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Dtsch Med Wochenschr 2016; 141(21): 1531-1536
DOI: 10.1055/s-0042-109043
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© Georg Thieme Verlag KG Stuttgart · New York

Hyper- und Hypokaliämien – „the silent killer“

„The silent killer: hyper- and hypokalaemia“
Mark Dominik Alscher
1   Robert-Bosch-Krankenhaus, Zentrum für Innere Medizin, Abteilung für Allgemeine Innere Medizin und Nephrologie
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Publikationsverlauf

Publikationsdatum:
17. Oktober 2016 (online)

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Zusammenfassung

Die Bestimmung der Kaliumkonzentration im Serum ist die Grundlage für die Diagnose von Störungen im Kaliumhaushalt. Die Konzentration resultiert aus dem Zusammenspiel von Kaliumaufnahme, -ausscheidung und interner Verteilung zwischen zellulären und extrazellulären Räumen. Störungen des Kaliumhaushaltes sind häufig. Dies ist Folge einer zunehmend älter werdenden Bevölkerung mit Erkrankungen, die einerseits häufig zu einer Diuretika-Therapie anderseits zu einer Nierenschädigung führen. Im ersten Fall finden sich überwiegend Hypokaliämien, im Letzteren nicht selten Hyperkaliämien. Beide führen zu einer erhöhten Mortalität, häufig ohne dass die Ursache dafür erkannt wird. Häufig firmieren die Todesfälle aufgrund der Herzrhythmusstörungen, welche zu einem Herzstillstand führen können (Kammerflimmern und Hypo-Asystolie) als „plötzlicher Herztod“. Ein pathophysiologisches Verständnis für das mögliche Auftreten und die rechtzeitige Entdeckung durch eine Kontrolle des Kaliums sind entscheidend, um die Mortalität zu senken.

Abstract

The estimation of potassium in the serum is basis for the diagnosis of potassium disturbances. The value is a result of intake, excretion and internal distribution of potassium between intra- and extracellular compartments of the body. Clinically, we often see disturbances of potassium. The causes are explained by an aging population with morbidities that warrant diuretic treatment on the one side, and chronic kidney diseases on the other. In the first cases, we see hypokalaemia, in the latter hyperkalaemia. Both can lead to increased mortalities which are often labelled as “sudden heart death” without finding the underlying mechanism to be potassium driven. This is due to the fact that cardiac arrhythmias (ventricular fibrillation, heart block) lead to cardiac arrest. The pathophysiological understanding of the principles is the key for the guidance of diagnosis and therapy of the disturbances of potassium metabolism. Only by that, a decrease in mortality can be accomplished.

