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Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Antihypertensive Drugs: Direct Renin Inhibitors01:25

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The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
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Renal Failure: Dose Adjustments01:11

Renal Failure: Dose Adjustments

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In patients with renal impairment, drugs undergo significant changes in their pharmacokinetics, which require dosage adjustments to ensure safe and effective therapy.
Reduced renal clearance and elimination rate are common outcomes of renal impairment. These alterations lead to a prolonged elimination half-life and an altered apparent volume of distribution for drugs. As a result, dosage adjustments are typically necessary to maintain optimal drug levels in the body.
However, dosage adjustments...
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Factors Affecting Renal Clearance: Drug's Physicochemical Properties and Plasma Levels01:31

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Renal clearance of a drug is influenced by various factors, including its physicochemical properties and plasma levels. These factors play a significant role in determining how efficiently the kidneys eliminate a drug.
One important factor is the drug's molecular size. The kidneys readily excrete smaller molecules below 300 Daltons (Da). On the other hand, molecules weighing between 300 and 500 Da are excreted through both urine and bile. Larger molecules above 500 Da tend to be excreted...
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Renal Drug Excretion: Tubular Secretion01:28

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Active tubular secretion is a robust, energy-demanding process that utilizes carrier systems to transport drugs into renal tubules. The active renal secretion systems include the organic anion transporter (OAT) for weak acids and the organic cation transporter (OCT) for weak bases. Structurally similar drugs can compete for the same transporter, potentially leading to drug accumulation and toxicity. However, this principle can be exploited therapeutically. One example is probenecid (Probalan),...
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Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors01:30

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

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Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
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Related Experiment Video

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Finerenone: Will It Be a Game-changer?

Dinesh Khullar1, Anish Kumar Gupta1, Kulwant Singh1

  • 1Department of Nephrology and Renal Transplant Medicine, Max Super Speciality Hospital Saket, New Delhi, India.

Cardiac Failure Review
|January 28, 2025
PubMed
Summary
This summary is machine-generated.

Finerenone, a non-steroidal mineralocorticoid receptor antagonist (MRA), effectively reduces heart failure hospitalizations and cardiovascular death in patients with type 2 diabetes and chronic kidney disease. It offers a safer alternative to steroidal MRAs, with fewer risks of hyperkalemia and acute kidney injury.

Keywords:
Heart failurechronic kidney diseaseclinical trialsfinerenonemineralocorticoid receptor antagonists

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Area of Science:

  • Cardiology
  • Nephrology
  • Endocrinology

Background:

  • Heart failure (HF) is a leading cause of cardiovascular death, with patients having chronic kidney disease (CKD) and type 2 diabetes (T2D) at higher risk.
  • Current guidelines inadequately address comorbidities in HF management.
  • Steroidal mineralocorticoid receptor antagonists (MRAs) are effective but carry risks like hyperkalemia and acute kidney injury (AKI).

Purpose of the Study:

  • To evaluate the efficacy and safety of finerenone, a non-steroidal MRA, in patients with HF and comorbidities.
  • To assess finerenone's impact on HF hospitalizations and cardiovascular outcomes.
  • To compare finerenone's safety profile with existing steroidal MRAs.

Main Methods:

  • Analysis of Phase III clinical trials including ARTS, ARTS-HF, FIDELIO-DKD, FIGARO-DKD, and FINEARTS-HF.
  • Inclusion of patients with HF with reduced, mildly reduced, or preserved ejection fraction, often with CKD and T2D.
  • Assessment of endpoints such as HF hospitalizations, cardiovascular death, hyperkalemia, and AKI.

Main Results:

  • Finerenone demonstrated significant reductions in HF hospitalizations (22% in FIDELIO-DKD/FIGARO-DKD) and cardiovascular death.
  • Fewer incidents of hyperkalemia and AKI were observed with finerenone compared to spironolactone.
  • Positive effects on cardiac and kidney tissues, including anti-inflammatory and anti-fibrotic properties, were noted in preclinical and clinical studies.

Conclusions:

  • Finerenone is a safe and effective non-steroidal MRA for managing HF, particularly in patients with CKD and T2D.
  • It offers a favorable risk-benefit profile compared to steroidal MRAs, reducing key adverse events.
  • Ongoing trials are exploring finerenone's role in diverse HF phenotypes and cardio-renal-metabolic disease management.