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This systematic review was performed to understand better the myriad presentations, various therapeutic options, response to therapy, and its clinical outcomes in hyperphosphatemic tumoral calcinosis (HTC). Full texts were selected according to strict inclusion criteria. All case reports of HTC wherein baseline phosphate was measured, treatment offered was mentioned, and information on follow-up and response to therapy that were available were included. A total of 43 of 188 eligible studies (N = 63 patients) met the inclusion criteria. A list of desired data was extracted and graded for methodological quality. A total of 63 individuals (Males = 33) were included from the 43 eligible case studies. The median age of the patients was 18 (IQR 8–32) years. The most frequently involved sites were the hip/gluteal region (34/63; 53.9%) followed by the elbow/forearm (26/63; 41.2%), and the shoulder (18/63; 28.5%). Three patients had conjunctival calcific deposits. The mean (SD) phosphate was 6.9 (1.1) mg/dL. Among the subjects, 36/63 (57.1%) underwent surgical excision with some form of medical therapy. Two patients underwent only surgical excision (2.1%). One patient was maintained on follow-up (1.6%) and 24/63 (38.1%) patients were treated with medical measures. The median (IQR) follow-up duration was 3 (1–9) years. Regression or reduction in lesion size was reported in 19/63 (30.2%) subjects; 20/63 (31.7%) showed progression, 24/63 (38.1%) had features of stable disease, and mortality was reported in 3 patients (4.7%). We report for the first time a detailed description of the clinical and therapeutic response of HTC. A combination of medical measures aimed at lowering serum phosphate appears to be the cornerstone of treatment, although clinical responses may vary. [ABSTRACT FROM AUTHOR]

Iron supplements and/or blood transfusions in combination with recombinant human erythropoietin injections are routinely used to correct renal anemia, which is a common complication of end-stage renal disease. However, massive blood transfusions and inadequate intravenous iron supplementation can lead to iron overload syndrome, and anemia is not always nephrogenic. A rare clinical case of a patient with end-stage chronic kidney disease with complex genesis of anemia, who is on hemodialysis, is presented. The case is interesting because the prescription of first-line drugs was life-threatening in nature, and sevelamer was the drug chosen for the correction of mineral-bone disorders.

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Aim: Bile acid sequestrants are cholesterol‐lowering drugs, which also improve glycaemic control in people with type 2 diabetes. The mechanism behind the glucose‐lowering effect is unknown but has been proposed to be mediated by increased glucagon‐like peptide‐1 (GLP‐1) secretion. Here, we investigated the glucose‐lowering effects of sevelamer including any contribution from GLP‐1 in people with type 2 diabetes. Materials and Methods: In a randomized, double‐blind, placebo‐controlled, crossover study, 15 people with type 2 diabetes on metformin monotherapy underwent two 17‐day treatment periods with the bile acid sequestrant sevelamer and placebo, respectively, in a randomized order and with an interposed wash‐out period of minimum 6 weeks. On days 15 and 17 of each treatment period, participants underwent experimental days with 4‐h liquid meal tests and application of concomitant infusion of exendin(9‐39)NH2 or saline. Results: Compared with placebo, sevelamer improved insulin sensitivity (assessed by homeostatic model assessment of insulin resistance) and beta‐cell sensitivity to glucose and lowered fasting and postprandial plasma glucose concentrations. In both treatment periods, exendin(9‐39)NH2 increased postprandial glucose excursions compared with saline but without absolute or relative difference between the two treatment periods. In contrast, exendin(9‐39)NH2 abolished the sevelamer‐induced improvement in beta‐cell glucose sensitivity. Conclusions: The bile acid sequestrant sevelamer improved insulin sensitivity and beta‐cell sensitivity to glucose, but using the GLP‐1 receptor antagonist exendin(9‐39)NH2 we were not able to detect a GLP‐1‐mediated glucose‐lowering effect of sevelamer in individuals with type 2 diabetes. Nevertheless, the sevelamer‐induced improvement of beta‐cell sensitivity to glucose was shown to be GLP‐1‐dependent. [ABSTRACT FROM AUTHOR]

