Abstract: TH-PO495

Effect of Losartan on Uric Acid in Patients with CKD

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 305 CKD: Clinical Trials and Tubulointerstitial Disorders

Authors

  • Patel, Komal, Northwell Health Lenox Hill Hospital, Paramus, New Jersey, United States
  • Rosenstock, Jordan L., None, New York, New York, United States
Background

Increased serum uric acid (UA) is a risk factor for end-stage renal disease and agents that lower it such as allopurinol may decrease renal disease progression. Losartan inhibits URAT1 mediated renal tubule urate reabsorption by the proximal tubule, which results in an increase in urate excretion. This appears to be an effect that is unique to losartan of all the angiotensin receptor blockers. Losartan has previously been shown to increase UA excretion and decrease serum UA levels in patients without kidney disease. However, the effects of losartan on serum and urine UA in patients with kidney disease is unknown. The purpose of this study was to evaluate the change in serum and urine UA levels among individuals with stage 3 chronic kidney disease (CKD3).

Methods

The study enrolled 15 individual outpatients with CKD 3 that were to be started on losartan as part of standard clinical care indications such as proteinuria or hypertension. Baseline serum UA and 24 hour urine for fractional excretion of uric acid (FeUA) were collected prior to starting losartan and after 30 days. Patients were excluded if they had started other medications affecting UA levels within 30 days or during study period.

Results

Mean baseline GFR was 42.07 + 6.05, and 60% were males. We found that serum UA 30 days post treatment was significantly lower than baseline (7.39 + 1.47 to 6.85 + 1.70) (p = 0.009). The median serum UA percent decrease from pre to post was 6% (p=0.008). However, the FE UA 30 days post treatment was not significantly different from baseline(p = 0.89).

Conclusion

This study did show a statistically significant change in serum UA levels in CKD 3 patients after the initiation of losartan. Though statistically sigfnicant, the small change in UA level may not be clinically meaningful. In patients without kidney disease levels may fall by as much as 20% and the difference suggests that renal disease may compromise the ability to respond to the uricosuric effect of losartan. Furthermore, we did not find a significant change in the FeUA. It has been suggested that the uricosuric effect with losartan is short lived as a new steady state is reached quickly, so 30 days may have been to long to recheck FeUA. This study involved a small cohort of patients, and a larger study is warranted to confirm our finding.