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Letters |
Western Reserve Care System, Dept. of Pathol. and Lab. Med., 500 Gypsy Lane, Youngstown, OH 44501
a author for correspondence.
To the Editor:
Continuous hemodialysis, either arteriovenous or veno-venous, is increasingly used in critically ill patients with acute renal failure. Trisodium citrate has become popular as a regional anticoagulant for these procedures to minimize the risk of hemorrhage and thrombocytopenia associated with heparin (1). Excess calcium citrate and citrate ions are removed by dialysis enhanced by calcium-free, alkali-free dialysate, thus requiring a CaCl2 infusion to maintain serum calcium. Noncritical hypocalcemia and metabolic alkalosis have been associated with such treatment (2).
We recently observed a patient who developed profound hypercalcemia
while undergoing continuous veno-venous hemofiltration dialysis
(CVVHD). This 76-year-old man had a long history of myasthenia gravis,
non-insulin-dependent diabetes mellitus, coronary artery disease, and
peripheral vascular disease. After an aortobifemoral bypass, he
developed an extensive left thigh hematoma and graft infection,
prompting two reexplorations and systemic antibiotic therapy. He
developed renal and hepatic failure as well as a coagulopathy. In
accordance with standard practice at our institution, CVVHD was
initiated with trisodium citrate anticoagulation in combination with a
calcium-free, alkali-free dialysate and CaCl2
infusion; total calcium at this time was 1.72 mmol/L. Over the next
72 h, 2.12 mol of trisodium citrate dihydrate and 0.37 mol of
CaCl2 were infused. The trisodium citrate infusion rate was
adjusted according to activated clotting time values. CaCl2
infusion was given to maintain a normal ionized calcium (1.13–1.30
mmol/L). Despite the large amount of CaCl2 infused, the
ionized calcium remained decreased. Because of this and the increased
activated clotting time values, the amounts of CaCl2 and
trisodium citrate infused were greater than the typical amounts given
for CVVHD. The patient also received multiple citrated blood products.
After three days of dialysis, the patient developed profound
hypercalcemia and acidosis (see Table 1
). The maximum total calcium, measured by the calcium/EDTA
o-cresolphthalein method on a Hitachi 747, was 4.67 mmol/L.
Total calcium was also measured by atomic absorption (4.37 mmol/L).
Serum citric acid concentrations were 22 and 17 mmol/L on two serum
specimens on March 11, 1996. Despite profound hypercalcemia,
hypercitric acidemia, and low ionized calcium, signs of hyper- or
hypocalcemia were not apparent. The patient's severe myasthenia gravis
probably masked typical symptoms. Despite continued CVVHD and
supportive care, the patient's condition deteriorated and he
died 5 days after initiation of dialysis.
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The distribution between protein-bound, complexed, and free calcium can be altered by many factors, such as calcium binding due to abnormal protein concentrations or structurally abnormal proteins, or the effects of heparin, bilirubin, and free fatty acids on protein. Bicarbonate, lactate, and phosphate also complex with calcium (3). This case illustrates the occurrence of hypercalcemia related to citrate accumulation and calcium complexing in continuous veno-venous hemofiltration dialysis, probably as a consequence of ineffective citrate removal and impaired hepatic metabolism (2)(4). Disparities between total and ionized calcium secondary to calcium citrate complexing have been reported in patients receiving citrated blood or other blood products and during donor plasmapheresis (5)(6). Although calcium citrate complexing is known to cause hypercalcemia in such cases, it is usually mild and resolves without treatment (3). The profound hypercalcemia with low ionized calcium in this case is a biochemical reflection of citrate accumulation in an unusual setting.
References
The following articles in journals at HighWire Press have cited this article:
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  C. Morath, N. Miftari, R. Dikow, C. Hainer, M. Zeier, S. Morgera, M. A. Weigand, and V. Schwenger Sodium citrate anticoagulation during sustained low efficiency dialysis (SLED) in patients with acute renal failure and severely impaired liver function Nephrol. Dial. Transplant., January 1, 2008; 23(1): 421 - 422. [Full Text] [PDF]
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