Article Text

Secondary hyperkalaemic paralysis
  1. Department of Neurology, MEDUNSA and Ga-Rankuwa Hospital, South Africa
  1. Professor R F Gledhill, Department of Neurology, PO Box 108, Medunsa 0204, South Africa. Telephone 0027 12 521 4136/4209; fax 0027 12 521 4758/560 0086.
  1. S EVERS
  1. Department of Neurology, University of Münster, Albert Schweitzer Strasse 33, D 48129 Münster, Germany

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    In their report describing a case of hyperkalaemic paralysis associated with renal failure and use of spironolactone, Evers et al 1 provide an illustration of the results obtained from conduction studies performed on the patient’s median sensory nerve. Utilising the calibration markers, the average amplitude of the sensory action potential (SAP) measures 10.6 μV before haemodialysis and 27.2 μV afterward. However, these measurements are recorded in table 1 as being 20.0 μV and 24.0 μV, respectively.

    An increase in SAP amplitude after normalisation of serum potassium concentration would offer additional support the authors’ suggestion that the pathological process causing weakness in secondary hyperkalaemic paralysis probably originates at the level of nerve rather than muscle.


    Evers replies:

    The figures in table 1 were indeed incorrect and the correct figures from the original data are 8 μV before haemodialysis and 24 μV after haemodialysis.

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