Patterns of chronic and transient hyperkalaemia and clinically important outcomes in patients with chronic kidney disease

Abstract

\n \n \n Whether hyperkalaemia in CKD is chronic or transient, and whether this has different outcome implications, is not known.\n \n \n \n This was an observational study of adults with CKD G3–5 from Stockholm, Sweden 2006–11. We examined individual trajectories of potassium from all measurements obtained through routine outpatient care. For each month of follow-up, we created a rolling assessment of the proportion of time in which potassium was abnormal during the previous 12 months. We defined patterns of hyperkalaemia as transient (≤50% of time during the previous year with potassium >5.0 mmol/L) and chronic (>50% of time with potassium >5.0 mmol/L), and examined whether previous hyperkalaemia pattern offers additional predictive value beyond that provided by the most recent (current) potassium value.\n \n \n \n We included 36 511 participants (56% women) with CKD G3–5 and median estimated glomerular filtration rate 46 mL/min/1.73 m2. Transient and chronic hyperkalaemia, respectively, were observed in 15% and 4% of patients with CKD G3a, and in 50% and 17% of patients with CKD G5. In fully adjusted models, transient (hazard ratio 1.36, 95% confidence interval 1.29–1.46) or chronic (1.16, 1.04–1.32) hyperkalaemia patterns, but not current hyperkalaemia, were associated with major adverse cardiovascular events (MACE), compared with normokalaemia. Transient hyperkalaemia (1.43, 1.35–1.52) and current potassium values, but not chronic hyperkalaemia, were associated with the risk of death.\n \n \n \n Between 4% and 17% of patients with CKD G3–5 develop chronic hyperkalaemia. In general, hyperkalaemia predicted MACE and death; however, the lack of effect of current potassium on MACE when adjusted for the previous pattern, and the stronger effects on death than on MACE, lead us to question whether hyperkalaemia is causal in these relationships.\n