Medications in Renal Failure That Affect the Calcium & Phosphorus Metabolism

Medications in Renal Failure That Affect the Calcium & Phosphorus Metabolism
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The kidneys filter the blood. They remove wastes, regulate the blood pressure, fluids, electrolytes, synthesis of red blood cells and vitamin D levels among other functions. Renal failure damages the ability of the body to regulate these functions. Medicines can be given to help regulate these electrolytes back to their normal values.

Calcium

In kidney failure, calcium levels in the blood drop. The parathyroid glands in the neck respond by secreting parathyroid hormone. This causes the bone to release calcium into the blood, making the bones weak and brittle, leading to osteoporosis. This condition is called renal osteodystrophy. Calcium administration helps to raise the calcium level, but not in the absence of vitamin D.

Vitamin D

Vitamin D can be taken in as a whole compound, or synthesized through the coordinated actions of the skin, kidneys and liver. In renal failure, since the kidneys are not working, vitamin D is not synthesized. One important function of vitamin D is to increase the absorption of calcium into the intestines. Vitamin D is given in order to raise the calcium levels.

Sevelamer

Another role of the kidneys is to lower phosphate levels when signaled by parathyroid hormone. Without proper kidney function, the phosphate levels rise in the blood. Sevelamer binds to phosphorus in food, preventing it from being absorbed into the blood stream. Side effects tend to be gastrointestinal, such as nausea and flatulence.

Aluminum Hydroxide and Lanthanum Carbonate

While sevelamer is a large compound, other phosphate binding molecules sometimes used in renal failure are smaller, such as the charged minerals aluminum and lanthanum. Like sevelamer, these agents work by binding to phosphate in the intestines, making an insoluble compound and making it unavailable to the body for absorption.

References

  • "Harrison's Principles of Internal Medicine"; Anthony S Fauci, et al.; 17th Ed 2008
  • "Robbins and Cotran Pathologic Basis of Disease"; Vinay Kumar, et al.; 8th Ed 2009

Article reviewed by Mia Paul Last updated on: Jul 11, 2011

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