Antidiuretic Function Before and During Treatment With SGLT2 Inhibitors (GliRACo1)

University of Turin

Status

Unknown

Conditions

Arterial Hypertension

Diabetes Mellitus, Type 2

Body Weight Changes

Treatments

Drug: SGLT2 inhibitor

Study type

Interventional

Funder types

Other

Identifiers

NCT03917758

GliRACo 1

Details and patient eligibility

About

Subjects treated with Canagliflozin, Dapagliflozin and Empagliflozin obtained improvement on blood pressure values, body weight and cardiovascular mortality but pathophysiological explanations of these effects are not yet known.

Full description

The pathophysiological explanations of the cardiovascular improvement of patients treated with SGLT2i are not yet known: osmotic diuresis and natriuresis, direct effects of weight reduction, increased in nitric oxide release, oxidative stress reduction, local renin-angiotensin-aldosterone system (RAAS) inhibition are the supposed mechanism. In the Literature the diuretic effect of SGLT2i therapy seems to be even stronger than thiazide or thiazide-like drugs. However, it is not defined the role of SGLT2i on antidiuretic function (RAAS, brain natriuretic peptide-BNP and antidiuretic hormone-ADH). Defining this relation could be important for:

knowing effect of SGLT2i on RAAS (drugs interferences are important particularly during case detection of primary aldosteronism);
discovering antidiuretic response to SGLT2i treatment and interactions between RAAS, BNP and ADH on the volume improvement induced by this new antidiabetic drugs.

In addition the aim of the study is to define effect of treatment on blood pressure and body composition.

Enrollment

30 estimated patients

Sex

All

Ages

18 to 80 years old

Volunteers

No Healthy Volunteers

Inclusion criteria

diabetic patients;
clinical indication to SGLT2i therapy.

Exclusion criteria

signs and symptoms of poor glycemic control (polydipsia, polyuria and weight loss);
HbA1c >10% or 86 mmol/mol;
Body Mass Index (BMI) > 40 Kg/m2;
personal history of primary and secondary aldosteronism;
personal history of heart failure;
personal history of acute kidney injury;
personal history of chronic kidney disease;
personal history of liver cirrhosis;
personal history of protein-wasting syndrome;
personal history of renin secreting tumor;
personal history of diabetes insipidus;
personal history of syndrome of inappropriate antidiuresis (SIAD);
personal history of hypocortisolism and hypercortisolism;
therapy with Angiotensin Converting Enzyme inhibitors;
therapy with Angiotensin Receptor Blockers;
therapy with renin inhibitors;
therapy with beta-blockers;
therapy with alfa2-receptors agonists;
therapy with Calcium Channel Blockers;
therapy with diuretics;
therapy with mineralocorticoid receptor antagonists;
therapy with non steroidal and steroidal anti-inflammatory drugs.