Regional citrate anticoagulation is an alternative to heparin in patients with bleeding diatheses who require continuous renal replacement therapy (CRRT). The short-term metabolic consequences that occur with citrate anticoagulation are well described and usually manageable if established protocols are followed vigilantly. Because of its customary short-term nature, the long-term consequences of CRRT with citrate are less often considered and have not been reported. The authors present the case of a woman with multisystem organ failure and prolonged acute renal failure who required CRRT for 120 days. Throughout her hospital course, adequate regional anticoagulation was achieved by blocking the coagulation cascade via the chelation of calcium by citrate. Despite an appropriate drop in the postfilter ionized calcium level, by 8 weeks after the initiation of CRRT, the patient was able to normalize serum calcium levels without the customary calcium infusion. Bone resorption owing to prolonged immobilization leading to hypercalcemia is a known complication of critically ill patients. This problem is more pronounced in patients with high bone turnover rates owing to conditions such as secondary hyperparathyroidism. In this particular case, the chelation of calcium by citrate masked the ensuing immobilization hypercalcemia, resulting in marked bone loss and bilateral spontaneous femoral fractures in the context of normal calcium levels. In critically ill patients sustained with prolonged CRRT with citrate anticoagulation, bone resorption and "relative" immobilization hypercalcemia may manifest as normal serum calcium levels in the face of falling calcium infusion rate requirements.