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

Start Date20 Mar 2024

Sponsor / Collaborator

Shahid Beheshti University of Medical Sciences

100 Clinical Results associated with Sevelamer Carbonate

100 Translational Medicine associated with Sevelamer Carbonate

100 Patents (Medical) associated with Sevelamer Carbonate

260

Literatures (Medical) associated with Sevelamer Carbonate

01 Jan 2026·EUROPEAN JOURNAL OF PHARMACOLOGY

Pharmacologic deprivation of serum inorganic phosphate ameliorates renal fibrosis via the modulation of systemic inflammation

Article

Author: Zhang, Yuan-Yuan ; Liao, Zi-Qiang ; Chen, Ze-Ning ; Deng, Zhi-Qiang ; Kang, Mei-Diao ; Tang, Qun ; Lv, Jin-Lei ; Luo, Rong-Guang ; Deng, Qing ; Liang, Qing-Rong

Renal fibrosis is a common feature of chronic kidney disease (CKD) and is characterized by interstitial fibrotic tissue deposition, impaired renal function, and interstitial inflammation. To date, there are no clinically effective therapeutic agents specifically approved for the treatment of renal fibrosis. Sevelamer, as a phosphate binder, was approved to treat hyperphosphatemia and was recently shown to have antifibrotic effects in preclinical studies. In this study, we established a folic acid (FA)-induced renal interstitial fibrosis mouse model and an in vitro model using human kidney-2 (HK-2) cells to evaluate the therapeutic effects and mechanisms of sevelamer in renal fibrosis. Our results revealed that sevelamer reduced serum phosphate levels in fibrotic mice and improved renal function by restoring serum creatinine (Scr), blood urea nitrogen (BUN), and uric acid (UA) levels. Sevelamer significantly alleviated tubular injury, reduced extracellular matrix (ECM) accumulation, decreased the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) in the serum, and mitigated renal inflammation. In vitro, sevelamer-induced phosphate deprivation inhibited HK-2 cell migration and epithelial‒mesenchymal transition (EMT), reducing the expression of fibrosis-associated proteins. Mechanistic studies revealed that low-phosphate stress induced by sevelamer suppressed the phosphorylation of IκBα and NF-κB-p65, inhibiting nuclear factor kappa B (NF-κB) signaling both in vivo and in vitro. As a result, sevelamer-mediated low-phosphate stress improved renal function, reduced ECM deposition, suppressed the expression of EMT markers in mouse kidneys and HK-2 cells, decreased inflammatory cytokine release, and attenuated NF-κB pathway activation. Sevelamer may be a potential therapeutic agent for the treatment of renal fibrosis.

01 Sep 2025·JOURNAL OF RENAL NUTRITION

Gastrointestinal Mucosal Cell Injury Caused by Sevelamer Crystals: Case Series and Literature Review

Review

Author: Ali, Umair ; Singh, Manisha ; Elbahnasawy, Enas ; Elkalashy, Ahmed ; Karakala, Nithin ; 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.

01 Apr 2025·Nephrologie & Therapeutique

The effects of resins added to the milk of children suffering from chronic kidney disease: a clinical relevance to control potassium and phosphate levels?

Article

Author: Ranchin, Bruno ; Naud, Corentin ; Bechara, Rouba ; Chambon, Véronique ; de Mul, Aurélie ; Bacchetta, Justine

Background:

In infants with chronic kidney disease (CKD), the management of nutrition and growth is highly challenging, particularly compared to older children. Management of hyperkalemia and hyperphosphatemia is difficult, and incorporating potassium and phosphate binders directly in formulas could be beneficial, as it avoids direct ingestion of resins by infants.

Materials and methods:

We conducted a study using Gallia® standard first-stage infant formula and Pregestimil®. We added either carbonate sevelamer (Renvela®, 200, 400 or 800 mg) or polystyrene sulfonate (Resikali®, 2000, 4000 or 8000 mg) to 90 ml of formula. Additionally, we evaluated the combined use of the resins with Gallia® by adding in 90 mL 200 mg/2000 mg, 400 mg/4000 mg, and 200 mg/4000 mg of Renvela® and Resikali®, respectively. The Milk was decanted for 10 minutes, and the resulting supernatants were weighted and analyzed for osmolality and pH. Sodium, potassium, chlore, bicarbonate, magnesium, glucose, calcium, phosphate, protein, cholesterol, triglycerides, iron, folate, vitamin B12 levels were measured after centrifugation.

