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Kidney Week

Abstract: TH-OR056

Diminished Efficacy of the Angiotensin Receptor Blocker Losartan During High Potassium Intake in CKD Patients

Session Information

Category: CKD (Non-Dialysis)

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

Authors

  • Wouda, Rosa Diana, Academic Medical Center, Amsterdam, Amsterdam, Netherlands
  • Waanders, Femke, Isala Klinieken, Zwolle, Netherlands
  • de Zeeuw, Dick, University Medical Center Grongingen, Groningen, Netherlands
  • Navis, Gerjan, University Medical Center Grongingen, Groningen, Netherlands
  • Vogt, Liffert, Academic Medical Center, Amsterdam, Amsterdam, Netherlands
Background

High potassium intake increases natriuresis and lowers blood pressure (BP). Whether these beneficial effects are also present in chronic kidney disease (CKD) patients and whether potassium intake affects BP and proteinuria-lowering efficacy of angiotensin receptor blockade (ARB) is unknown. We set out to address the effect of potassium intake on BP and proteinuria response to losartan in non-diabetic proteinuric CKD patients.

Methods

We performed a post-hoc analysis of a placebo-controlled interventional cross-over study in which 33 non-diabetic proteinuric patients (mean baseline proteinuria 3.8 g/d) were treated for 6 weeks with placebo, losartan 100mg, and losartan/hydrochlorothiazide (HCT) 100mg/25mg, respectively. Patients underwent the 3 interventions during both a habitual (~200 mmol/d) and low-sodium diet (<100 mmol/d), in randomized order. To analyze the effects potassium intake, we categorized patients based on median split of 24-hour urinary potassium excretion, reflecting potassium intake.

Results

Mean potassium intake was stable during all 6 treatment periods. Patients with high potassium intake (≥92 mmol/d) had similar BP reductions across all treatments as compared to low potassium intake (<92 mmol/d), whereas a lower proteinuria reduction (p=0.014) was observed for all treatments. Proteinuria reduction to losartan monotherapy and to losartan/HCT, respectively, was significantly lower during high potassium intake (20% vs 41%, p=0.011; and 48% vs 64%, p=0.036). These differences in antiproteinuric response abolished when adding a low sodium diet. In multiple regression analysis, potassium intake was a significant independent predictor of the antiproteinuric response to losartan monotherapy (-23%, 95%CI -37, -8%), but not to losartan combined with HCT.

Conclusion

In proteinuric CKD patients, the proteinuria, but not BP-lowering response to losartan was hampered during high potassium intake. Differences disappeared after low sodium diet, suggesting that intervention in sodium status outweighs the modulating effects of potassium intake on ARB efficacy.

Funding

  • Commercial Support