title: Clinical factors affecting serum potassium concentration in cardio-renal decompensation syndrome.
abstract: BACKGROUND
  Renin-angiotensin-aldosterone system (RAAS) inhibitors are currently indispensable for the treatment of heart failure. It is well known that hyperkalemia is likely to occur in renal failure; however, it has not yet been clarified how the serum potassium concentration changes as heart failure progresses. Currently, the cardio-renal decompensation syndrome holds that the serum potassium concentration is altered similarly by both heart failure and renal failure; however, there are no definitive reports on this. In order to use RAAS inhibitors more safely and effectively in heart failure, it is necessary to understand the factors affecting serum potassium concentration in the clinical setting.
  
  
  RESULTS
  We examined the clinical factors affecting serum potassium concentration in 1035 consecutive patients with cardiovascular disease who were hospitalized in our institution. Multiple regression analysis showed that the independent factors associated with an elevated serum potassium concentration were renal insufficiency evaluated by estimated glomerular filtration rate (eGFR) (P<0.0001), diabetes mellitus evaluated by HbA(1c) (P=0.0005) and the use of RAAS inhibitors (P=0.0010). The independent factors associated with a decreased serum potassium concentration were mean blood pressure (P<0.0001), heart failure evaluated by log BNP (P=0.0164) and the use of diuretics (P=0.0232).
  
  
  CONCLUSIONS
  The serum potassium concentration decreases with the severity of heart failure if renal function is preserved. From the perspective of potassium homeostasis, we could use the RAAS inhibitors more aggressively in patients with heart failure who do not have renal failure.
authors.affiliation: Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan.
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Ueno
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
authors.forename: Masafumi
authors.initials: M
authors.lastname: Nakayama
authors.forename: Megumi
authors.initials: M
authors.lastname: Yamamuro
authors.forename: Tsunenori
authors.initials: T
authors.lastname: Nishijima
authors.forename: Kenichi
authors.initials: K
authors.lastname: Kusuhara
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Nagayoshi
authors.forename: Sunao
authors.initials: S
authors.lastname: Kojima
authors.forename: Koichi
authors.initials: K
authors.lastname: Kaikita
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sumida
authors.forename: Seigo
authors.initials: S
authors.lastname: Sugiyama
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002648:Child; D018450:Disease Progression; D004232:Diuretics / Q000627:therapeutic use*; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006333:Heart Failure / Q000097:blood / Q000150:complications / Q000188:drug therapy; D006801:Humans; D006947:Hyperkalemia / Q000097:blood / Q000150:complications / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D011188:Potassium / Q000097:blood*; D012044:Regression Analysis; D051437:Renal Insufficiency / Q000097:blood / Q000150:complications / Q000188:drug therapy; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D012720:Severity of Illness Index; D013148:Spironolactone / Q000627:therapeutic use*; D055815:Young Adult
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D004232:Diuretics; D020097:Natriuretic Peptide, Brain; D013148:Spironolactone; D011188:Potassium