Introduction: Case reports have suggested a causative role between sevelamer use and subsequent gastrointestinal bleeding (GIB), but no large observational studies have evaluated this association. Methods: Using the United States Renal Data System database from 2015 to 2019, we examined the association between initiation of sevelamer (vs. non-sevelamer containing phosphate binders) and GIB hospitalization as well as all-cause mortality among individuals on hemodialysis. We emulated a target trial using Cox regression models and inverse probability of treatment weights to estimate the adjusted hazard ratios (HR) across outcomes and subgroups. Results: Among 21,354 new users of phosphate binders (11,276 sevelamer and 10,078 non-sevelamer) with baseline lab data (calcium, phosphorus, hemoglobin, and albumin), there were 2,811 GIB hospitalizations and 5,920 deaths after a median follow-up of 1.3 years. Compared with the initiation of non-sevelamer binders, sevelamer was not associated with an increased risk of GIB hospitalization (89 vs. 90 events per 1,000 person-years; IPTW-HR: 0.98, 95% CI: 0.91–1.06) or all-cause mortality (220 vs. 224 events per 1,000 person-years; IPTW-HR: 0.98, 95% CI: 0.93–1.03). Subgroup analyses (such as diabetes and anti-coagulation use) were generally consistent, and there was no association between sevelamer dose and GIB hospitalization. Conclusion: Among patients requiring hemodialysis, sevelamer (vs. non-sevelamer) containing phosphate binders was not associated with increased risk of GIB hospitalization. [ABSTRACT FROM AUTHOR]

Introduction: Hyperphosphatemia is an independent risk factor for mortality in chronic kidney disease (CKD) patients. Objectives: This systematic review and meta-analysis aimed to investigate the effect of Sevelamer on serum phosphorus levels in CKD and hemodialysis patients. Materials and Methods: The data were obtained after searching the international databases of Cochrane, PubMed, Scopus, Web of Science, and the Google Scholar search engine until February 28, 2023. The heterogeneity of articles was assessed using the I2 index. The data were analyzed in STATA 14, and P values < 0.05 were considered significant. Findings: A total of 22 articles were assessed with a total sample size of 3221. Sevelamer reduced calcium levels in CKD and hemodialysis patients compared with those in the comparison group (standardized mean difference [SMD]: -0.67; 95% CI: -1.23, -0.11); however, sevelamer had no significant effect on serum parathyroid hormone (PTH) levels (SMD: 0.07; 95% CI: -0.39, 0.54) and Ca × P product (SMD: -0.20; 95% CI: -0.41, 0). A significant decrease in serum phosphorus level was observed in patients who had taken sevelamer for a maximum of 12 weeks compared with the comparison group (SMD: -0.27; 95% CI: -0.54, -0.01); however, no significant decrease in serum phosphorus level was observed in patients who had taken sevelamer for more than 12 weeks. A significant decrease in serum phosphorus level was observed in sevelamer users compared to placebo group members (SMD: -0.36; 95% CI: -0.68, -0.05). Conclusion: The administration of sevelamer reduced serum phosphorus levels in CKD and hemodialysis patients compared with those in the placebo group in the short term. Therefore, physicians are recommended to prescribe sevelamer for a maximum period of three months. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO website (ID: CRD42023406804). [ABSTRACT FROM AUTHOR]

Rationale and objective: Data suggest that non-calcium-based binders, and specifically sevelamer, may lead to lower rates of death when compared with calcium-based binders in end-stage renal disease (ESRD) patients. However, the association between sevelamer use and mortality for those with non-dialysis-dependent chronic kidney disease (NDD-CKD) patients has been uncertain. Study design: Our research is presented in a prospective cohort study. Setting and participants: A total of 966 participants with NDD-CKD stages 4–5 were enrolled in the PECERA study from 12 centers in Spain. Exposure: The participants were treated with sevelamer. Outcome: This study yielded all-cause and cardiovascular mortality outcomes. Analytical approach: We conducted an association analysis between mortality and sevelamer use with time-dependent Cox proportional hazards models. Results: After a median follow-up of 29 months (IQR: 13–36 months), death occurred in 181 participants (19%), with cardiovascular (n = 95, 53%) being the leading cause of death. In a multivariable model, the adjusted hazard ratios (HRs) for patients under sevelamer treatment were 0.44 (95% CI, 0.22 to 0.88) and 0.37 (95% CI, 0.18 to 0.75) for all-cause and cardiovascular mortality, respectively, compared with those of untreated patients. Limitations: Some limitations include potential confusion via indication bias; causal statements about these associations cannot be made due to the observational nature of this study. Conclusions: In this prospective NDD-CKD cohort study, the administration of sevelamer was independently associated with lower all-cause and cardiovascular mortality, suggesting that non-calcium-based phosphate binders might be the first-line therapy for phosphate lowering in this population. Further interventional studies clarifying the risks and benefits of phosphate binders in NDD-CKD are warranted. [ABSTRACT FROM AUTHOR]

