Primary aldosteronism (PA) is associated with higher renal damage than essential hypertension (HT). In particular, the prevalence of chronic kidney disease increases after treatment for PA, as actual renal damage may be underestimated in untreated PA due to glomerular hyperfiltration. Previous studies have indicated the role of the renin-angiotensin-aldosterone system in renal dysfunction in type 2 diabetes (T2DM) patients, but whether PA causes additional renal function damage in T2DM is unclear. The aim of this study was to investigate this issue. A retrospective review of all T2DM outpatients who visited our high-volume center for PA in the FY 2017 was carried out. We segregated patients that underwent PA treatment (PA group) and those without PA (non-PA group). Treatment for PA was defined as adrenalectomy or the use of aldosterone receptor antagonists (MRAs). Untreated PA was excluded, since renal damage might be underestimated in these patients. We compared the renal function between these two groups. There were 83 patients in the PA group and 1580 patients in the non-PA group. In the PA group, 21 patients underwent adrenalectomy, 60 patients underwent MRA treatment, and 2 patients underwent both. Compared to the non-PA group, patients in the PA group were younger (62 [55-69] vs. 66 [55-75] years, p=0.014), and had a higher BMI (25.9 [23.8-27.8] vs. 24.8 [21.7-28.1] kg/m2, p=0.019) and lower HbA1c (6.8 [6.5-7.1] vs. 7.3 [6.7-8.0]%, p<0.001). In the renal function evaluation, the PA group had significantly lower eGFR (66.3 [52.4-78.2] vs. 70.5 [56.0-85.6] ml/min/1.73 m2, p=0.047) than the non-PA group. Multiple regression analysis revealed that PA was a factor for decreased eGFR, independent from age, sex, BMI, HbA1c, and HT (p=0.007). PA induced a 3.3 (95% CI: 0.90-5.7)-ml/min/1.73 m2 decrease in eGFR, equivalent to 3.8 years of aging. Our results show that PA was a risk factor for renal dysfunction independent from HT in T2DM patients. To prevent the progression of renal failure, PA should not be overlooked.


S. Katsuragawa: None. Y. Tsurutani: Research Support; Self; Astellas Pharma Inc. T. Takiguchi: None. J. Saito: None. T. Nishikawa: None.

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