RSS-Feed abonnieren
PDF herunterladen
DOI: 10.1055/s-0042-109043
Hyper- und Hypokaliämien – „the silent killer“
„The silent killer: hyper- and hypokalaemia“Publikationsverlauf
Publikationsdatum:
17. Oktober 2016 (online)
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.
-
Literatur
- 1 Weiner ID, Wingo CS. Hyperkalemia: a potential silent killer. J Am Soc Nephrol 1998; 9: 1535-1543
- 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
- 3 Unwin RJ, Luft FC, Shirley DG. Pathophysiology and management of hypokalemia: a clinical perspective. Nat Rev Nephrol 2011; 7: 75-84
- 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.
- 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
- 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
- 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
- 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
- 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
- 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
- 11 Perez GO, Oster JR, Rogers A. Acid-base disturbances in gastrointestinal disease. Dig Dis Sci 1987; 32: 1033-1043
- 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
- 13 Haberer JP, Jouve P, Bedock B, Bazin PE. Severe hypokalaemia secondary to overindulgence in alcohol-free “pastis”. Lancet 1984; 1: 575-576
- 14 Harris RT. Bulimarexia and related serious eating disorders with medical complications. Ann Intern Med 1983; 99: 800-807
- 15 Mehler PS. Hypokalemia: A Marker of Covert Bulimia Nervosa. Am J Med 2015; 128: e37
- 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
- 17 16. Kuhlmann U, Böhler J, Luft FC. et al. Nephrologie. 6. Aufl. Stuttgart: Thieme; 2015
- 18 Zietse R, Zoutendijk R, Hoorn EJ. Fluid, electrolyte and acid-base disorders associated with antibiotic therapy. Nat Rev Nephrol 2009; 5: 193-202
- 19 Kleta R, Basoglu C, Kuwertz B oking E New treatment options for Bartter’s syndrome. N Engl J Med 2000; 343: 661-662
- 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
- 21 Briet M, Schiffrin EL. Aldosterone: effects on the kidney and cardiovascular system. Nature reviews Nephrology 2010; 6: 261-273
- 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
- 23 Kuhlmann U, Böhler J, Luft FC et al. Nephrologie. 6. Aufl. Stuttgart: Thieme; 2015: 322-345
- 24 Weiner ID, Wingo CS. Hypokalemia-consequences, causes, and correction. J Am Soc Nephrol. 1997; 8: 1179-1188
- 25 Funder JW. Apparent mineralocorticoid excess. Endocrinol Metab Clin North Am. 1995; 24: 613-621
- 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
- 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
- 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
- 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
- 30 Hung AM, Hakim RM. Dialysate and serum potassium in hemodialysis. Am J Kidney Dis. 2015; 66: 125-132
- 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