This study was designed to examine the relative safety and efficacy of sevelamer in the treatment of chronic kidney disease (CKD) patients in comparison to placebo, calcium carbonate (CC), or lanthanum carbonate (LC). The PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure (CNKI) databases were searched for articles published through 18 June 2022. The quality of relevant studies was independently analyzed by two investigators who also extracted data from these manuscripts as per Cochrane Collaboration Handbook 5.3. The safety and efficacy of sevelamer as a treatment for hyperphosphatemia in CKD patients were then examined through a meta-analysis, with the primary patient-level outcomes of interest in this analysis being all-cause mortality and the incidence of gastrointestinal adverse effects. Vascular calcification score was also examined as an intermediate outcome, while serum biochemical parameters including levels of phosphate (P), calcium (Ca), intact parathyroid hormone (iPTH), lipids, C-reactive protein (CRP), or fibroblast growth factor-23 (FGF-23) were additionally assessed. In total, this meta-analysis incorporated data from 34 randomized controlled trials (RCTs) enrolling 2802 patients. Sevelamer was associated with reduced all-cause mortality (RR 0.28, CI 0.19 − 0.41, very low certainty) and Vessel calcification score (RR −0.58, CI −1.11 to −0.04, low certainty) and induced less hypercalcemia (MD −0.28, CI 0.40 to −0.16, low certainty) and hyperphosphatemia (MD −0.22, CI −0.32 to −0.13, low certainty) when compared with Ca-based binders in CKD5D individuals. No significant differences in gastrointestinal adverse events (GAEs) incidence were observed. These data suggest that sevelamer may represent a beneficial means of protecting CKD patients against death and vessel calcification when used to treat hyperphosphatemia, while we found no clinically important benefits in decreasing gastrointestinal adverse effects. [ABSTRACT FROM AUTHOR]

Introduction: Hyperphosphatemia is an independent risk factor for mortality in chronic kidney disease (CKD) patients. Objectives: This systematic review and meta-analysis aimed to investigate the effect of Sevelamer on serum phosphorus levels in CKD and hemodialysis patients. Materials and Methods: The data were obtained after searching the international databases of Cochrane, PubMed, Scopus, Web of Science, and the Google Scholar search engine until February 28, 2023. The heterogeneity of articles was assessed using the I2 index. The data were analyzed in STATA 14, and P values < 0.05 were considered significant. Findings: A total of 22 articles were assessed with a total sample size of 3221. Sevelamer reduced calcium levels in CKD and hemodialysis patients compared with those in the comparison group (standardized mean difference [SMD]: -0.67; 95% CI: -1.23, -0.11); however, sevelamer had no significant effect on serum parathyroid hormone (PTH) levels (SMD: 0.07; 95% CI: -0.39, 0.54) and Ca × P product (SMD: -0.20; 95% CI: -0.41, 0). A significant decrease in serum phosphorus level was observed in patients who had taken sevelamer for a maximum of 12 weeks compared with the comparison group (SMD: -0.27; 95% CI: -0.54, -0.01); however, no significant decrease in serum phosphorus level was observed in patients who had taken sevelamer for more than 12 weeks. A significant decrease in serum phosphorus level was observed in sevelamer users compared to placebo group members (SMD: -0.36; 95% CI: -0.68, -0.05). Conclusion: The administration of sevelamer reduced serum phosphorus levels in CKD and hemodialysis patients compared with those in the placebo group in the short term. Therefore, physicians are recommended to prescribe sevelamer for a maximum period of three months. Registration: This study has been compiled based on the PRISMA checklist, and its protocol was registered on the PROSPERO website (ID: CRD42023406804).

