Calcium & Renal Failure

Calcium & Renal Failure
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The human body must perform a delicate balancing act to maintain normal levels of calcium, phosphorus and other minerals in the blood. The kidneys play a central role in this balancing act, as they filter excess minerals from the circulatory system. In people with kidney failure, this filtering ability declines, resulting in low or high levels of some substances. Those with renal failure undergo regular testing to determine their calcium levels.

Hypocalcemia

Hypocalcemia refers to abnormally low levels of calcium in the blood. In some people with kidney disease, the kidneys excrete too much calcium, resulting in lower calcium levels. Damaged kidneys also have difficulty maintaining a normal amount of phosphorus in the blood. When phosphorus levels get too high, calcium levels decrease. Another cause of hypocalcemia in people with renal failure is reduced ability to form vitamin D-3. Vitamin D aids in the absorption of calcium, so reduced absorption leads to less calcium in the bloodstream.

Hypercalcemia

Physicians use the term "hypercalcemia" to describe abnormally high levels of calcium in the blood. In acute renal failure patients, high phosphorus levels cause calcium deposits to form in the soft tissues of the body. This reduces the amount of calcium available for circulation in the blood, causing a condition called secondary hyperparathyroidism. The parathyroid glands react by producing more parathyroid hormone, a chemical that regulates calcium and vitamin D levels. When kidney function starts to improve, the excess parathyroid hormone causes temporary hypercalcemia. Several factors contribute to the development of hypercalcemia in people with chronic renal failure. These factors include excessive use of vitamin D supplements, loss of mobility and the use of calcium-based antacids.

Effects

Calcium imbalance has serious consequences for people with chronic kidney disease. Hypocalcemia causes seizures, emotional problems, muscle spasms, congestive heart failure and muscle stiffness. Hypercalcemia causes cognitive dysfunction, increased urinary frequency, kidney stone formation, high blood pressure, muscle weakness and calcification of the blood vessels.

Renal Osteodystrophy

The National Institute of Diabetes and Digestive and Kidney Diseases estimates that 90 percent of people receiving dialysis treatment for kidney disease also develop a condition called renal osteodystrophy. This bone disease occurs when someone with renal failure experiences decreased calcium levels or increased phosphorus levels over a long period. When calcium levels decline, parathyroid hormone takes calcium out of the bones and sends it to the bloodstream. When this happens many times, the bones get weak. The bones also lose calcium when phosphorus levels get too high. Renal osteodystrophy causes joint pain, fractures, joint pain and loss of mobility.

Treatment

Treatment for acute hypocalcemia involves the intravenous administration of calcium. The Cleveland Clinic Center for Continuing Education explains that calcium gluconate has better results than calcium chloride because it causes less damage if it leaks out of the IV tubing and into the surrounding tissues. Chronic cases of hypocalcemia require treatment with calcium and vitamin D supplements.

The treatment for hypercalcemia depends on how severe it is and whether the patient is experiencing any symptoms. If calcium levels are not dangerously high and the patient has no symptoms, treatment is not necessary. Symptomatic patients with calcium levels of 12 to 14 mg/dL should receive treatment with medications that block the absorption of calcium or increase the excretion of calcium in the urine. A calcium level higher than 14 mg/dL requires treatment even if the patient does not have any symptoms.

References

Article reviewed by Libby Swope Wiersema Last updated on: May 22, 2011

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