Response to a Hypocalcemic Challenge
Because some calcium is always lost in urine, even a short period of total fasting can produce a mild hypocalcemic challenge. More severe challenges are produced by a diet deficient in calcium or anything that might interfere with calcium absorption by renal tubules or the intestine. The parathyroid glands are exquisitely sensitive to even a small decrease in ionized calcium and promptly increase PTH secretion (Fig. 18). Effects of PTH on calcium reabsorption from the glomerular filtrate coupled with some calcium mobilization from bone are evident after about an hour, providing the first line of defense against a hypocalcemic challenge. These actions are adequate only to compensate for a mild or
The importance of the negative feedback effects of 1,25(OH)2D3 on PTH secretion is highlighted by the condition known as renal osteodystrophy that is found in patients with chronic renal failure.
This disorder is characterized by abnormalities in bone mineralization due largely to secondary hyperparathyroidism that results from inability to synthesize 1,25(OH)2D3.
brief challenge. When the hypocalcemic challenge is large and sustained, additional, delayed responses to PTH are needed. After about 12-24 hr, increased formation of 1,25(OH)2D3 increases the efficiency of calcium absorption from the gut. Osteoclastic bone resorption in response to both PTH and 1,25(OH)2D3 taps the almost inexhaustible reserves of calcium in the skeleton. If calcium intake remains inadequate, skeletal integrity may be sacrificed in favor of maintaining blood calcium concentrations.
Hypercalcemia is rarely seen under normal physiologic circumstances, but it may be a complication of a variety of pathologic conditions usually accompanied by increased blood concentrations of PTH or PTHrP. An example of hypercalcemia that might arise under physiologic circumstances is the case when a person who has been living for some time on a low-calcium diet ingests calcium-rich food. Under the influence of high concentrations of PTH and 1,25(OH)2D3 that would result from calcium insufficiency, osteoclastic activity transfers bone mineral to the extracellular fluid. In addition, calcium absorptive mechanisms in the intestine and renal tubules are stimulated to their maximal efficiency. Consequently the calcium that enters the gut is absorbed efficiently and blood calcium is increased by a few tenths of a milligram per deciliter. Calcitonin secretion is promptly increased and would provide some benefit through suppression of osteoclastic activity. Although PTH secretion promptly decreases, and its effects on calcium and phosphate transport in renal tubules quickly diminish, several hours pass before hydroxylation of 25 OH-D3 and osteoclastic bone resorption diminish. Even after its production is shut down, many hours are required for responses to 1,25(OH)2D3 to decrease. Although some calcium phosphate may crystallize in demineralized osteoid, renal loss of calcium is the principal means of lowering blood calcium. The rate of renal loss, however, is limited to only 10% of the calcium present in the glomerular filtrate, or about 40 mg/hr, even after complete shutdown of PTH-sensitive transport.
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