Results:

With polystyrene sulfonate, potassium levels in milk decreased in a dose-dependent manner, by 36%, 52% and 68%, respectively. Polystyrene sulfonate also reduced magnesium levels and increased both calcium concentration (from 9.7 to 21 mmol/L) and osmolality (from 359 to 423 mOsm/kg). No significant effect on phosphate was observed. Sevelamer decreased both calcium and phosphate concentrations in a dose-dependent manner, by 14%, 26% and 29%, and by 24%, 36% and 40%, respectively. Sevelamer also increased pH from 6.9 to 9.1, and decreased folate levels by 32%, 66% and 81% respectively, from 465 to 88 mmol/L. The combined use of sevelamer and polystyrene sulfonate results in decreased levels of potassium (by 45%, 59% and 59%, respectively), phosphate (by 38%, 39% and 36%, respectively), and folate, albeit with a slighter increase in pH. Osmolality remained unchanged and no other relevant differences were observed.

Conclusion:

Pretreating formulas with resins is a reproducible and straightforward method when specific diets for CKD are unavailable. However, it is important to keep in mind that resins may impact the overall composition (osmolality) and the concentration of other nutrients (folates).

News (Medical) associated with Sevelamer Carbonate

08 May 2026

·www.prnewswire.com

Alebund Pharmaceuticals Announces Completion of Patient Enrollment in Global Phase III Pivotal Multi-Regional Clinical Trial of AP301 for Hyperphosphatemia

