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Preparing your E-Poster
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E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
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Abstract titles should be brief and reflect the content of the abstract.
Hyperkalemia is a common metabolic complication of chronic kidney disease (CKD) and may limit the use of renin–angiotensin system inhibitors (RASi), a cornerstone therapy for slowing CKD progression. Metabolic acidosis, another frequent complication of CKD, contributes to extracellular potassium shift and impaired renal potassium excretion, thereby predisposing to hyperkalemia. However, the degree that metabolic acidosis affects the risk of hyperkalemia across different stages of CKD remains unclear. Understanding this relationship is essential for improving patient management and monitoring in clinical practice.
This cross-sectional analysis of baseline data was conducted using the Thai CKD Project, an ongoing multicenter prospective cohort enrolling adults with CKD stages G3–G5 (eGFR ≤60 mL/min/1.73 m²) from 41 hospitals across Thailand. Hyperkalemia was defined as serum potassium ≥5.0 mmol/L and ≥5.5 mmol/L (sensitivity threshold). The prevalence of hyperkalemia was examined across CKD stages and stratified by the presence of metabolic acidosis (serum bicarbonate <22 mmol/L). Logistic regression analyses were performed to identify factors associated with hyperkalemia.
Among 3,344 participants (mean age 69 ± 12 years; 45% female), the overall prevalence of hyperkalemia was 9.7% (K ≥ 5.0 mmol/L) and 1.7% (K ≥ 5.5 mmol/L). The prevalence of hyperkalemia increased progressively with CKD severity and was higher among patients with metabolic acidosis (Figure 1). In univariate analysis, advanced CKD stages (G3b–G5), metabolic acidosis, and mineralocorticoid receptor antagonists (MRA) use were significantly associated with hyperkalemia (Table 2).
In multivariable analyses, independent predictors of K ≥ 5.0 mmol/L included CKD stage G3b (OR 1.57, 95% CI 1.03–2.44, p = 0.041), CKD stage G4 (OR 3.17, 95% CI 2.13–4.86, p < 0.001), CKD stage G5 (OR 3.31, 95% CI 1.99–5.58, p < 0.001), metabolic acidosis (OR 1.47, 95% CI 1.12–1.91, p = 0.005), RASi use (OR 1.39, 95% CI 1.08–1.79, p = 0.010), and MRA use (OR 2.25, 95% CI 1.20–3.98, p = 0.007). At the stricter cutoff of K ≥ 5.5 mmol/L, significant predictors were CKD stage G4 (OR 4.19, 95% CI 1.61–14.39, p = 0.008), metabolic acidosis (OR 3.18, 95% CI 1.84–5.54, p < 0.001), and MRA use (OR 3.33, 95% CI 1.09–9.04, p = 0.032).
Hyperkalemia was common among CKD patients and increased with disease severity, especially in the presence of metabolic acidosis. Lower serum bicarbonate, advanced CKD stage, and MRA therapy were consistent risk factors, whereas RAS inhibitor use was mainly associated with mild hyperkalemia, and SGLT2 inhibitor use showed no significant association. These findings emphasize the importance of personalized risk evaluation and early correction of metabolic derangements to optimize outcomes in CKD.
