Key result
Abstract lacks quantitative results linking kidney tubule biomarkers to incident hypertension.
Why the study?
Few studies have related urinary biomarkers of kidney tubule injury and dysfunction to the risk of developing hypertension.
Are urinary biomarkers of kidney tubule injury and dysfunction associated with the risk of incident hypertension in community-living individuals?
Cohort
Are urinary biomarkers of kidney tubule injury and dysfunction associated with the risk of incident hypertension in community-living individuals?
Answers are grounded in this paper and cite their sources.
No quantitative results reported; leaves open whether kidney tubule biomarkers predict incident hypertension in community cohorts.
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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Malhotra et al. (2022) conducted a cohort in Incident hypertension. Biomarkers of kidney tubule injury and dysfunction was evaluated on Incident hypertension.
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