Supported Research

General Audience Summary

Background: Hypertension (high blood pressure) management generally involves a ‘one size fits all’ approach. Employing a more personalized approach targeting the specific cause of an individual patient’s hypertension provides the opportunity to improve long-term health. Primary aldosteronism (PA) is a very common, yet often unrecognized, cause of hypertension caused by excess production of a hormone called aldosterone. Excess aldosterone causes the body to retain salt, raises blood pressure, and damages the kidneys. Indeed, PA leads to disproportionately high rates of kidney disease compared with other forms of hypertension. Importantly, the adverse health consequences of PA are preventable with early treatment using medications (called mineralocorticoid receptor antagonists) that directly block the effects of aldosterone. These medications used to treat PA are distinct from the blood pressure medications that are routinely used to treat other forms of hypertension. Recently, a growing body of evidence has demonstrated that milder forms of PA (‘Subclinical PA’) are exceedingly common in the general population yet go undetected in modern-day medical practice. Whether Subclinical PA leads to increased rates of kidney disease remains unknown.

Purpose: To study the impact of Subclinical PA on kidney disease.

Procedure: We will investigate Subclinical PA using CARTaGENE – a study which enrolled over 20,000 Québec residents in 2009-2010 and captured a vast amount of health information on these individuals. A subset of these individuals had blood and urine samples collected and stored both at the beginning of the study and 7 years later. We will use the stored blood and urine samples to measure aldosterone levels among these individuals to identify those with Subclinical PA and compare their rates of kidney disease to those participants without Subclinical PA. We will also employ a state-of-the-art technique called proteomics which will allow us to study the effects of aldosterone at the molecular level to gain an understanding of the precise mechanisms by which Subclinical PA may damage the kidney.

Outcome: We anticipate that individuals with Subclinical PA will develop higher rates of kidney disease compared to individuals without Subclinical PA.

Relevance to Patients: If indeed individuals with Subclinical PA experience higher rates of kidney disease, the logical next step will be to study whether using medications that specifically target Subclinical PA (and are not used routinely in the treatment of hypertension) will prevent kidney disease in this large, but currently unrecognized, population. This study will provide a much-needed step toward a more personalized approach to hypertension management that will serve to prevent future kidney disease.