Hypocalciuric Effect of Lithium in Man

Miller, Paul D.; Dubovsky, Steven; Schrier, Robert W.; McDonald, Keith M.; Arnaud, C. D.

doi:10.1007/978-1-4613-4217-5_19

Cited by 16 publications

(12 citation statements)

References 24 publications

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“…Our data support the hypothesis that the previously reported systemic effects of lithium on mineral metabolism in man and experimental animal models (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) may be a function of the varying skeletal response to the lithium ion. …”

Section: Discussionsupporting

confidence: 90%

“…Our cointrol value for the periosteal mineralization rate, 3.57+0.43 gnm/day, correlates with the value of 3.2 ,tm/dav reported by previous investigators as the periosteal f'ormation rate in the femur of rats of similar weight (22). Subsequent studies by others with the rat tibia have reported periosteal and endosteal formation rates of 6.0 ,um/day and 2.9…”

Section: Discussionsupporting

confidence: 90%

“…Lithium treatment in man has been reported to induce hypercalcemia with elevated levels of parathyroid hormone and magnesium (2), hypocalciuria without alterations in response to parathyroid hormone (3)(4)(5), and renal tubular acidosis (6). In the rat, lithium has been noted to have no effect on serum calcium (7,8) or to result in hypercalcemia (9) and hypercalciuria (9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

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Lithium inhibition of bone mineralization and osteoid formation.

Baran¹,

Schwartz²,

Bergfeld³

et al. 1978

J. Clin. Invest.

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A B S T R A C T Lithium chloride administration to growing rats, which resulted in circulating lithium levels of 1.4 meq/liter, was attended by significant suppression of bone mineralization and organic matrix synthesis as assessed by tetracycline labeling and histological quantitation of osteoid, respectively. These effects of lithium were not associated with changes in animal behavior, nor were there any significant differences in blood levels of calcium, phosphorus, alkaline phosphatase, creatinine, pH, or parathyroid hormone. The data suggest that lithium inhibition of bone mineralization is secondary to suppression of osteoid formation.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Lithium inhibition of bone mineralization and osteoid formation.

Baran¹,

Schwartz²,

Bergfeld³

et al. 1978

J. Clin. Invest.

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“…However, acute lithium in fusions paradoxically increase the fractional excretion of calcium. A possible explanation for the hypocalciuria ob served in lithium-treated rats is that parathyroid hormone levels are elevated [10,28], however, our animals did not have significant elevations of their plasma calcium con centrations. It is possible that following each daily dose of lithium, urinary calcium excretion briefly increases and then PTH secretion is stimulated to produce calcium reten tion and homeostasis.…”

Section: Discussionmentioning

confidence: 68%

“…It is possible that following each daily dose of lithium, urinary calcium excretion briefly increases and then PTH secretion is stimulated to produce calcium reten tion and homeostasis. Such a mechanism would explain some of the divergent reported results of lithium on urinary calcium excretion [2,6,18,28,29,36], A reduction of plasma potassium levels in lithium-treated rats may simply reflect the effects of an increase in distal nephron flow [25] or else a possible intracellular potassium shift due to a mild volume contraction alkalosis. The latter is more likely as total body potassium (as well as total body sodium, calcium and phosphate) was found to be un altered by lithium treatment [unpublished results].…”

Section: Discussionmentioning

confidence: 99%

Effect of Lithium Treatment on Rat Renal Tubule Function

Carney¹,

Wong²,

Dirks³

1980

Nephron

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Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10–12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting rystem was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal sats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented; thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.

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Effects of Lithium Carbonate on Human Calcium Metabolism

Mallette¹,

Eichhorn²

1986

Arch Intern Med

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Hypocalciuric Effect of Lithium in Man

Cited by 16 publications

References 24 publications

Lithium inhibition of bone mineralization and osteoid formation.

Lithium inhibition of bone mineralization and osteoid formation.

Effect of Lithium Treatment on Rat Renal Tubule Function

Effects of Lithium Carbonate on Human Calcium Metabolism

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