Abstract and Introduction
Objective: Primary aldosteronism (PA) is a major cause of secondary hypertension and is associated with chronic renal injury. The glomerular filtration rate (GFR) in PA rapidly decreases after the removal of glomerular hyperfiltration due to aldosterone excess by adrenalectomy (ADX) or mineralocorticoid receptor antagonist (MRA) treatment and is stable in the long term. However, the effects of these treatments on the long-term renal function of PA patients with chronic kidney disease (CKD) is not well understood.
Design and Patients: In this single-center, retrospective study, acute and chronic changes in the estimated GFR (eGFR) were examined in 107 patients with PA, including 49 patients with post-treatment CKD defined as eGFR < 60 ml/min/1.73 m2.
Results: The reduction in eGFR observed 1 month after ADX in the CKD group (N = 31) was −20.1 ± 8.2 ml/min/1.73 m2. Multivariate analysis showed that pre-treatment eGFR and plasma aldosterone concentration were independent predictive factors of the acute reduction in eGFR after ADX. The reduction of eGFR observed 1 month after MRA administration in the post-treatment CKD group (N = 18) was −9.2 ± 5.9 ml/min/1.73 m2. Multivariate analysis showed that the duration of hypertension and pre-treatment eGFR were independent predictive factors of the acute reduction in eGFR after ADX administration. In 20 patients with CKD (N = 12 ADX and N = 8 MRA) followed for more than 5 years post-treatment, there was no further significant decline in eGFR over a follow-up period of 7 (6, 8) years nor any difference between the two treatment modalities.
Conclusions: Our study suggests that treatment of PA in stage 3 CKD is safe and useful in preventing renal injury.
Primary aldosteronism (PA) is a major cause of secondary hypertension, accounting for approximately 10% of patients with hypertension.[1,2] Previous epidemiologic studies have revealed that patients with PA have more severe cardiovascular and renal complications than age-, sex-, and blood pressure-matched patients with essential hypertension.[3,4] Two therapeutic options are recommended for the treatment of PA: adrenalectomy (ADX) for patients with unilateral aldosterone-producing adenoma or medical treatment based on mineralocorticoid receptor antagonists (MRA) for patients with bilateral PA.
A series of clinical studies have shown that renal hemodynamic alteration due to hyperaldosteronism results in glomerular hyperfiltration,[5,6] which is a cause of chronic renal injury. The glomerular filtration rate (GFR) in PA rapidly decreases after the removal of aldosterone excess by ADX[5,8–10] or the blockade of aldosterone action by MRA. To prevent renal injury in the long term, complete removal of glomerular hyperfiltration by ADX or a sufficient dose of MRA is recommended for patients with PA. A previous clinical study showed that long-term chronic changes after ADX or MRA administration in patients with PA was not greater than that of essential hypertension.
Focusing on PA with chronic kidney disease (CKD), long-term changes in renal function after treatment of PA have not been fully investigated. Recently, a multicenter database in Japan showed that 19.6% of patients with PA already suffered from overt CKD that might be due to several causes: age, diabetes mellitus, and/or long-term duration of hyperaldosteronism. Previous studies have shown that masked CKD was uncovered and exacerbated by PA treatment in some patients with PA,[14,15] and a low preoperative estimated GFR (eGFR) was suggested to be a risk factor for CKD after adrenalectomy. One case of PA with CKD required haemodialyses after MRA treatment. This led us to carefully consider ADX or MRA treatment for PA with low eGFR. Therefore, the effect of PA treatment on renal function in PA patients with CKD should be examined not only in the short term but also in the long term (i.e., more than 5 years). This study retrospectively examined the short- and long-term changes in GFR after ADX or MRA administration in patients with PA, especially those with CKD, in a single center.
Clin Endocrinol. 2023;98(3):323-331. © 2023 Blackwell Publishing