患有IgA脏病的Sparsentan:来自随机,双盲,主控临床试验的预规定的中间分析
Hiddo J L Heerspink1, Jai Radhakrishnan2, Charles E Alpers3
1Department of Clinical Pharmacy and Pharmacology, University of Groningen, Groningen, Netherlands; The George Institute for Global Health, University of New South Wales, Sydney, NSW, Australia.
Lancet (London, England)
|April 4, 2023
概括
与伊尔贝萨坦相比,斯帕森坦显著减少了IgA脏病患者的蛋白尿症. 在中间分析中,这种新型的双内末素和血管素受体抗剂的安全性与伊尔贝萨坦相似.
科学领域:
- 肝脏病学
- 药理学
- 临床试验
背景情况:
- 抗体A病是一种慢性病.
- 斯帕森坦是一种新型的双内甲蛋白和血管素受体抗剂.
- 目前针对IgA瘤的治疗方法存在局限性.
研究的目的:
- 评估斯帕森坦在患有IgA脏病的成年人中的疗效和安全性.
- 为了比较sparsentan和irbesartan之间的蛋白尿减少.
- 评估治疗出现的不良事件.
主要方法:
- 一个国际的,随机的,双盲的,主动控制的第3期试验 (PROTECT研究).
- 404名患有IgA脏病和蛋白尿症的参与者接受了斯帕森坦 (400毫克/ 天) 或伊尔贝萨坦 (300毫克/ 天).
- 主要终点是36周尿蛋白与肌素比率的变化.
主要成果:
- 在36周后,与伊尔贝萨坦 (-15. 1%) 相比,Sparsentan在蛋白尿症中显示出较大的统计显著减少.
- 这意味着蛋白尿的相对降低为41%有利于sparsentan.
- 治疗出现的不良事件在各组之间是相似的,没有报告严重的安全问题.
结论:
- 在IgA脏病患者中,Sparsentan可显著降低蛋白尿.
- 斯帕森坦的安全性与伊尔贝萨坦相似.
- 进一步的研究将确定sparsentan的长期脏保护潜力.
相关概念视频
Antihypertensive Drugs: Direct Renin Inhibitors
721
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,...
721
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
475
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...
475
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
232
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
232
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists
207
Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme...
207
Dipeptidyl Peptidase 4 Inhibitors
220
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
220
Open Angle Glaucoma: Treatment
505
In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Drugs such as carbonic anhydrase inhibitors, α2- and...
505