Schlüsselwörter

Hyperkaliämie - Hyperkaliämie - Kalium - Mortalität

Keywords

Hyperkalaemia - hypokalaemia - potassium - mortality
 

  • Literatur

  • 1 Weiner ID, Wingo CS. Hyperkalemia: a potential silent killer. J Am Soc Nephrol 1998; 9: 1535-1543
    PubMedGoogle Scholar
  • 2 Conway R, Creagh D, Byrne DG et al. Serum potassium levels as an outcome determinant in acute medical admissions. Clin Med (Lond) 2015; 15: 239-243
    CrossrefPubMedGoogle Scholar
  • 3 Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nat Rev Nephrol 2011; 7: 75-84
    CrossrefPubMedGoogle Scholar
  • 4 Krogager ML, Torp-Pedersen C, Mortensen RN et al. Short-term mortality risk of serum potassium levels in hypertension: a retrospective analysis of nationwide registry data. Eur Heart J 2016 Apr 20. DOI: 10.1093/eurheartj/ehw129.
    PubMedGoogle Scholar
  • 5 Chang AR, Sang Y, Leddy J et al. Antihypertensive Medications and the prevalence of kyperkalemia in a large health system. Hypertension 2016; 67: 1181-1188
    CrossrefPubMedGoogle Scholar
  • 6 Goyal A, Spertus JA, Gosch K, Venkitachalam L, Jones PG, Van den Berghe G et al. Serum potassium levels and mortality in acute myocardial infarction. JAMA. 2012; 307 (2) 157-64
    CrossrefPubMedGoogle Scholar
  • 7 Jensen HK, Brabrand M, Vinholt PJ et al. Hypokalemia in acute medical patients: risk factors and prognosis. Am J Med 2015; 128: 60-7 e1
    CrossrefPubMedGoogle Scholar
  • 8 Salah K, Pinto YM, Eurlings LW et al. Serum potassium decline during hospitalization for acute decompensated heart failure is a predictor of 6-month mortality, independent of N-terminal pro-B-type natriuretic peptide levels: An individual patient data analysis. Am Heart J 2015; 170: 531-542 e1
    CrossrefPubMedGoogle Scholar
  • 9 Luo J, Brunelli SM, Jensen DE, Yang A. Association between serum potassium and outcomes in patients with reduced kidney function. Clin J Am Soc Nephrol 2016; 11: 90-100
    CrossrefPubMedGoogle Scholar
  • 10 Squires RD, Huth EJ. Experimental potassium depletion in normal human subjects. I. Relation of ionic intakes to the renal conservation of potassium. J Clin Invest 1959; 38: 1134-1148
    CrossrefPubMedGoogle Scholar
  • 11 Perez GO, Oster JR, Rogers A. Acid-base disturbances in gastrointestinal disease. Dig Dis Sci 1987; 32: 1033-1043
    CrossrefPubMedGoogle Scholar
  • 12 Alscher DM, Herrlinger K, Stange EF. [Disturbances in volume and electrolytes with intestinal and kidney diseases]. Internist (Berl) 2006; 47: 1110 112–114, 115–120
    CrossrefPubMedGoogle Scholar
  • 13 Haberer JP, Jouve P, Bedock B, Bazin PE. Severe hypokalaemia secondary to overindulgence in alcohol-free “pastis”. Lancet 1984; 1: 575-576
    PubMedGoogle Scholar
  • 14 Harris RT. Bulimarexia and related serious eating disorders with medical complications. Ann Intern Med 1983; 99: 800-807
    CrossrefPubMedGoogle Scholar
  • 15 Mehler PS. Hypokalemia: A Marker of Covert Bulimia Nervosa. Am J Med 2015; 128: e37
    PubMedGoogle Scholar
  • 16 Rabelink TJ, Koomans HA, Hene RJ, Dorhout Mees EJ. Early and late adjustment to potassium loading in humans. Kidney Int 1990; 38: 942-947
    CrossrefPubMedGoogle Scholar
  • 17 16. Kuhlmann U, Böhler J, Luft FC. et al. Nephrologie. 6. Aufl. Stuttgart: Thieme; 2015
    Artikel in Thieme ConnectGoogle Scholar
  • 18 Zietse R, Zoutendijk R, Hoorn EJ. Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol 2009; 5: 193-202
    CrossrefPubMedGoogle Scholar
  • 19 Kleta R, Basoglu C, Kuwertz B oking E New treatment options for Bartter’s syndrome. N Engl J Med 2000; 343: 661-662
    CrossrefPubMedGoogle Scholar
  • 20 Loffing J, Zecevic M, Feraille E et al. Aldosterone induces rapid apical translocation of ENaC in early portion of renal collecting system: possible role of SGK. Am J Physiol Renal Physiol 2001; 280: F675-682
    PubMedGoogle Scholar
  • 21 Briet M, Schiffrin EL. Aldosterone: effects on the kidney and cardiovascular system. Nature reviews Nephrology 2010; 6: 261-273
    CrossrefPubMedGoogle Scholar
  • 22 Meyer-Lehnert H, Kramer HJ, Heck I et al. [Severe periodic hypokalemic paralysis. Prevention using beta-receptor blockade]. Dtsch Med Wochenschr 1987; 112: 1173-1177
    Artikel in Thieme ConnectPubMedGoogle Scholar
  • 23 Kuhlmann U, Böhler J, Luft FC et al. Nephrologie. 6. Aufl. Stuttgart: Thieme; 2015: 322-345
    Artikel in Thieme ConnectGoogle Scholar
  • 24 Weiner ID, Wingo CS. Hypokalemia-consequences, causes, and correction. J Am Soc Nephrol. 1997; 8: 1179-1188
    PubMedGoogle Scholar
  • 25 Funder JW. Apparent mineralocorticoid excess. Endocrinol Metab Clin North Am. 1995; 24: 613-621
    PubMedGoogle Scholar
  • 26 Thomas RM, Ruel E, Shantavasinkul PC, Corsino L. Endocrine hypertension: An overview on the current etiopathogenesis and management options. World J Hypertens. 2015; 5: 14-27
    PubMedGoogle Scholar
  • 27 Simon DB, Karet FE, Hamdan JM et al. Bartter’s syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2. Nat Genet. 1996; 13: 183-188
    CrossrefPubMedGoogle Scholar
  • 28 Simon DB, Nelson-Williams C, Bia MJ et al. Gitelman’s variant of bartter’s syndrome, inherited hypokalaemic alkalosis, is caused by mutations in the thiazide-sensitive Na-Cl cotransporter. Nat Genet. 1996; 12: 24-30
    CrossrefPubMedGoogle Scholar
  • 29 Torres VE, Young Jr. WF, Offord KP, Hattery RR. Association of hypokalemia, aldosteronism, and renal cysts. N Engl J Med. 1990; 322: 345-351
    CrossrefPubMedGoogle Scholar
  • 30 Hung AM, Hakim RM. Dialysate and serum potassium in hemodialysis. Am J Kidney Dis. 2015; 66: 125-132
    CrossrefPubMedGoogle Scholar
  • 31 Blumberg A, Roser HW, Zehnder C, Muller-Brand J. Plasma potassium in patients with terminal renal failure during and after haemodialysis; relationship with dialytic potassium removal and total body potassium. Nephrol Dial Transplant. 1997; 12: 1629-1634
    CrossrefPubMedGoogle Scholar