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Renal function–related pathways encompass the complex network of physiological and molecular processes responsible for maintaining kidney homeostasis, including glomerular filtration, tubular reabsorption, and endocrine regulation [1.1.2, 1.2.4]. These pathways involve critical signaling systems such as the renin-angiotensin-aldosterone system (RAAS), the sodium-glucose cotransporter (SGLT) axis, and oxidative stress response mechanisms like the Nrf2/HO-1 pathway [1.1.2, 1.3.2]. Dysregulation of these pathways is a hallmark of chronic kidney disease (CKD), diabetic nephropathy, and hypertension, leading to progressive renal fibrosis and loss of function [1.3.2]. While the term does not refer to a single molecular target, it represents a therapeutic focus where drugs like ACE inhibitors, ARBs, and SGLT2 inhibitors are used to modulate specific components to preserve renal health [1.3.2]. Clinical assessment of these pathways relies on biomarkers such as estimated glomerular filtration rate (eGFR) and albuminuria to monitor disease progression and treatment efficacy [1.2.1, 1.2.3]. Research indicates that these pathways are also involved in systemic conditions, such as mediating the link between insulin resistance and cardiovascular outcomes [1.2.3]. In oncology, alterations in these pathways have been identified as potential mechanisms for symptoms like cancer-related fatigue [1.3.1]. Therapeutic strategies often aim to restore the balance of these pathways to prevent progression to end-stage renal disease [1.1.1].
Drugs targeting these pathways typically act by inhibiting the renin-angiotensin-aldosterone system (RAAS), blocking sodium-glucose cotransporters (SGLT2), or modulating mineralocorticoid receptors to reduce intraglomerular pressure, inflammation, and fibrosis.
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