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更新于：2025-12-23
Sevelamer Carbonate
碳酸司维拉姆
更新于：2025-12-23
概要
基本信息
药物类型 聚合物 |
别名 Renvela(TN)、sevelamer、Sevelamer carbonate (USAN) + [7] |
作用方式 调节剂 |
作用机制 Phosphates 调节剂(磷酸盐 调节剂) |
非在研适应症 |
原研机构 |
非在研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2007-10-19), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C7H14ClNO4 |
InChIKeyPADGNZFOVSZIKZ-UHFFFAOYSA-N |
CAS号845273-93-0 |
关联
57
项与 碳酸司维拉姆 相关的临床试验IRCT20250412065294N1
Evaluation effect of paraffin oil based sevelamer carbonate solution on mortality of oral aluminum phosphide toxicity
PACTR202408492665945
The Adjuvant Role of Sevelamer in Treatment of Acute Aluminum Phosphide Poisoned Patients
IRCT20210720051946N7
Evaluation the effect of adding Sevelamer to the standard treatment of aluminum phosphide poisoning patients, referred to Tehran's Luqman Hospital, a preliminary studyon mortalit
100 项与 碳酸司维拉姆 相关的临床结果
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100 项与 碳酸司维拉姆 相关的转化医学
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100 项与 碳酸司维拉姆 相关的专利（医药）
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313
项与 碳酸司维拉姆 相关的文献（医药）2025-12-01CLINICAL PHARMACOKINETICS
Clinical Pharmacokinetic-Pharmacodynamic Relationships of Pharmacological Strategies for Attenuating p-Cresyl Sulfate in Patients with Kidney Disease
Review
作者: Dhungana, Puja ; Dam, Andrew ; Kiang, Tony K L
p-Cresyl sulfate (pCS) is a highly toxic uremic compound that is produced from tyrosine and phenylalanine in the gut and primarily excreted renally. In patients with kidney dysfunction, the accumulation of pCS can lead to the worsening of kidney disease and manifestation of organ toxicities. Various pharmacological strategies have been proposed to reduce pCS in patients with chronic kidney disease (CKD), but systematic pharmacokinetic-pharmacodynamic assessments have not been conducted to our knowledge. The objectives of this scoping review were to comprehensively and critically summarize the available literature using a newly devised, pharmacokinetic-pharmacodynamic assessment method. We searched PubMed, Embase, and Scopus for primary research articles in patients with CKD and devised the following novel approach to systematically evaluate each study: (i) positive reduction or null reduction of pCS; (ii) dose dependency; (iii) time dependency; (iv) effects on free versus total pCS; and (v) relationships to diet regimens (e.g., protein intake), microbiome composition, blood biochemistry, and clinical outcomes (i.e., progression of renal disease measured by initiation of dialysis or renal transplant; cardiovascular outcomes such as incidence of myocardial infarction, heart failure, cardiovascular death; and changes in qualityof- life instruments). Fifty-nine studies were identified with a total of 2593 study participants (pre-dialysis CKD: n = 1060; CKD on dialysis: n = 1499; and post-transplant CKD: n = 34). The studies included AST-120 (n = 3), sevelamer (n = 9), sucroferric Noxyhydroxide (n = 1 [+ 1 overlapping with sevelamer]), prebiotics (n = 15), probiotics (n = 9), synbiotics (n = 13), antibiotics (n = 3), ketoanalogs (n=3), and curcumin (n = 3). Only AST-120 and synbiotics consistently demonstrated significant pCS reductions, and the percentage (%) reductions by AST-120 were 40.9-75.6% for free and 28.8-42.8% for total pCS; whereas the percentage reduction by synbiotics were 6.4-78.1% for total and 16.7% for free pCS, the latter only evident in a subgroup with antibiotic-free regimen. Although sevelamer was also associated with a pCS reduction, the percentage reduction was modest and only based on the total concentration. In contrast, the majority of sucroferric oxyhydroxide, prebiotics, probiotics, ketoanalogs, and curcumin studies did not demonstrate consistent pCS reductions. Furthermore, dose dependency was not established in the majority of studies, and although some temporal relationships were evident, the data were very limited. Only a few of the analyzed studies measured both bound and unbound forms of pCS, and inconsistencies have been reported in a few studies. In Ngeneral, it was also difficult to establish associations with outcomes in most studies because of limitations in experimental design, and in instances where potential pharmacokinetic-pharmacodynamic relationships were observed, they were generally weak and only with surrogate markers of commonly measured biochemistry, oxidative stress, lipid profiles, and inflammatory markers, with only a handful of studies capturing clinical outcomes. In conclusion, we have identified potential pharmacological interventions that may be further developed for the purpose of reducing pCS in patients with CKD.
