The main features of treatment are to augment calcium intake (as calcium carbonate) and to limit phosphate intake. (See Chapter 7.) About 2 grams of calcium carbonate should be taken daily. Many preparations are available, all equally effective. Phosphate intake should be limited to about 400 mg per day. Blood levels of both parathyroid hormone and vitamin D are more responsive to a low-phosphorus diet than to calcium supplementation.
With such treatment, many of these abnormalities disappear, but sometimes it is necessary to administer an active form of vitamin D. Occasionally it is necessary to surgically remove the parathyroid glands.
In evaluating serum calcium concentration, it is important to recall that about half of serum calcium is bound to albumin. Hence, when albumin concentration is low, total serum calcium may be low even though nonprotein-bound calcium (the biologically important quantity) is normal. A simple formula gives a good estimate of nonprotein-bound calcium (Ca2+) based on total serum calcium (Ca) and albumin (Alb) concentration: Ca2+ = Ca - 1.25(Alb). Among my patients, I have rarely seen low levels of nonprotein-bound calcium. High values are even less common.
I have rarely seen excess calcium levels in patients taking calcium carbonate, which is effective even though it is poorly absorbed. Calcium acetate (PhosLo) is better absorbed but may lead to high readings. This may not be a serious problem in dialysis patients, but in predialysis patients, glomerular filtration rate may decrease sharply and may not recover. Calcium carbonate is the much safer option, in my experience.
Serum phosphate in patients on the supplemented very-low-protein diet is usually within normal limits, except in a few patients with very severe renal failure. This is because a low-protein diet is almost always a low-phosphate diet, too; dietary phosphate is highest in foods high in protein. (See chapter 7.)
Some nephrologists have recommended the use of the activated form of vitamin D, calcitriol, in all patients, at a dose of about 0.25 mcg daily. I have used this in a few patients with low serum calcium levels (corrected for albumin) but not otherwise. A recent study from Japan indicates that patients approaching dialysis who have relatively low serum levels of calcitriol are more likely to have low serum levels of albumin, as well. My experience also leads me to believe that the low levels of calcitriol may cause low levels of albumin, but this is an unproven assumption.
If calcitriol treatment is overdone, the first ill effect to be seen is an elevation of serum calcium concentration above normal (hypercalcemia), which can cause a sharp fall in kidney function. Usually kidney function recovers when serum calcium returns to normal, but not always.
As renal failure progresses, phosphate accumulates in the blood, and vitamin D synthesis is further impaired. Both of these changes tend to stimulate the secretion of parathyroid hormone even more. The parathyroid glands enlarge and may in fact get so big that they cannot shut off. As noted earlier, they may have to be surgically removed. These high levels of parathyroid hormone in turn contribute to bone disease, which can be incapacitating in poorly treated patients whose phosphate level stays very high. One sign of this condition is a high level in the blood of the enzyme alkaline phosphatase, released from the bone. Consequent bone pain and fractures can be disabling.
A low-protein, low-phosphate diet, supplemented by ketoacids as calcium salts, may correct this condition completely. Some physicians have maintained that calcium administered as salts of ketoacids is particularly well absorbed. However, this has not been well established, and these salts carry the risk of inducing a high blood calcium concentration.
Alternatively, we can try to reduce intestinal absorption of phosphate. The most commonly used agent for this purpose is calcium carbonate, which, as discussed earlier, should always be part of a low-protein regimen. It combines with phosphate in the gut to form the insoluble salt calcium phosphate, which is excreted in the stool. Many preparations of calcium carbonate are available, generally without a prescription.
In years gone by, patients commonly took aluminum salts, such as aluminum hydroxide, to control phosphate absorption. The body absorbs only small amounts of these salts. Ingestion leads to the formation of another insoluble salt, aluminum phosphate, that is excreted in the stool. These salts are also widely used as antacids. Scientists have established that enough aluminum is absorbed from these salts to cause serious bone damage in patients with chronic renal failure. Nerve and blood cell toxicity also may occur. Today, however, aluminum salts are rarely used to reduce phosphate absorption, and also patients with renal failure should avoid using them as antacids.
Sevelamer, a newly introduced polymer, reduces phosphate absorption and is highly effective but also highly expensive. The more affordable option is for patients to take calcium supplements and reduce phosphate intake.
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