Renal Excretion of Calcium

Peacock, M.

doi:10.1007/978-1-4471-1437-6_6

Cited by 15 publications

(14 citation statements)

References 151 publications

(161 reference statements)

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“…Renal calcium excretion is regulated by two main mechanisms: tubular calcium reabsorption and filtered calcium load (29). Disruption of either or both of these mechanisms leads to abnormal calcium homeostasis.…”

Section: Renal Calcium Excretionmentioning

confidence: 99%

“…GFR hypercalcemia develops when the input of calcium to the circulation exceeds its removal by the kidney's filtration rate independent of the tubular calcium reabsorption rate (29). This readily occurs in children and patients with CKD (25).…”

Section: Renal Calcium Excretionmentioning

confidence: 99%

“…Finally, the dose response between serum phosphate and FGF-23 concentrations is much less rapid than that between calcium and its regulating hormones. On the other hand, renal excretion of phosphate is as closely regulated as calcium, and the kidney is the main organ that regulates both calcium (29) and phosphate homeostasis (41).…”

Section: Phosphate Homeostasismentioning

confidence: 99%

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Calcium Metabolism in Health and Disease

Peacock

2010

Clinical Journal of the American Society of Nephrology

691

502

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This brief review focuses on calcium balance and homeostasis and their relationship to dietary calcium intake and calcium supplementation in healthy subjects and patients with chronic kidney disease and mineral bone disorders (CKD-MBD). Calcium balance refers to the state of the calcium body stores, primarily in bone, which are largely a function of dietary intake, intestinal absorption, renal excretion, and bone remodeling. Bone calcium balance can be positive, neutral, or negative, depending on a number of factors, including growth, aging, and acquired or inherited disorders. Calcium homeostasis refers to the hormonal regulation of serum ionized calcium by parathyroid hormone, 1,25-dihydroxyvitamin D, and serum ionized calcium itself, which together regulate calcium transport at the gut, kidney, and bone. Hypercalcemia and hypocalcemia indicate serious disruption of calcium homeostasis but do not reflect calcium balance on their own. Calcium balance studies have determined the dietary and supplemental calcium requirements needed to optimize bone mass in healthy subjects. However, similar studies are needed in CKD-MBD, which disrupts both calcium balance and homeostasis, because these data in healthy subjects may not be generalizable to this patient group. Importantly, increasing evidence suggests that calcium supplementation may enhance soft tissue calcification and cardiovascular disease in CKD-MBD. Further research is needed to elucidate the risks and mechanisms of soft tissue calcification with calcium supplementation in both healthy subjects and CKD-MBD patients.

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Section: Renal Calcium Excretionmentioning

confidence: 99%

Section: Renal Calcium Excretionmentioning

confidence: 99%

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Calcium Metabolism in Health and Disease

Peacock

2010

Clinical Journal of the American Society of Nephrology

691

502

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“…Once absorbed, the major flow of calcium is to bone and to kidney. In the kidney about 98% of the 9000 mg calcium that is filtered each day is reabsorbed, mainly under the regulation of serum parathyroid hormone (PTH) concentrations [28]. The 2% unreabsorbed calcium appears in urine as an obligatory calcium loss.…”

Section: Functionmentioning

confidence: 99%

Effects of Calcium and Vitamin D Insufficiency on the Skeleton

Peacock

1998

Osteoporos Int

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“…Fasting urinary calcium excretion adjusted for creatinine clearance (UCa E ) was derived by the formula: UCa E ϭ (Ca U ϫ Cr S )/Cr U (16). Creatinine clearance was estimated from the serum creatinine concentration, 24-h urinary creatinine concentration, and volume.…”

Section: Methodsmentioning

confidence: 99%

Effects of Lithium Therapy on Bone Mineral Metabolism: A Two-Year Prospective Longitudinal Study¹

Mak

Shek

Chow³

et al. 1998

The Journal of Clinical Endocrinology & Metabolism

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Many studies showed an increased occurrence of primary hyperparathyroidism during lithium therapy. We studied 53 patients receiving lithium therapy prospectively for 2 yr. Serum PTH levels were unequivocally elevated. The baseline PTH level was 2.8 +/- 1.2 pmol/L and increased progressively to 3.9 +/- 1.5 pmol/L after 2 yr (P < 0.0005). There was no change in serum calcium, alkaline phosphatase, inorganic phosphate concentrations or tubular reabsorption of phosphate in relation to glomerular filtration rate. Fasting urinary reabsorption of calcium increased significantly (P < 0.0005), which was concordant with the PTH change. Fasting and 24-h urinary excretion of calcium decreased significantly (P < 0.0005), suggesting reduced, rather than enhanced, bone resorption as in primary hyperparathyroidism. This may be the main mechanism in maintaining normocalcemia, despite PTH elevation, during lithium therapy.

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Renal Excretion of Calcium

Cited by 15 publications

References 151 publications

Calcium Metabolism in Health and Disease

Calcium Metabolism in Health and Disease

Effects of Calcium and Vitamin D Insufficiency on the Skeleton

Effects of Lithium Therapy on Bone Mineral Metabolism: A Two-Year Prospective Longitudinal Study¹

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Renal Excretion of Calcium

Cited by 15 publications

References 151 publications

Calcium Metabolism in Health and Disease

Calcium Metabolism in Health and Disease

Effects of Calcium and Vitamin D Insufficiency on the Skeleton

Effects of Lithium Therapy on Bone Mineral Metabolism: A Two-Year Prospective Longitudinal Study1

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Effects of Lithium Therapy on Bone Mineral Metabolism: A Two-Year Prospective Longitudinal Study¹