1. Calcium concentration and Ca2+ -ATPase activity under basal conditions and after maximal stimulation with calmodulin were measured in erythrocytes from 32 patients with end-stage renal failure on haemodialysis and from 27 healthy subjects.

2. In patients with renal failure the Ca2+ concentration in erythrocytes was elevated compared with healthy subjects (4.27 ± 1.02 versus 2.86 ± 0.57 μmol/l, P < 0.05).

3. Basal Ca2+ -ATPase activity was lower in the patients with renal failure than in healthy subjects (4.62 ± 1.34 versus 5.43 ± 1.23 pmol of phosphate min−1 10−6 erythrocytes). After maximal stimulation, Ca2+−ATPase activity reached 6.93 ± 2.81 pmol of phosphate min−1 10−6 erythrocytes in the patients with renal failure, whereas in healthy subjects stimulation yielded a Ca2+−ATPase activity of 32.54 ± 8.48 pmol of phosphate min−1 10−6 erythrocytes.

4. Incubation of erythrocytes from healthy subjects with plasma from uraemic patients caused inhibition of Ca2+−ATPase. Likewise, the ultrafiltrate from plasma obtained by haemofiltration treatment inhibited Ca2+−ATPase.

5. Gel chromatography of the ultrafiltrate and laser desorption/ionization mass spectroscopy revealed that a fraction containing substances with a molecular mass of about 300 Da inhibited Ca2+−ATPase.

6. It is concluded that, in uraemia, a Ca2+−ATPase inhibitor accumulates in the plasma, and this could contribute to the toxicity of uraemia by inhibiting cellular Ca2+ transport in erythrocytes and possibly other tissues.

This content is only available as a PDF.
You do not currently have access to this content.