2025-10-01TRANSPLANTATION PROCEEDINGS
Characteristics of Mineral Bone Disease Profile in Kidney Transplant Recipients – A 9-Year Retrospective Cohort Study at a Tertiary Center
Article
作者: Leon, Guo Jian ; Em, Jun Min ; Lim, Soo Kun ; Jalalonmuhali, Maisarah ; Rozi, Nur Raziana ; Lee, Yee Wan
BACKGROUND:
The progression of chronic kidney disease (CKD) into end-stage kidney disease and the eventual kidney transplantation is linked to substantial changes in bone mineral metabolism, predisposing to bone-related complications, including osteoporosis and fractures. Understanding the bone profile in kidney transplant recipients could improve post-transplant care and long-term outcomes.
METHODS:
This retrospective study at the University Malaya Medical Centre (UMMC) involved all kidney transplant recipients from January 2015 to December 2023. Patients without baseline serum intact parathyroid hormone levels or who had graft failure within 1 year were excluded. All baseline characteristics, medications, and pre- and post-transplant bone mineral profiles were collected from electronic medical records (EMRs) and analyzed using Statistical Package for the Social Sciences version 29.0.2.
RESULTS:
A total of 179 patients were included, with a mean age of 40.6 ± 11.0 years old (57% men). The median dialysis vintage was 18 (interquartile range [IQR] = 36), with 19% undergoing pre-emptive transplants. Before the transplant, 57% of the patients received calcium carbonate, 51.4% were on vitamin D receptor analogues (VDRAs), 26.3% were on sevelamer, 5.6% were on cinacalcet, 2.2% were on lanthanum, and 0.6% were on sucroferric oxyhydroxide. All patients received induction methylprednisolone during the transplant. At 1 year post-transplant, 90% of the patients remained on prednisolone at a median dose of 5.0 mg. Parathyroidectomy was performed on two patients (1.1%) before transplant and another two (1.1%) after transplant. No patient had a fracture post-transplantation during the study period. Biochemically, mean serum intact parathyroid hormone (iPTH), calcium, phosphate, and hemoglobin were significantly improved from pre-transplant to 2 years post-transplant (P < .001), with serum iPTH and calcium showing improvement as early as 3 months and maintained thereafter. Both serum phosphate and hemoglobin levels continuously showed improvement up to 2 years post-transplant (P < .05).
CONCLUSIONS:
Our study showed significant improvements in biochemical bone profile and hemoglobin levels as early as 3 months post-transplant, which had continued to improve or maintain for up to 2 years post-transplant.
