Calcium Homeostasis in Immobilization: An Example of Resorptive Hypercalciuria

Abstract

Prolonged immobilization may result in hypercalcemia, hypercalciuria, and osteoporosis. Although bone resorption is central to this syndrome, the mechanism of resorption is uncertain. In particular, the role of systemic calcium-regulating hormones remains unclear. In 14 immobilized subjects we measured fasting calcium excretion, 24-hour urinary calcium excretion during restricted calcium intake, the renal phosphorus threshold, plasma 1,25-dihydroxyvitamin D, nephrogenous cyclic AMP, and immunoreactive parathyroid hormone. Mean serum calcium levels were normal, but fasting and 24-hour calcium excretion were markedly elevated (0.28 mg per deciliter of glomerular filtrate and 314 mg per 24 hours, respectively). The mean levels of serum phosphorus (4.8 mg per deciliter) and the renal phosphorus threshold (4.3 mg per deciliter) were elevated. Mean plasma 1,25-dihydroxyvitamin D was strikingly reduced (9.9 pg per milliliter), as were nephrogenous cyclic (0.64 nmol per deciliter of glomerular filtrate) and immunoreactive parathyroid hormone in both assays. These findings indicate that the parathyroid--1,25-dihydroxyvitamin D axis is suppressed in patients with immobilization-induced hypercalciuria, as would be predicted by a model of resorptive hypercalciuria.

Influence of physical mobility and season on 25-hydroxyvitamin D-parathyroid hormone interaction and bone remodelling in the elderly

“…We conclude that, in institutionalized elderly, immobility has a strong impact on bone metabolism. This might counteract the development of 28 HPT through increased serum calcium (15), which is consistent with our ®nding of a positive correlation between mobility score and both serum calcium and urinary DPD. These results are similar to those seen in younger persons during shortterm bed rest (16) and in astronauts during space¯ight (17), with primary bone loss as a result of immobility or weightlessness-induced negative calcium balance.…”

Bone loss in spinal cord-injured patients: from physiopathology to therapy

“…3 During the first months following injury, the releasing of the mineral phase modifies calcium homeostasis. 37,38 Hypercalcemia and hypercalciuria, [37][38][39][40] which lead to the development of renal calculi 41 and to alterations in the calciotropic hormonal profile, 2,3,38,[42][43][44] are the most commonly encountered abnormalities. Histomorphometric data demonstrated that the principal cause of bone loss is the increase in bone resorption as defined by an augmentation in eroded surfaces and of the number of osteoclasts.…”

Urinary catheter blockage depends on urine pH, calcium and rate of flow

“…Following spinal cord injury urine Ca increases and alimentary Ca absorption is inhibited. 20 At this time changes in Ca intake have negligible in¯uence on urine Ca 21 and urine Ca concentration can be lowered only by increasing the intake of¯uid. If urine Ca remains high in a paraplegic after 9 months or in a tetraplegic more than 18 months after onset of the cord lesion consideration may be given to reducing Ca intake.…”