Litzow J R, Lemann J, Lennon E J
J Clin Invest. 1967 Feb;46(2):280-6. doi: 10.1172/JCI105530.
Small but statistically significant negative calcium balances were found in each of eight studies in seven patients with chronic azotemic renal disease when stable metabolic acidosis was present. Only small quantities of calcium were excreted in the urine, but fecal calcium excretion equaled or exceeded dietary intake. Complete and continuous correction of acidosis by NaHCO(3) therapy reduced both urinary and fecal calcium excretion and produced a daily calcium balance indistinguishable from zero. Apparent acid retention was found throughout the studies during acidosis, despite no further reduction of the serum bicarbonate concentration. The negative calcium balances that accompanied acid retention support the suggestion that slow titration of alkaline bone salts provides an additional buffer reservoir in chronic metabolic acidosis. The treatment of metabolic acidosis prevented further calcium losses but did not induce net calcium retention. It is suggested that the normal homeostatic responses of the body to the alterations in ionized calcium and calcium distribution produced by raising the serum bicarbonate might paradoxically retard the repair of skeletal calcium deficits.
在七名患有慢性氮质血症性肾病的患者中,当存在稳定的代谢性酸中毒时,八项研究中的每一项都发现了虽小但具有统计学意义的负钙平衡。尿液中仅排出少量钙,但粪便钙排泄量等于或超过饮食摄入量。通过碳酸氢钠治疗完全且持续地纠正酸中毒可减少尿液和粪便中的钙排泄,并产生与零无显著差异的每日钙平衡。在整个酸中毒研究期间,尽管血清碳酸氢盐浓度没有进一步降低,但仍发现明显的酸潴留。伴随酸潴留的负钙平衡支持了这样一种观点,即在慢性代谢性酸中毒中,碱性骨盐的缓慢滴定提供了额外的缓冲储备。代谢性酸中毒的治疗可防止进一步的钙流失,但不会引起净钙潴留。有人认为,身体对因提高血清碳酸氢盐而导致的离子钙和钙分布变化的正常稳态反应可能反常地阻碍骨骼钙缺乏的修复。