May 6, 2026 -- Alebund Pharmaceuticals (Jiangsu) Limited ("Alebund" or the "Company"), an integrated biopharmaceutical company focusing on developing innovative therapies for the treatment of renal diseases and related chronic conditions, today announced the completion of patient enrollment in the global Phase III pivotal multi-regional clinical trial (RESPOND-2, Study AP301-HP-03) of AP301, a novel fiber-iron-based phosphate binder, for the treatment of hyperphosphatemia. The trial was conducted in the United States and China, led by Dr. Geoffrey A. Block of U.S. Renal Care, with Professor Xiaoqiang Ding, Director of the Department of Nephrology, Zhongshan Hospital, Fudan University serving as the China principal investigator, and enrolled a total of 282 chronic kidney disease ("CKD") patients on maintenance dialysis with hyperphosphatemia — 138 in the U.S. and 144 in China. As a next-generation fiber-iron-based phosphate binder, AP301 is designed to have a higher phosphate-binding capability, favorable gastrointestinal tolerability, minimal risk of iron overload, and no requirement for chewing before swallowing, with the potential to improve treatment adherence and effectively control hyperphosphatemia. RESPOND-2 is a double-blind, randomized, multi-regional Phase III clinical trial conducted in the U.S. and China. The study planned to enroll 264 CKD patients aged 12 years and above on maintenance dialysis with hyperphosphatemia, with 282 patients actually enrolled. The study comprises three treatment phases: an 8-week double-blind dose titration phase (AP301 versus AP301 ineffective low dose, 2:1 randomization), a 24-week open-label treatment phase, and a 3-week double-blind randomized withdrawal phase (AP301 maintenance dose versus AP301 ineffective low dose, 1:1 re-randomization). The primary endpoint is the change in serum phosphate levels from baseline to the end of the dose titration phase (AP301 versus AP301 ineffective low dose). The key secondary endpoint is the change in serum phosphate level from the end of the open-label treatment phase to the end of the randomized withdrawal phase (AP301 maintenance dose versus AP301 ineffective low dose). Based on existing clinical data for AP301, the Company reached an agreement with the FDA that this global Phase III multi-regional clinical trial will serve as the single pivotal study to support U.S. registration of AP301. Hyperphosphatemia is one of the most common complications in CKD patients, affecting approximately 95% of dialysis-dependent CKD patients and approximately 15% of non-dialysis CKD patients. According to KDIGO (Kidney Disease: Improving Global Outcomes) guidelines, hyperphosphatemia is defined as a serum phosphate level exceeding 4.5 mg/dL (1.45 mmol/L), with the target serum phosphate range for dialysis patients being 3.5–5.5 mg/dL (1.13–1.78 mmol/L) [1]. Chronically elevated serum phosphate is a central driver of CKD-mineral and bone disorder (CKD-MBD), leading to serious complications including vascular calcification, secondary hyperparathyroidism, and renal osteodystrophy, and is an independent risk factor for cardiovascular events and all-cause mortality in dialysis patients [2]. For CKD patients on dialysis, regular dialysis alone is insufficient to clear the accumulated phosphorus in the body, and the effect of dietary phosphorus restriction is limited. Oral phosphate binders remain the primary treatment for hyperphosphatemia. However, existing phosphate binders are commonly associated with gastrointestinal side effects, high pill burden, and systemic absorption in some agents, resulting in poor patient compliance and inadequate treatment duration. According to the Dialysis Outcomes and Practice Patterns Study (DOPPS) data, approximately 76% of dialysis patients in China, 52% in the U.S., and 39% in Japan fail to achieve target serum phosphate levels [3]. Data from the China Dialysis Calcification Study (CDCS) further showed that the serum phosphate us target attainment rate among Chinese dialysis patients within the 3.5–5.5 mg/dL range was only 40.1% [4]. AP301 demonstrated robust and clinically meaningful efficacy in the completed China pivotal Phase III clinical trial (RESPOND-1, Study AP301-HP-02) [5]. The study was led by Professor Li Zuo, Director of the Department of Nephrology at Peking University People's Hospital, and randomized 474 participants across 50 investigational sites in China. At Week 12, AP301 was non-inferior to sevelamer carbonate, a phosphate binder widely used in clinical practice, in reducing serum phosphate levels (reductions from baseline of -0.72 mmol/L [-2.22 mg/dL] vs. -0.70 mmol/L [-2.17 mg/dL]), respectively; the upper bound of the 95% confidence interval (CI) for the between-group difference (0.06 mmol/L [0.20 mg/dL]) was below the pre-defined non-inferiority margin of 0.19 mmol/L (0.59 mg/dL), demonstrating that AP301 met the pre-specified non-inferiority criterion versus sevelamer carbonate. At Week 27, participants receiving the AP301 maintenance dose achieved clinically and statistically superior serum phosphate control compared with the ineffective low dose group, with a between-group difference of -0.58 mmol/L (-1.8 mg/dL) (PBased on the results of AP301 China pivotal phase III clinical trial and other accumulated clinical data, Alebund has obtained alignment with NMPA and plans to submit a New Drug Application (NDA) in China in the near future. Jin Tian, M.D., Co-founder and Chief Medical Officer of Alebund Pharmaceuticals, commented: "The on-time completion of patient enrollment in AP301's global Phase III pivotal multi-regional clinical trial reflects Alebund's ability to advance high-quality global clinical development, which is an important milestone in the global registrational development of AP301." Hyperphosphatemia is one of the most common complications in CKD patients. The long-term elevated serum phosphate levels could cause multiple complications such as secondary hyperparathyroidism, renal osteodystrophy, and vascular calcification. It is an independent risk factor of cardiovascular events and all-cause mortalities. Good control of serum phosphate levels could effectively improve the patients' outcome. For CKD patients undergoing dialysis treatment, regular dialysis is not sufficient to remove the excess serum phosphate in the body. Considering the limitations of low-phosphate diet which might cause dystrophia, oral use of phosphate binders is the prevailing treatment for hyperphosphatemia. However, existing phosphate binders lead to low patient compliance, with less than 50% of patients achieving good phosphate control, due to gastrointestinal side effects and high pill burden, etc. According to the Global and Chinese Hyperphosphatemia Drug Industry Blue Book by China Insights Consultancy in 2023, the out-of-target rate of serum phosphate level in dialysis patients in Chinese mainland was significantly higher than that in other countries and regions. There remains substantial room for improvement in terms of the proportion of patients using phosphate binders and duration of their usage. According to CIC, by 2035, the market size of serum phosphorus-lowering products in China is expected to reach RMB 10 billion while the global market size is forecasted to reach USD 6 billion. Alebund was founded in Shanghai in 2018. The Company focuses on the discovery, development, manufacturing, and commercialization of novel therapies primarily for kidney diseases and their complications, as well as other chronic conditions, to bring better therapeutic options to patients in China and globally. Alebund has built a diversified and balanced pipeline of seven drug candidates and one commercialized product (Mircera®) targeting a broad range of renal indications, including chronic kidney disease (CKD) and CKD complications, such as hyperphosphatemia, renal anemia, IgA nephropathy, diabetic kidney disease, focal segmental glomerulosclerosis (FSGS), and autosomal dominant polycystic kidney disease (ADPKD). Alebund has completed the construction of its manufacturing site in Yangzhou that will supply both drug substance and drug products of our product candidates, including AP301, upon commercial launch. Alebund has also established a dedicated in-house commercialization team in China responsible for promoting our renal products. The content above comes from the network. if any infringement, please contact us to modify.

