Abstract

Hypertension (HTN) is the leading cause of premature death worldwide, affecting >1 billion people, and is a major risk factor for the onset and progression of chronic kidney disease (CKD) and cardiovascular disease (CVD) [1, 2]. While mechanisms leading to essential HTN remain elusive, many have hypothesized that abnormal salt and water regulation by the kidney tubules may be contributory [3, 4]. Contemporary clinical tests evaluate and assess kidney glomerular function but not tubule function. Kidney damage and tubulointerstitial injury may lead to neurohormonal activation, inflammation and impaired sodium and potassium handling, which may contribute to the development of HTN through mechanisms independent of estimated glomerular filtration (eGFR) [3]. Recent investigations have identified several urinary biomarkers of kidney tubule injury and dysfunction and multiple prior studies have demonstrated that these biomarkers are associated with the loss of kidney function in ambulatory populations, independent of eGFR or albuminuria [5, 6]. However, few studies have related tubule function biomarkers to the risk of developing HTN [7].

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