Abstract: TH-PO443

Time-Updated Analysis of Potassium Intake, Serum Potassium, and Outcomes after Kidney Transplantation

Session Information

Category: Nutrition, Inflammation, and Metabolism

  • 1401 Nutrition, Inflammation, Metabolism


  • Verschuur, Lara Christine, University Medical Center Groningen, Groningen, Netherlands
  • Gomes Neto, Antonio, University Medical Center Groningen, Groningen, Netherlands
  • Eisenga, Michele F., None, Groningen, Groningen, Netherlands
  • Navis, Gerjan, None, Groningen, Groningen, Netherlands
  • Bakker, Stephan J.L., University Medical Center Groningen, Groningen, Netherlands
  • De Borst, Martin H., University Medical Center Groningen, Groningen, Netherlands

Low potassium (K+) intake has been associated with an increased risk of hypertension, cardiovascular events, and mortality in patients with chronic kidney disease and in the general population. Kidney transplant recipients (KTRs) may nevertheless refrain from increasing K+ intake because of fear for hyperkalemia, which may be often unjustified.


We assessed the relationship between paired measurements of 24-hour urinary K+ excretion, as a proxy for K+ intake, and serum K+ in 1,108 with eGFR >15 mL/min/1.73 m2. We subsequently analyzed associations of K+ intake with death-censored graft failure (DCGF) and all-cause mortality using time-updated Cox regression, adjusted for potential confounders, including age, sex, time-matched estimated GFR (eGFR, CKD-EPI), systolic blood pressure, and use of diuretics or RAAS-inhibitors.


KTRs (55% men) were 44±13 yrs old at transplantation. Data from 8,904 paired urinary and serum K+ measurements were available. When considering intra-individual median K+ excretion, K+ excretion was 2.6 [2.0-3.1] g/d (median [IQR]). K+ intake was below the WHO-recommended intake (90-120 mmol/d, 3.5-4.7 g/d) in 87.4% of KTR. K+ intake decreased with advancing stages of CKD (P-trend<0.001). Overall, K+ intake explained 1.3% of the variation in serum K+; in stage 4 CKD it explained 1.0%. In multivariable linear regression, eGFR, diuretics use, sex, BMI, and ACE-inhibitor use (all P<0.05) were the main independent determinants of serum K+ (R2=0.12), whereas K+ excretion was no significant independent determinant (P=0.16). During median follow-up for 14.3 [9.2-20.3] years, 291 patients developed DCGF and 676 patients died. In time-updated multivariable Cox regression analysis, K+ intake was inversely associated with the risk of DCGF (fully adjusted HR 0.60 [95% CI 0.49-0.74] per 1 g/d increase in K+ intake, P<0.0001) and mortality (0.76 [0.63-0.91], P<0.0001). Adjustment for serum K+ did not materially change the results.


K+ intake is low in the vast majority of KTR. The minimal impact of K+ intake on serum K+ and the association of low K+ intake with an increased risk of adverse outcomes suggest that dietary K+ intake should be stimulated in most KTRs.