Clinical Result

18 Mar 2026

·www.biospace.com

R1 Leads Busy Fundraising Day With $77.5M Series A Raise for Kidney Disease

iStock, Nauval Wildani Alongside R1 Therapeutics, Mestag Therapeutics and iDEL Therapeutics also brought in money on Tuesday, helping to push their respective cancer portfolios forward. Biopharma had a fruitful fundraising day on Tuesday, led by R1 Therapeutics’ oversubscribed series A haul to advance novel treatments for kidney diseases. The California-based startup is coming onto the biopharma scene with $77.5 million in initial funds, according to a Tuesday news release , as well as a potentially first-in-class drug to help temper phosphate levels in patients with chronic kidney disease. Abingworth, F-Prime and DaVita Venture Group co-led the moneymaking push. R1 will use its series A proceeds to advance the global development of AP306, a pan phosphate transporter inhibitor that the biotech claims is “the only agent that blocks the ‘active’ transport” of phosphate. Other phosphate-lowering agents only passively restrict its transport, R1 said. AP306 was originally developed by Chugai and came to R1 via the China-based biotech Alebund Pharmaceuticals, which gave R1 an exclusive worldwide sublicense to the drug—though the specific financial terms of this agreement remain under wraps. Alebund will retain ownership over AP306 in the Greater China region. AP306 has already completed Phase 2a testing in China, with results in February 2025 demonstrating a significant decrease from baseline in serum phosphate levels. Compared with Sanofi’s phosphate binder Renvela, approximately 20% more patients on AP306 achieved the range of phosphate levels recommended in the Kidney Disease: Improving Global Outcomes guidelines. R1 plans to collaborate with Alebund on a global Phase 2b study for AP306, set to begin later this year, according to the press release. The drug “represents a fundamentally new approach to treating hyperphosphatemia,” R1 CEO Krishna Polu said in a statement. “AP306 has the potential to deliver superior efficacy with substantially lower pill burden compared to current phosphate binder therapies.” Also bringing in money on Tuesday was Mestag Therapeutics, which raised $40 million in a push backed by some of the industry’s biggest names, including Johnson & Johnson, Forbion and Google Ventures. The financing will help bankroll the Phase 1 STARLYS study of Mestag’s bispecific antibody for solid tumors. STARLYS is set to start mid-2026, according to the biotech’s press announcement. iDEL Therapeutics also closed its seed round on Tuesday, raising €9 million (about $10.4 million). The company’s technology involves directly delivering cancer drugs into the cytosol of cancer cells, an approach that can be applied to both large and small molecules. Thursday’s proceeds will help push two proprietary lead programs toward the clinic. IDEL is backed by BiomedVC with participation from NRW.Venture, KHAN Technology Transfer Fund II and Gründerfonds Ruhr.