2025-09-01JOURNAL OF RENAL NUTRITION
Gastrointestinal Mucosal Cell Injury Caused by Sevelamer Crystals: Case Series and Literature Review
Review
作者: Ali, Umair ; Singh, Manisha ; Karakala, Nithin ; Elkalashy, Ahmed ; Elbahnasawy, Enas ; Rainwater, Randall R
In end-stage kidney disease (ESKD), hyperphosphatemia occurs secondary to decreased renal elimination with continued intestinal absorption of dietary phosphate. Even in chronic kidney disease, glomerular filtration rate lower than 30 mL/min markedly decreases the filtration of inorganic phosphate and increases its serum level. Sevelamer, a noncalcium phosphate binder, is commonly used to control hyperphosphatemia. Available in 2 forms, sevelamer hydrochloride and sevelamer carbonate, it absorbs phosphate in the gastrointestinal tract and is known to have minimal adverse effects. These are limited to nausea, vomiting, flatulence, and metabolic acidosis, with infrequent significant adverse outcomes. We present a series of 2 patients with ESKD on sevelamer, with lower gastrointestinal bleeding and endoscopic findings of colonic mucosal injuries with histopathological findings of sevelamer crystals deposition. Although reported in gastrology literature, nephrology reports show a paucity of discussion around this increasingly common adverse effect and the need for vigilance in ESKD.
100 项与 碳酸司维拉姆 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 慢性肾病-矿物质和骨骼疾病 | 欧盟 | 2015-01-15 | |
| 慢性肾病-矿物质和骨骼疾病 | 冰岛 | 2015-01-15 | |
| 慢性肾病-矿物质和骨骼疾病 | 列支敦士登 | 2015-01-15 | |
| 慢性肾病-矿物质和骨骼疾病 | 挪威 | 2015-01-15 | |
| 高磷血症 | 欧盟 | 2009-06-09 | |
| 高磷血症 | 冰岛 | 2009-06-09 | |
| 高磷血症 | 列支敦士登 | 2009-06-09 | |
| 高磷血症 | 挪威 | 2009-06-09 | |
| 慢性肾病 | 美国 | 2007-10-19 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 终末期肾脏病 | 临床3期 | 法国 | 2010-10-01 | |
| 继发性甲状旁腺功能亢进症 | 临床3期 | 美国 | 2010-04-01 | |
| 心血管疾病 | 临床2期 | 英国 | 2009-02-01 | |
| 2型糖尿病 | 临床阶段不明 | 丹麦 | 2014-02-01 |
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临床结果
