Effects of endogenous estrogen on renal calcium and phosphate handling in elderly women

• Published in: American journal of physiology: endocrinology and metabolism Vol. 288; no. 2; pp. E430 - E435
• Main Authors: Dick, I. M, Devine, A, Beilby, J, Prince, R. L
• Format: Journal Article
• Language: English
• Published: United States 01.02.2005
• Subjects: Aged; Aging - metabolism; Calcium - urine; Estrogens - administration & dosage; Estrogens - pharmacokinetics; Female; Hormone Replacement Therapy; Humans; Kidney - drug effects; Kidney - metabolism; Osteoporosis, Postmenopausal - prevention & control; Parathyroid Hormone - administration & dosage; Parathyroid Hormone - pharmacokinetics; Phosphates - urine; Risk Assessment - methods; Risk Factors; Women's Health
• ISSN: 0193-1849; 1522-1555
• DOI: 10.1152/ajpendo.00140.2004

1 School of Medicine and Pharmacology, University of Western Australia; 2 The Western Australian Centre for Pathology and Medical Research; 3 Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital; and 4 Western Australian Institute of Medical Research, Nedlands Western Australia, Australia Submitted 24 March 2004 ; accepted in final form 30 September 2004 High postmenopausal endogenous estrogen concentrations are an important determinant of preservation of bone mass and reduced fracture in elderly women. Calcium supplementation can also reduce bone loss in these patients, suggesting an interaction between estrogen deficiency and calcium balance. Potential mechanisms of estrogen on calcium transport include direct effects on the bone, the kidney, and the bowel. Previous studies have demonstrated effects of estrogen on renal phosphate handling. We have used a cross-sectional, population-based analysis of biochemical data obtained from ambulant elderly women to determine the association of endogenous estradiol with urine calcium and phosphorus excretion. The subjects were 293 postmenopausal women >70 yr old. Factors associated with renal calcium and phosphate excretion were measured, including the filtered calcium and phosphate load, parathyroid hormone (PTH), estradiol, and sex hormone-binding globulin (SHBG). The free estradiol concentration (FE) was calculated from a previously described formula. A high plasma estradiol concentration ( r 2 = 0.023, P = 0.01) and a high FE ( r 2 = 0.045, P = 0.001) were associated with reduced renal calcium excretion. The estradiol and FE effect on renal calcium excretion remained significant after adjusting for calcium filtered at the glomerulus and serum PTH. A high FE was associated with a reduced renal phosphate threshold in univariate analysis ( r 2 = 0.023, P = 0.010). The effect remained significant after adjustment for serum PTH. The size of the effect of the FE was of the same order of magnitude as the effect of PTH on reducing renal calcium excretion and increasing renal phosphate excretion. These data support in vitro and animal data demonstrating an effect of estradiol on renal calcium and phosphate handling and indicate that, in elderly postmenopausal women, the effect is of a similar magnitude to the well-recognized effects of PTH on these physiologically regulated parameters. estradiol; calcium homeostasis; phosphate homeostasis; renal tubular calcium reabsorption; osteoporosis Address for reprint requests and other correspondence: I. M. Dick, School of Medicine and Pharmacology, Univ. of Western Australia, 4th Floor G Block, Sir Charles Gairdner Hospital, Nedlands, WA, Australia 6009 (E-mail: iand{at}cyllene.uwa.edu.au )