Renal calcium and phosphate handling is an important contributor to mineral homeostasis and bone health and the androgen receptor (AR) is highly expressed in the kidney. We investigated the short term effects of androgen deprivation on renal calcium and phosphate reabsorption, independent of their effects on bone. Two weeks following orchidectomy (ORX) of adult mice, bone loss occurred along with hypercalciuria, which was similarly prevented by testosterone and dihydrotestosterone supplementation. Treatment with bisphosphonates prior to ORX also inhibited hypercalciuria, indicating that the calcium flux originated from the bone. Renal calcium and phosphate transporter expression was increased post-ORX, independent of bisphosphonates. Furthermore, androgen deprivation appeared to stimulate local synthesis of 1,25(OH)₂D₃. When bisphosphonate-treated mice were fed a low calcium diet, bone resorption was no longer blocked and secondary hyperparathyroidism developed, which was more pronounced in ORX mice than sham-operated mice. In conclusion, this study shows that androgen deprivation increased renal calcium and phosphate transporter expression, independent of bone, and underlines the importance of adequate intestinal calcium supply in circumstances of androgen deprivation and bisphosphonate treatment.

肾脏钙和磷酸盐的处理是矿物质体内稳态和骨骼健康的重要因素，并且雄激素受体（AR）在肾脏中高度表达。我们调查了雄激素剥夺对肾脏钙和磷酸盐重吸收的短期影响，而与它们对骨骼的影响无关。成年小鼠的睾丸切除术（ORX）后两周，发生骨质流失和高钙尿症，这同样可以通过补充睾丸激素和二氢睾丸激素来预防。在ORX之前用双膦酸盐治疗也抑制了高钙尿症，表明钙通量起源于骨骼。肾钙和磷酸盐转运蛋白表达增加ORX后，独立于双膦酸盐。此外，雄激素剥夺似乎刺激了1,25（OH）_2的局部合成D ₃。当双膦酸盐治疗的小鼠饲喂低钙饮食时，骨吸收不再受阻，继发性甲状旁腺功能亢进发展，这在ORX小鼠中比假手术小鼠更为明显。总之，这项研究表明，雄激素剥夺增加了肾脏钙和磷酸盐转运蛋白的表达，独立于骨骼，并强调了在雄激素剥夺和双膦酸盐治疗的情况下，充足的肠道钙供应的重要性。