We describe the clinical evolution of a patient with tumoral calcinosis due to a pathogenic variant in the GALNT3 gene presented with a large mass overlying her left hip associated complicated by inflammatory flares. Therapy (sevelamer, acetazolamide, and probenecid) was unsuccessful in preventing tumour surgeries, therefore, interleukin-1β monoclonal antibody therapy was added; this was successful in the prevention of tumour re-growth. This case highlights the importance of assessing and treating the inflammatory aspect of calcinotic tumour.

AbstractThis study was designed to examine the relative safety and efficacy of sevelamer in the treatment of chronic kidney disease (CKD) patients in comparison to placebo, calcium carbonate (CC), or lanthanum carbonate (LC). The PubMed, Embase, Cochrane Library, and China National Knowledge Infrastructure (CNKI) databases were searched for articles published through 18 June 2022. The quality of relevant studies was independently analyzed by two investigators who also extracted data from these manuscripts as per Cochrane Collaboration Handbook 5.3. The safety and efficacy of sevelamer as a treatment for hyperphosphatemia in CKD patients were then examined through a meta-analysis, with the primary patient-level outcomes of interest in this analysis being all-cause mortality and the incidence of gastrointestinal adverse effects. Vascular calcification score was also examined as an intermediate outcome, while serum biochemical parameters including levels of phosphate (P), calcium (Ca), intact parathyroid hormone (iPTH), lipids, C-reactive protein (CRP), or fibroblast growth factor-23 (FGF-23) were additionally assessed. In total, this meta-analysis incorporated data from 34 randomized controlled trials (RCTs) enrolling 2802 patients. Sevelamer was associated with reduced all-cause mortality (RR 0.28, CI 0.19 − 0.41, very low certainty) and Vessel calcification score (RR −0.58, CI −1.11 to −0.04, low certainty) and induced less hypercalcemia (MD −0.28, CI 0.40 to −0.16, low certainty) and hyperphosphatemia (MD −0.22, CI −0.32 to −0.13, low certainty) when compared with Ca-based binders in CKD5D individuals. No significant differences in gastrointestinal adverse events (GAEs) incidence were observed. These data suggest that sevelamer may represent a beneficial means of protecting CKD patients against death and vessel calcification when used to treat hyperphosphatemia, while we found no clinically important benefits in decreasing gastrointestinal adverse effects.

Nonalcoholic fatty liver disease is a rapidly rising problem in the 21st century and is a leading cause of chronic liver disease that can lead to end-stage liver diseases, including cirrhosis and hepatocellular cancer. Despite this rising epidemic, no pharmacological treatment has yet been established to treat this disease. The rapidly increasing prevalence of nonalcoholic fatty liver disease and its aggressive form, nonalcoholic steatohepatitis (NASH), requires novel therapeutic approaches to prevent disease progression. Alterations in microbiome dynamics and dysbiosis play an important role in liver disease and may represent targetable pathways to treat liver disorders. Improving microbiome properties or restoring normal bile acid metabolism may prevent or slow the progression of liver diseases such as NASH. Importantly, aberrant systemic circulation of bile acids can greatly disrupt metabolic homeostasis. Bile acid sequestrants are orally administered polymers that bind bile acids in the intestine, forming nonabsorbable complexes. Bile acid sequestrants interrupt intestinal reabsorption of bile acids, decreasing their circulating levels. We determined that treatment with the bile acid sequestrant sevelamer reversed the liver injury and prevented the progression of NASH, including steatosis, inflammation, and fibrosis in a Western diet-induced NASH mouse model. Metabolomics and microbiome analysis revealed that this beneficial effect is associated with changes in the microbiota population and bile acid composition, including reversing microbiota complexity in cecum by increasing Lactobacillus and decreased Desulfovibrio The net effect of these changes was improvement in liver function and markers of liver injury and the positive effects of reversal of insulin resistance.

