Primary Aldosteronism Results in a Decline in Estimated Glomerular Filtration Rate Independent of Blood Pressure: A Case-Control Study.

BACKGROUND

Primary aldosteronism (PA) is the predominant cause of secondary hypertension, leading to cardiovascular and renal damage. However, current epidemiology findings on the association between PA and estimated glomerular filtration rate (eGFR) remain inconsistent.

METHODS

A 1:1 gender- and age-matched case-control study was conducted among participants with PA, essential hypertension (EH), and normotension, with 204 participants in each group. Multiple linear regression was used to explore the correlations of PA with eGFR. Subgroup analyses were conducted to examine variations in the PA-eGFR association. Mediation analysis was performed to explore the role of inflammatory markers in this relationship.

RESULTS

Compared to the EH group, the PA group showed no significant differences in systolic blood pressure (SBP), diastolic blood pressure (DBP), or eGFR but exhibited significantly higher levels of plasma aldosterone concentration (PAC) and aldosterone-to-renin ratio (ARR), along with lower plasma renin concentration (PRC) levels. PA was associated with a decline in eGFR after adjusted potential confounders. When stratified the PA patients into three groups according to the levels of PAC, PRC and ARR, patients in the highest PAC groups, the lowest PRC group, and the highest ARR group had much lower eGFR compared to the EH group. The inverse associations mentioned above remained significant even further adjusted for SBP or DBP, respectively. Age (β = -0.422 [95% CI: -1.28, -0.606], p < 0.001), PRA (β = -0.225 [95% CI: -0.035, -0.006], p = 0.005), and uric acid (UA) (β = -0.285 [95% CI: -0.035, -0.006], p < 0.001) were inversely associated with eGFR (p < 0.05) in PA patients. Lymphocyte-to-monocyte ratio attributed a proportion of 7.62% for the total effect.

CONCLUSION

Our study indicates that PA is associated with lower eGFR independent of blood pressure, and the adverse effects might be greater than negative controls or EH patients. Inflammation could be a potential mediator of this detrimental effect. In PA, elevated UA may promote crystal formation and glomerular obstruction, contributing to renal dysfunction.