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Abstract: PO0563

Tolerance for Potassium Supplementation in Patients with CKD

Session Information

Category: CKD (Non-Dialysis)

  • 2102 CKD (Non-Dialysis): Clinical, Outcomes, and Trials

Authors

  • Gritter, Martin, Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
  • Yeung, Stanley M.H., Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
  • Wouda, Rosa D., Amsterdam Universitair Medische Centra, Amsterdam, Noord-Holland, Netherlands
  • Vogt, Liffert, Amsterdam Universitair Medische Centra, Amsterdam, Noord-Holland, Netherlands
  • De Borst, Martin H., Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
  • Rotmans, Joris I., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
  • Hoorn, Ewout J., Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
Background

Recent studies have shown an association between higher potassium (K+) intake and better kidney outcomes in patients with chronic kidney disease (CKD). However, K+ supplementation in CKD may be limited by the risk of hyperkalemia (>5.5 mEq/L). In this study in patients with CKD our aims were to (1) analyze the effect of K+ supplementation on whole-blood K+ (WBK+), (2) identify factors associated with a rise in WBK+, and (3) identify risk factors for hyperkalemia.

Methods

To do so, we analyzed the results of the 2-week open-label run-in phase of a randomized clinical trial studying the renoprotective effect of long-term K+ supplementation in patients with progressive CKD and hypertension.

Results

In 151 patients (67±11 years, 74% males, eGFR 32±9 ml/min/1.73 m2, 83% on renin-angiotensin inhibitors), K+ supplementation (40 mEq/day) increased urinary K+ excretion from 73±24 to 106±28 mEq/day, WBK+ from 4.3±0.5 to 4.7±0.5 mEq/L, and plasma aldosterone from 294 (210-447) to 366 (271-504) pg/mL (P<0.001 for all). The majority of patients (n=138, 91%) remained normokalemic. K+ supplementation had no significant effect on urinary sodium excretion (158±62 to 155±68 mEq/day), systolic blood pressure (132±15 to 132±15 mmHg), or eGFR (32±9 to 32±8 mL/min/1.73 m2). Multivariable linear regression identified that age (β 0.008, 95%CI 0.001 to 0.02), female sex (β 0.2, 95%CI 0.001 to 0.3), renin-angiotensin inhibitor use (β 0.2, 95%CI 0.05 to 0.4), diuretic use (β -0.1, 95%CI -0.3 to 0.0), baseline WBK+ (β -0.3, 95%CI -0.5 to -0.2), and baseline bicarbonate (β -0.03, 95%CI -0.06 to -0.01) are independently associated with a change in WBK+ after K+ supplementation. The 13 patients who developed hyperkalemia (WBK+ 5.8±0.2 mEq/L) were older (74±7 vs. 66±11 years), more often had diabetes (69 vs. 36%), had lower eGFR (26±8 vs. 33±8 ml/min/1.73 m2), lower baseline bicarbonate (22.5±3.8 vs. 24.8±3.4 mEq/L), and higher baseline WBK+ (4.8±0.4 vs. 4.2±0.4 mEq/L, P<0.05 for all).

Conclusion

In conclusion, the majority of patients with advanced CKD remains normokalemic upon K+ supplementation, despite the use of renin-angiotensin inhibitors. This short-term study illustrates the feasibility of investigating the renoprotective potential of K+ supplementation in patients with CKD and provides the characteristics of patients in whom this is safe.

Funding

  • Private Foundation Support