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Related Concept Videos

Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

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

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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: Angiotensin II Receptor Blockers01:30

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In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
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Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

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Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
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Renal Drug Clearance: Overview01:06

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Renal clearance is a crucial parameter in pharmacokinetics that quantifies the rate at which the kidneys excrete a drug. It represents a constant fraction of the central volume of distribution containing the drug that the kidney eliminates per unit of time.
Renal clearance can be calculated using different methods. One approach is to divide the urinary drug excretion rate by the plasma drug concentration. This method directly measures renal clearance, indicating the kidneys' efficiency in...
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Aliskiren and the dual complement inhibition concept.

Maria Vanessa Perez-Gomez1,2,3, Alberto Ortiz1,2,3

  • 1IIS-Fundacion Jimenez Diaz, School of Medicine, Universidad Autonoma de Madrid, Madrid, Spain.

Clinical Kidney Journal
|February 22, 2020
PubMed
Summary

High-dose aliskiren shows promise as an adjunct therapy for haemolytic uraemic syndrome (HUS). This direct renin inhibitor may also benefit other complement-mediated kidney diseases, including C3 glomerulopathy.

Keywords:
aliskirencomplementdense deposit diseasehaemolytic uraemic syndromeparoxysmal nocturnal haemoglobinuriarenin

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Area of Science:

  • Nephrology
  • Complement System Biology
  • Pharmacology

Background:

  • A recent report details high-dose aliskiren use alongside eculizumab for a patient with haemolytic uraemic syndrome (HUS).
  • Renin's complement factor 3 (C3) activating properties have been identified.
  • Aliskiren has been successfully used in C3 glomerulopathy and dense deposit disease cases.

Discussion:

  • This study explores the implications of renin's role in complement activation for kidney diseases.
  • It examines the potential of aliskiren in treating HUS and C3 glomerulopathy.
  • The discussion extends to immunoglobulin A nephropathy and the concept of dual complement inhibition.

Key Insights:

  • Direct renin inhibition with aliskiren is a potential therapeutic strategy for complement-mediated nephropathies.
  • Renin's direct activation of the complement system offers new therapeutic targets.
  • Adjunctive therapy with aliskiren may improve outcomes in HUS and C3 glomerulopathy.

Outlook:

  • Further research is warranted to elucidate the role of renin in complement-mediated kidney diseases.
  • Clinical trials investigating dual complement inhibition strategies could offer new treatment paradigms.
  • Exploring aliskiren's efficacy in a broader range of nephropathies is a future direction.