Cardiorenal benefits of finerenone: protecting kidney and heart

González-Juanatey, José Ramón; Górriz, José Luis; Ortíz, Alberto; Valle, Alfonso Salguero del; Soler, María José; Fácila, Lorenzo

doi:10.1080/07853890.2023.2171110

Cited by 14 publications

(1 citation statement)

References 66 publications

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“…Sodium-glucose co-transporter-2 (SGLT2) inhibitors, glucagon-like peptide 1 (GLP1) receptor agonists, and non-steroidal mineralocorticoid receptor antagonists have recently been shown to have important renoprotective effects in patients with diabetes, which is also paralleled by a significant and important reduction in cardiovascular morbidity and mortality [ 1 , 2 , 3 ].…”

Section: Introductionmentioning

confidence: 99%

The Pillars for Renal Disease Treatment in Patients with Type 2 Diabetes

Kearney

Gnudi

2023

Pharmaceutics

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The diabetes epidemic and the increasing number of patients with diabetic chronic vascular complications poses a significant challenge to health care providers. Diabetic kidney disease is a serious diabetes-mediated chronic vascular complication and represents a significant burden for both patients and society in general. Diabetic kidney disease not only represents the major cause of end stage renal disease but is also paralleled by an increase in cardiovascular morbidity and mortality. Any interventions to delay the development and progression of diabetic kidney disease are important to reduce the associated cardiovascular burden. In this review we will discuss five therapeutic tools for the prevention and treatment of diabetic kidney disease: drugs inhibiting the renin–angiotensin–aldosterone system, statins, the more recently recognized sodium-glucose co-transporter-2 inhibitors, glucagon-like peptide 1 agonists, and a novel non-steroidal selective mineralocorticoid receptor antagonist.

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Section: Introductionmentioning

confidence: 99%

The Pillars for Renal Disease Treatment in Patients with Type 2 Diabetes

Kearney

Gnudi

2023

Pharmaceutics

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Rediscovery of the implication of albuminuria in heart failure: emerging classic index for cardiorenal interaction

Min,

Matsumoto,

Asakura

et al. 2024

ESC Heart Failure

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The development of new drugs and device therapies has led to remarkable advancements in heart failure (HF) treatment in the past couple of decades. However, it becomes increasingly evident that guideline‐directed medical therapy cannot be one‐size‐fits‐all across a wide range of ejection fractions (EFs) and various aetiologies. Therefore, classifications solely relying on EF and natriuretic peptide make optimization of treatment challenging, and there is a growing exploration of new indicators that enable efficient risk stratification of HF patients. Particularly when considering HF as a multi‐organ interaction syndrome, the cardiorenal interaction plays a central role in its pathophysiology, and albuminuria has gained great prominence as its biomarker, independent from glomerular filtration rate. Albuminuria has been shown to exhibit a linear correlation with cardiovascular disease and HF prognosis in multiple epidemiological studies, ranging from normal (<30 mg/g) to high levels (>300 mg/g). However, on the other hand, it is only recently that the details of the pathological mechanisms that give rise to albuminuria have begun to be elucidated, including the efficient compaction/tightening of the glomerular basement membrane by podocytes and mesangial cells. Interestingly, renal disease, diabetes, and HF damage these components associated with albuminuria, and experimental models have demonstrated that recently developed HF drugs reduce albuminuria by ameliorating these pathological phenotypes. In this review, facing the rapid expansion of horizons in HF treatment, we aim to clarify the current understanding of the pathophysiology of albuminuria and explore the comprehensive understanding of albuminuria by examining the clinically established evidence to date, the pathophysiological mechanisms leading to its occurrence, and the outcomes of clinical studies utilizing various drug classes committed to specific pathological mechanisms to put albuminuria as a novel axis to depict the pathophysiology of HF.

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