Phase 1Phase 2License out/inClinical Result

17 Mar 2026

·firstwordpharma.com

Kidney biotech R1 Therapeutics emerges with $77.5M, new way to tackle phosphate control in CKD

R1 Therapeutics launched Tuesday with $77.5 million in hand and a lead asset called AP306 that it believes will improve outcomes for chronic kidney disease (CKD) patients by controlling hyperphosphataemia via a new mechanism. Rather than depending on the burdensome binder drugs patients have used for years, the California-based biotech aims to block phosphate absorption directly in the gut.It also announced a partnership with Alebund Pharmaceuticals to license global rights to AP306 outside China. Although exact terms of the deal weren't disclosed, Alebund said that it is eligible to receive milestone payments of up to low triple-digit millions of US dollars, as well as tiered sales royalties in the low double-digit percentage range. Alebund added that it also holds "a substantial non-dilutive equity interest in R1."AP306, also known as EOS789, is designed to inhibit all three phosphate transporters — NaPi-IIb, PiT-1 and PiT-2 — blocking phosphate uptake in the gut. It was discovered by Chugai Pharmaceutical and licensed to Alebund in 2021 for an undisclosed upfront payment and potential milestones.Current phosphate binders have been the standard of care for 60 years, but are limited by low binding capacity, high pill burden and poor gastrointestinal (GI) tolerability. More recently, Ardelyx's Xphozah (tenapanor) was approved by the FDA to lower serum phosphorus in CKD patients on dialysis as an add-on therapy that targets the NHE3 sodium transporter, though R1 says managing hyperphosphataemia continues to be an area of high unmet need."By blocking the active transport of phosphate through three different phosphate transporters in the GI tract, initial clinical studies suggest AP306 has the potential to deliver superior efficacy with substantially lower pill burden compared to current phosphate binder therapies," said R1 CEO Krishna Polu, adding the experimental drug, if successful, "should redefine the class of phosphate lowering therapies."Advancing to Phase IIbIn a Phase IIa study in dialysis patients, AP306 met its primary endpoint, reducing serum phosphate by 2.51 mg/dL from baseline at 12 weeks in haemodialysis patients with hyperphosphataemia, compared with a 1.08 mg/dL reduction for Sanofi's phosphate binder Renagel/Renvela (sevelamer). The study also suggested AP306 was safe and well tolerated, with a markedly lower dose burden than standard binders, which often require patients to take up to nine to 15 pills a day, R1 says on its website.A Phase IIb study of AP306 as monotherapy for hyperphosphatemia in patients with CKD is slated to start later this year in the US and China, with Alebund serving as a collaborative development partner on the drug.The oversubscribed series A financing was co-led by Abingworth, F-Prime and DaVita Venture Group, with participation from Curie.Bio, SymBiosis and US Renal Care.

Phase 2Clinical ResultPhase 1License out/in

100 Deals associated with Sevelamer Carbonate

External Link

KEGG	Wiki	ATC	Drug Bank
D06642	Sevelamer Carbonate	V03AE02	DB00658

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Chronic Kidney Disease-Mineral and Bone Disorder	European Union	Sanofi Winthrop Industrie SA	15 Jan 2015
Chronic Kidney Disease-Mineral and Bone Disorder	Iceland	Sanofi Winthrop Industrie SA	15 Jan 2015
Chronic Kidney Disease-Mineral and Bone Disorder	Liechtenstein	Sanofi Winthrop Industrie SA	15 Jan 2015
Chronic Kidney Disease-Mineral and Bone Disorder	Norway	Sanofi Winthrop Industrie SA	15 Jan 2015
Hyperphosphatemia	European Union	Sanofi Winthrop Industrie SA	09 Jun 2009
Hyperphosphatemia	Iceland	Sanofi Winthrop Industrie SA	09 Jun 2009
Hyperphosphatemia	Liechtenstein	Sanofi Winthrop Industrie SA	09 Jun 2009
Hyperphosphatemia	Norway	Sanofi Winthrop Industrie SA	09 Jun 2009
Chronic Kidney Diseases	United States	Genzyme Corp.	19 Oct 2007

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Hyperparathyroidism, Secondary	Phase 3	United States	Genzyme Corp.	01 Apr 2010
Kidney Failure, Chronic	Phase 3	United States	Genzyme Corp.	01 Jan 2006
Cardiovascular Diseases	Phase 2	United Kingdom	Genzyme Corp.	01 Feb 2009
Diabetes Mellitus, Type 2	Clinical	Denmark	Sanofi	01 Feb 2014

