Renal secondary hyperparathyroidism results from a severe increase in PTH that occurs because the kidneys can no longer filter and secrete sufficient amounts of Pj ions each day. As the blood concentration of Pi increases, the serum PTH also rises in an attempt to correct the error (increase of serum Pi ). The action of PTH on bone tissue then predominates, and the rate of bone turnover continues to increase, unless corrected by renal dialysis or kidney transplantation. Without correction, the net result is a
Figure IV. B.5.4. Mechanism through which a low dietary calcium:phosphorus ratio contributes to the development of a persistently elevated parathyroid hormone (PTH) concentration in the blood.
Figure IV. B.5-5- Comparison of parathyroid hormone (PTH) responses of normal and high dietary phosphorus (Pj) and effects of PTH on bone mass.
Continuing increase in the serum Pj concentration and a rapid thinning of bone tissue at practically every site in the body. If severe enough, this condition can result in fractures at almost any skeletal location. Oral phosphate binders, such as aluminum or magnesium hydroxides, are usually administered to patients to reduce the amount of Pi absorbed by the small intestine and to enhance calcium absorption, but this strategy typically is not sufficient to stem the gradual increase in serum PTH as the disease progresses.
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