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http://dx.doi.org/10.1373/clinchem.2005.061184 | DOI Listing |
Cureus
December 2024
Department of Medicine, Jawaharlal Nehru Medical College and Hospital, Aligarh Muslim University, Aligarh, IND.
Primary aldosteronism (PA) is a common cause of secondary hypertension, with familial hyperaldosteronism (FH) contributing to a lesser number of cases. FH type IV, a rare subtype, has hardly been reported as a subtype of PA cases. We present a case of a 27-year-old female who presented to the emergency department with circumoral tingling and numbness.
View Article and Find Full Text PDFJCEM Case Rep
January 2025
Division of Diabetology and Metabolism, Department of Internal Medicine, Tokyo Women's Medical University School of Medicine, Shinjuku-ku, Tokyo 162-8666, Japan.
A 37-year-old man presented with symptoms of polyuria and weight loss over the past year. Initial laboratory examination showed elevated blood glucose level (468 mg/dL [25.9 mmol/L]; normal reference range [RR], 75-109 mg/dL [4.
View Article and Find Full Text PDFJ Saudi Heart Assoc
December 2024
College of Medicine, University of Sharjah, Sharjah, United Arab Emirates.
Objectives: Zilebesiran is an investigational RNA interference therapeutic designed to lower blood pressure by targeting the hepatic production of angiotensinogen, the most upstream precursor of the renin-angiotensin-aldosterone system. This approach aims to offer long-lasting blood pressure control with potentially fewer doses compared to traditional antihypertensive medications. The objective of this systematic review and meta-analysis was to assess the antihypertensive efficacy of zilebesiran in patients with hypertension.
View Article and Find Full Text PDFNat Rev Nephrol
January 2025
AHEPA Hospital, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece.
Diuretic drugs act on electrolyte transporters in the kidney to induce diuresis and are often used in chronic kidney disease (CKD), given that nephron loss creates a deficit in the ability to excrete dietary sodium, which promotes an increase in plasma volume. This rise in plasma volume is exacerbated by CKD-induced systemic and intra-renal activation of the renin-angiotensin-aldosterone-system, which further limits urinary sodium excretion. In the absence of a compensatory decrease in systemic vascular resistance, increases in plasma volume induced by sodium retention can manifest as a rise in systemic arterial blood pressure.
View Article and Find Full Text PDFCureus
December 2024
Department of Endocrinology, Metabolism, Rheumatology and Nephrology, Faculty of Medicine, Oita University, Yufu, JPN.
Background: The uremic toxin indoxyl sulfate (IS) is an important factor in chronic kidney disease (CKD) progression. Inhibitors of the renin-angiotensin system and add-on therapy with mineralocorticoid receptor (MR) antagonists can help reduce proteinuria and suppress CKD progression. However, the association between IS and MR activation remains unknown.
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