Calcium and Phosphorus Fluxes During Hemodialysis With Low Calcium Dialysate

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We evaluated the acute effects of varying dialysate calcium concentration on plasma concentrations and dialyzer fluxes of calcium and phosphorus in adult hemodialysis patients. Seven individuals with stable end-stage renal failure were dialyzed 4 hours, three times weekly. The effects of dialysates containing 1.75, 1.25, or 0.75 mmol/L (70.1, 50.1, or 30.1 mg/L) of calcium were compared. Each patient was studied once at each bath calcium concentration. Compared with the predialysis mean value of 2.27 mmol/L (9.1 mg/dL), plasma total calcium concentration increased, remained constant, or decreased with the 1.75-,1.25-, or 0.75-mmol/L calcium dialysates, respectively. The 0.75-mmol/L calcium dialysate did not cause signs or symptoms of hypocalcemia (and the plasma calcium concentration did not fall below 1.80 mmol/L [7.2 mg/dL). Plasma phosphorus concentrations decreased equally from a predialysis mean value of 2.16 mmol/L (6.7 mg/dL), regardless of the dialysate calcium concentration. After 4 hours of treatment with the three different dialysates, the cumulative calcium fluxes were significantly different. With 1.75 mmol/L calcium, mean bodily calcium accumulation was 21.9 mmol (879 mg). With 1.25 mmol/L, there was no net calcium flux. With 0.75 mmol/L, mean patient calcium loss was 5.8 mmol (231 mg). Mean phosphorus removal after 4 hours was 32.5 mmol (1,006 mg) and was unaffected by dialysate calcium concentration. We conclude that (1) during hemodialysis with 1.75 mmol calcium/L, net calcium flux into the patients is substantial, whereas during hemodialysis with 0.75 mmol calcium/L, calcium losses are modest; (2) a single 4-hour treatment with a dialysate containing 0.75 mmol calcium/L is safe, provided that predialysis plasma calcium concentration is not low; and (3) variations in dialysate calcium concentration within the clinically relevant range do not affect phosphorus removal by hemodialysis. We caution against the extrapolation of our results in these acute studies to chronic treatment with low calcium dialysates, which could aggravate secondary hyperparathyroidism if intestinal calcium absorption fails to replace dialytic losses.

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    Supported in part by grants from the Medical Research Institute Council of the Michael Reese Hospital and Medical Center and the National Institute of Diabetes and Digestive and Kidney Diseases (Grant No. DK35985).

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