Nephrol Dial Transplant Vol. 19 No. 9 © ERA-EDTA 2004; all rights reserved
Editorial Comment
Hyperkalaemia: again
Nephrology, Department of Medicine, University Medical Center C. G. Carus, Dresden, Germany
Correspondence and offprint requests to: Peter Gross, MD, Nephrologie, Medizinische Klinik III, Universitätsklinikum C. G. Carus, Fetscherstrasse 74, D-01307 Dresden, Germany. Email: peter.gross@mailbox.tu-dresden.de
Keywords: aldosterone antagonists; hyperkalaemia; hyporeninaemic hypoaldosteronism
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Introduction |
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Before 1999—and if one was a nephrologist— it was rare to be called to consult on a case of hyperkalaemia. No doubt cases of hyperkalaemia occurred at that time, too—for instance in patients in the moderate to advanced stages of renal failure—but physicians apparently had sufficient understanding of kidney function to call for dialysis treatment or similar alternative measures where appropriate and take care of severe hyperkalaemia. This has changed recently. Now, it is almost routine to be called by the Emergency Room because of ‘another severe’ hyperkalaemia—and one that is not related to uraemia. Why?
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Hyperkalaemia has changed with the advent of the RALES study |
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In 1999 the ‘randomized aldactone evaluation study investigators’ (RALES [6]) reported the results of a 24 month observation in 1663 patients with advanced congestive heart failure (CHF). In that landmark trial which had been conducted in a prospective controlled fashion, the addition of spironolactone to the patients’ treatment improved morbidity and mortality
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Hyperkalaemia is now common and it may be fatal |
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What went wrong after RALES? |
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What are the risk factors for hyperkalaemia in the setting of ACE inhibitors plus mineralocorticoid antagonist? |
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Future perspectives |
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Anything else new in ‘Hyperkalaemia-land’? |
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Hyporeninaemic hypoaldosteronism (hypo-hypo): an old foe that doesn’t go away |
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The treatment of hyperkalaemia |
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Conclusion |
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