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04485039 (CTgov)	Phase 4	Smallpox	44	Tecovirimat (TPOXX: Oral Antiviral)	vpaoimytpn(cggpfcyjll) = ongghgdfnv txhmnuxnby (vhyixzyguv, 39.6) View more	-	09 Oct 2024
				Tecovirimat+sevelamer carbonate oral tablet (TPOXX: Oral Antiviral and Sevelamer Carbonate)	mtgpozcumq(dvemjlkveo) = kaqtqydvsj opfmaurvcq (ekrvtifalq, pbfbvvfams - nysbsnpniy) View more
NCT03644264 (Pubmed)	Phase 3	Hyperphosphatemia	286	Sucroferric oxyhydroxide	ulxkpviuuw(nirubxmdbm) = ivzckqqjaw lbbhtmuuag (wnqdgbeaen )	Positive	20 Jul 2023
				Sevelamer carbonate	ulxkpviuuw(nirubxmdbm) = tzwigmgblh lbbhtmuuag (wnqdgbeaen )
NCT03988920 (NORMALIZE, CTgov)	Phase 4	Hyperphosphatemia \| Kidney Failure, Chronic	172	Sevelamer Carbonate+Tenapanor (Tenapanor w/Sevelamer)	wdsnknfizu = zgplzrjprq amodddoobz (ltuxauqjyo, mbfauzjrbf - uchgnsjckv) View more	-	29 Mar 2023
				Sevelamer Carbonate+Tenapanor (Sevelamer w/Tenapanor)	wdsnknfizu = pudoxevdoz amodddoobz (ltuxauqjyo, wbmovsrqnn - ifbhfyzyln) View more
ASN2022	Not Applicable	Chronic Kidney Diseases hyperphosphatemia	-	Sevelamer	lrkmswjkrs(nuqwwukdos): HR = 0.84 (95% CI, 0.79 - 0.91) View more	Positive	05 Nov 2022
				Sevelamer (Cardiopulmonary Bypass (CPB))
NCT03001011 (RECOVER \| P0880, CTgov)	Phase 3	Hyperphosphatemia \| Chronic Kidney Diseases	202	Placebo (Placebo)	dgfigqaryp(wcfumhefex) = syebnmigxr ikiyhpumfa (ztvohzaisf, pvygbfyahv - yfywxozqda) View more	-	28 Jul 2020
				Sevelamer Carbonate (GZ419831) (Renvela)	dgfigqaryp(wcfumhefex) = rjkkhgnuzg ikiyhpumfa (ztvohzaisf, vzesedglbs - pmerwaneqm) View more
NCT01574326 (Pubmed \| Pediatr Nephrol) Manual	Phase 2	Hyperphosphatemia \| Chronic Kidney Diseases	66	sevelamer carbonate	zdqbujqfri(obsqkjxgmz): difference = -0.90, P-Value = 0.001 View more	Positive	01 Feb 2018
				Placebo
NCT01220843 (FRENCH, Pubmed) Manual	Phase 3	Chronic Kidney Diseases	96	Sevelamer	yxlfsmrcgy(qqojarznzj) = qvctmyfcya crydvfgbce (yzisccfkbp )	Negative	07 Dec 2017
				Placebo	yxlfsmrcgy(qqojarznzj) = tjphyszhqa crydvfgbce (yzisccfkbp )
NCT01238588 (CTgov)	Not Applicable	Hyperphosphatemia \| Inflammation \| Plaque, Atherosclerotic	24	Renvela+Sevelamer Carbonate	wttcxqmqyv(ryulgxnatq) = wrerjlcavb agfliogrmz (ovjymetbsz, ynwmiwzawt - dwvjmdzxpk) View more	-	21 Jun 2017
NCT00999037 (CTgov)	Not Applicable	Hyperparathyroidism, Secondary \| Chronic Kidney Diseases	18	Sevelamer Carbonate (Renvela)	qdtkkjgarx(jrnuasxjaf) = xgkkrnfqzq lpbherrwgw (sjzrnicath, 41) View more	-	31 Mar 2017
				Placebo (Placebo)	qdtkkjgarx(jrnuasxjaf) = ckwujucqql lpbherrwgw (sjzrnicath, 46) View more
NCT01574326 (phase 2 study, ASN2016)	Phase 2	Hyperphosphatemia \| Chronic Kidney Diseases	101	Sevelamer Carbonate	jphzhnrqfo(vrlyndaaes) = oiquebvqks kcngyvcudx (llziobvbcd )	Positive	15 Nov 2016

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