Relationship between serum aldosterone levels and urinary sodium excretion in patients with diabetes in the presence and absence of renin angiotensin aldosterone blockade — ASN Events
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Relationship between serum aldosterone levels and urinary sodium excretion in patients with diabetes in the presence and absence of renin angiotensin aldosterone blockade (#284)

Renata Libianto 1 2 , John Moran 3 , Richard MacIsaac 4 5 , Felicity Pyrlis 6 , Sara Baqar 6 , George Jerums 4 6 , Elif Ekinci 6 7 8
  1. The University of Melbourne, Parkville, VIC, Australia
  2. UROP student, Bio21, Melbourne, Australia
  3. Intensive Care Consultant, Queen Elizabeth Hospital, Adelaide, Australia
  4. Professorial Fellow, The University of Melbourne, Melbourne, Australia
  5. Director of Endocrinology, St Vincent's Health, Melbourne, Australia
  6. Endocrinology Consultant, Austin Health, Melbourne, Australia
  7. Research Fellow, The University of Melbourne, Melbourne, Australia
  8. Research Fellow, Menzies School of Public Health, Melbourne, Australia

Background: Current guidelines recommend that people with hypertension and diabetes should reduce their salt intake[1]. However, in a previous study in patients with type 2 diabetes, we have shown that low 24-hour urinary sodium excretion (mmol/24h, 24hUNa), is associated with increased mortality[2]. In the general population, low salt intake is associated with increased plasma renin activity (PRA) and serum aldosterone concentration[3]. The current study investigated the relationship between 24hUNa, PRA, aldosterone and brain natriuretic peptide (BNP) in patients with diabetes.

Methods: In a cross-sectional study, clinical characteristics, 24hUNa, PRA, aldosterone, and BNP were recorded in 329 consecutive patients attending diabetes clinics at Austin Health. A subgroup of 46 patients was not taking medications which interfere with the renin-angiotensin-aldosterone system (RAAS). The relationship between 24hUNa with aldosterone, PRA and BNP was examined by Pearson correlation. A linear regression model which included PRA and 24hUNa was generated to predict aldosterone levels.

Results: Mean age was 64 years, 60% were males, mean HbA1c was 7.7±1.3% (mean±SD), and 77% had type 2 diabetes. In the total study group, there was a negative correlation between serum aldosterone and 24hUNa (r= -0.14, p=0.04). This relationship was most pronounced in the subgroup of patients not taking agents which interfere with RAAS (r= -0.36, p=0.02). Using a linear regression model, PRA and 24hUNa significantly predicted aldosterone levels in people not taking RAAS interfering medications (F=6.8, p=0.002)(Figures 1A,1B). However, this relationship was not seen in subjects receiving RAAS modulating medications. There was no significant correlation between 24hUNa and PRA or BNP. There was also no significant correlation between aldosterone and 24h urinary potassium excretion or serum potassium.

Conclusions: The relationship between 24hUNa and aldosterone was masked in people with diabetes taking RAAS modifying medications. This study highlights the difficulties in further delineating the mechanisms linking low urinary salt excretion and increased mortality in people with diabetes.

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  1. P Elliott, et al. BMJ, 1996. 312: p. 1249-1253.
  2. EI Ekinci, et al. Diabetes Care, March 2011. 34: p. 703-709.
  3. NA Graudal, et al. American Journal of Hypertension, January 2012. 25(1): p. 1-15.