalate absorption with subsequent hyperoxaluria.

Additional treatments

Other therapies include the use of increased dietary fiber, such as rice, oat, and wheat bran supplements, as relatively mild intestinal calcium binders. Bisphosphonates, such as alendronate (Fosamax), increase bone deposition of calcium, thus removing it from the circulation before it can be excreted. This improves bone calcium density and helps to reduce urinary calcium levels.

Optimization of all other urinary stone risk factors is highly recommended. This would include increasing urinary volume, reducing dietary oxalate, and using potassium citrate as needed. Purine intake should be restricted if uric acid levels are elevated.

Pentosan polysulphate (Elmiron) may potentially have use in difficult calcium oxalate stone cases. Although it has no effect specifically on calcium excretion, pentosan polysulphate appears to reduce calcium oxalate crystallization and crystal aggregation, which reduces new kidney stone formation rates. [50, 51, 52]

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