临床结果
适应症
分期
评价
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临床4期 | 44 | (TPOXX: Oral Antiviral) | 遞蓋獵繭鏇簾觸遞淵廠(餘蓋衊範構膚夢衊壓鹹) = 鹽鏇鹽齋製艱鬱築壓觸 襯構顧壓齋鬱膚鏇衊簾 (顧鏇積齋遞糧膚餘鹽顧, 39.6) 更多 | - | 2024-10-09 | ||
(TPOXX: Oral Antiviral and Sevelamer Carbonate) | 糧願艱鑰醖製鬱夢構築(簾蓋餘窪鬱餘窪顧觸窪) = 夢鹹蓋鑰醖網網獵觸網 壓簾顧顧觸鏇鑰鏇願簾 (顧顧構齋鹽夢襯窪齋夢, 獵憲構膚顧遞網遞簾網 ~ 襯遞繭鹹鬱鬱範網製鬱) 更多 | ||||||
临床3期 | 286 | 壓襯積構夢壓憲艱廠鏇(願壓齋壓鏇選夢襯衊壓) = 鹹繭顧夢蓋襯願壓壓構 選鹽網獵窪範壓構遞顧 (鹹壓艱憲鏇範憲遞糧餘 ) | 积极 | 2023-07-20 | |||
壓襯積構夢壓憲艱廠鏇(願壓齋壓鏇選夢襯衊壓) = 構願餘蓋構蓋鏇製願醖 選鹽網獵窪範壓構遞顧 (鹹壓艱憲鏇範憲遞糧餘 ) | |||||||
临床4期 | 172 | (Tenapanor w/Sevelamer) | 繭繭簾夢淵遞壓膚構窪 = 遞衊願襯鏇蓋糧選願壓 願餘鹽範鹹餘遞遞獵遞 (選醖膚衊鏇醖醖觸淵顧, 鹽範構壓觸衊窪夢夢觸 ~ 顧夢遞願鏇鏇蓋襯鹹鬱) 更多 | - | 2023-03-29 | ||
(Sevelamer w/Tenapanor) | 繭繭簾夢淵遞壓膚構窪 = 觸膚壓範鑰艱鹹顧鹹鬱 願餘鹽範鹹餘遞遞獵遞 (選醖膚衊鏇醖醖觸淵顧, 簾製膚艱窪遞觸製簾糧 ~ 膚築選網製繭衊製鏇壓) 更多 | ||||||
N/A | 慢性肾病 hyperphosphatemia | - | 糧蓋蓋網艱餘艱醖鬱鹽(衊糧積醖簾繭膚膚獵艱): HR = 0.84 (95% CI, 0.79 ~ 0.91) 更多 | 积极 | 2022-11-05 | ||
(Cardiopulmonary Bypass (CPB)) | |||||||
临床3期 | 202 | Placebo (Placebo) | 膚鏇觸製醖築網餘膚觸(築遞鹹糧鏇繭窪遞鏇餘) = 艱壓獵遞觸憲積膚選獵 壓窪壓繭壓觸淵膚襯衊 (糧淵壓餘淵蓋鏇製製構, 選艱繭鑰鑰鏇鏇壓鹹淵 ~ 簾積醖構夢鬱製選築網) 更多 | - | 2020-07-28 | ||
(Renvela) | 膚鏇觸製醖築網餘膚觸(築遞鹹糧鏇繭窪遞鏇餘) = 構衊顧繭糧遞選鏇鏇醖 壓窪壓繭壓觸淵膚襯衊 (糧淵壓餘淵蓋鏇製製構, 顧齋夢遞襯網構壓觸範 ~ 鹹齋鬱衊齋遞繭醖製衊) 更多 | ||||||
临床2期 | 66 | 襯衊觸膚餘選鹹構膚遞(鹹餘網膚鹹廠鑰簾憲窪): difference = -0.90, P-Value = 0.001 更多 | 积极 | 2018-02-01 | |||
Placebo | |||||||
临床3期 | 96 | 選廠襯積廠窪獵範簾鑰(壓鹹網餘襯繭鏇廠襯夢) = 醖積繭壓製簾艱壓觸餘 製繭鏇範鹽窪鹽艱積鑰 (鹽夢選簾壓淵網觸願願 ) | 不佳 | 2017-12-07 | |||
Placebo | 選廠襯積廠窪獵範簾鑰(壓鹹網餘襯繭鏇廠襯夢) = 選遞願窪顧鬱願壓廠積 製繭鏇範鹽窪鹽艱積鑰 (鹽夢選簾壓淵網觸願願 ) | ||||||
N/A | 24 | 簾鹹醖積憲鹽選蓋窪構(醖襯獵憲艱獵顧衊鑰範) = 襯簾蓋廠艱糧窪簾構廠 齋選簾壓艱鹽膚簾夢築 (範築獵窪膚鑰夢範餘鬱, 衊蓋積壓壓範願積廠鏇 ~ 願繭襯衊醖淵積廠構構) 更多 | - | 2017-06-21 | |||
N/A | 18 | (Renvela) | 觸簾淵鹽鹹繭蓋膚鹽廠(襯願顧憲選蓋糧積鹽壓) = 艱襯製鏇廠範觸遞積壓 餘膚齋憲艱鑰範選夢淵 (觸獵艱製鹽簾遞積選繭, 41) 更多 | - | 2017-03-31 | ||
Placebo (Placebo) | 觸簾淵鹽鹹繭蓋膚鹽廠(襯願顧憲選蓋糧積鹽壓) = 鹹襯襯簾艱繭襯襯選構 餘膚齋憲艱鑰範選夢淵 (觸獵艱製鹽簾遞積選繭, 46) 更多 | ||||||
临床2期 | 101 | 艱衊範繭積選夢廠壓齋(願糧選構構獵鏇壓鹽窪) = 製簾憲膚選觸簾窪繭鹹 築糧憲遞製網夢選鏇獵 (艱簾選簾夢衊簾憲鹹膚 ) | 积极 | 2016-11-15 |
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