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Abstract: PO1788

Suppressed Renin Activity in CKD: Are We Missing Primary Hyperaldosteronism?

Session Information

Category: Hypertension and CVD

  • 1402 Hypertension and CVD: Clinical, Outcomes, and Trials

Authors

  • Sohail, Mohammad Ahsan, Cleveland Clinic, Cleveland, Ohio, United States
  • Nakhoul, Georges, Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
  • Arrigain, Susana, Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
  • Schold, Jesse D., Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
  • Taliercio, Jonathan J., Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
  • Thomas, George, Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
  • Mehdi, Ali, Cleveland Clinic Glickman Urological and Kidney Institute, Cleveland, Ohio, United States
Background

Primary hyperaldosteronism (PA) is more prevalent than once thought and associated with adverse kidney and cardiovascular outcomes. A prior analysis of the CKD registry at the Cleveland Clinic in patients without a diagnosis of PA showed that the lowest quartile of plasma renin activity (PRA) had more severe hypertension and faster eGFR decline. We hypothesized that some of these patients with suppressed PRA may have undiagnosed PA.

Methods

We reviewed patients in the Cleveland Clinic CKD registry with documented PRA and absolute plasma aldosterone concentration (PAC). Patients in the lowest PRA quartile were identified and stratified by PAC/PRA ratio. A cutoff ratio of >20 was considered suggestive of PA regardless of the PAC. Characteristics and outcomes of these two subgroups were compared using t-tests, chi-square tests, Kaplan-Meier analyses and Cox models.

Results

276 patients were identified for this analysis. Median PRA and PAC were 0.5 ug/L/hr and 8.7 ng/dl respectively. 141 (51%) patients had a PAC/PRA ratio of ≥20 with a median PAC of 14.6 ng/dl in this subgroup. Patients with PAC/PRA of ≥20 vs. <20 had significantly lower eGFR (mean: 50.7 vs. 55.4 mL/min/1.73 m2; p=0.009), more resistant hypertension (63.1% vs. 48.9%; p=0.044), lower serum potassium values (mean: 3.9 vs. 4.2 mmol/L; p<0.001), and higher serum bicarbonate levels (mean: 26.4 vs. 25.3 mmol/L; p=0.001). With median follow up of 4.2 years, there was no difference in mortality between the two subgroups on adjusted cox model analysis (HR for >20 vs.<20: 0.83, 95%CI: 0.47,1.47). No difference in ESKD-free survival at 5 years was noted but the event rate was low (92.6 vs. 91.9 for >20 vs.<20; p=0.77).

Conclusion

Our analysis indicates that some CKD patients with suppressed PRA may have underlying PA. More than half of our suppressed PRA cohort had elevated PAC/PRA ratio ≥20 suggestive of PA. The biochemical profile and severe hypertension further supports this diagnosis. We hypothesize that the diagnosis of PA was possibly ruled out because of the “not very high” PAC. Given the limitations of the spot PAC/PRA screen owing to diurnal PAC variations, a suppressed PRA should merit an in-depth evaluation for undiagnosed PA regardless of the PAC. Making this diagnosis is critical since it has significant therapeutic implications.