BackgroundPhosphate binders are commonly used in the treatment of patients with hyperphosphatemia. While phosphate binders are used to lower phosphate, the effects of specific phosphate binder types on vitamin D metabolism are unknown.MethodsWe performed a secondary analysis of the Phosphate Normalization Trial in which patients with moderate to advanced chronic kidney disease were randomized to receive either placebo, sevelamer carbonate, lanthanum carbonate or calcium acetate for 9 months. We evaluated changes in serum concentrations of vitamin D metabolites including 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], the ratio of 24,25(OH)2D3 to 25-hydroxyvitamin D [the vitamin D metabolite ratio (VMR)] and the ratio of serum 1,25(OH)2D to 25-hydroxyvitamin D.ResultsCompared with placebo, randomization to the calcium acetate arm was associated with a 0.6 ng/mL (95% CI 0.2, 1) and 13.5 pg/ng (95% CI 5.5, 21.5) increase in 24,25(OH)2D and VMR, respectively, and a 5.2 pg/mL (95% CI 1.1, 9.4) reduction in 1,25(OH)2D. Randomization to sevelamer carbonate was associated with a 0.5 ng/mL (95% CI -0.9, -0.1) and 11.8 pg/ng (95% CI -20, -3.5) reduction in 24,25(OH)2D3 and VMR, respectively. There was no association of the sevelamer arm with the change in 1,25(OH)2D3, and randomization to lanthanum carbonate was not associated with a change in any of the vitamin D metabolites.ConclusionAdministration of different phosphate binders to patients with moderate to severe CKD results in unique changes in vitamin D metabolism.

Arsenic trioxide (As2O3, ATO) has limited therapeutic benefit to treat solid tumors, whether used alone or in combination. Nanoscale drug delivery vehicles have great potential to overcome the limitation of the utility of ATO by rapid renal clearance and dose-limiting toxicity. Polymeric materials ranging from gelatin foam to synthetic polymers such as poly(vinyl alcohol) were developed for vascular embolic or chemoembolic applications. Recently, we have introduced sevelamer, an oral phosphate binder, as a new polymeric embolic for vascular interventional therapy. In this paper, sevelamer arsenite nanoparticle with a polygonal shape and a size of 50–300 nm, synthesized by anionic exchange from sevelamer chloride, was developed as a Pi-responsive bifunctional drug carrier and embolic agent for chemoembolization therapy. At the same arsenic dosage, sevelamer arsenite-induced severer tumor necrosis than ATO on the VX2 cancer model. In vitro tests evidenced that Pi deprivation by sevelamer could enhance ATO’s anticancer effect. The results showed that ATO in Pi starvation reduced cell viability, induced more apoptosis, and diminished the mitochondrial membrane potential (Δψm) of cells since Pi starvation helps ATO to further down-regulate Bcl-2 expression, up-regulate Bax expression, enhance the activation of caspase-3 and increase the release of cytochrome c, and the production of excessive reactive oxygen species (ROS). Sevelamer arsenite not only plays a Pi-activated nano-drug delivery system but also integrated anticancer drug with embolic for interventional therapy. Therefore, our results presented a new administration route of ATO as well as an alternative chemoembolization therapy.

It is a decade-long controversy that transarterial chemoembolization (TACE) has definite priority over transarterial embolization (TAE) in treating patients with hepatocellular carcinoma (HCC), since HCC cells are regularly resistant to chemotherapy by enhanced expression of proteins that confer drug resistance, and ABC transporters pump the intracellular drug out of the cell. We addressed this issue by modulating the chemo-environment. In an animal model, sevelamer, a polymeric phosphate binder, was introduced as an embolic agent to induce intratumoral inorganic phosphate (Pi) starvation, and trans-arterially co-delivered with doxorubicin (DOX). The new type of TACE was named as DOX-TASE. This Pi-starved environment enhanced DOX tumoral accumulation and retention, and DOX-TASE thereby induced more severe tumor necrosis than that induced by conventional TACE (C-TACE) and drug-eluting bead TACE (D-TACE) at the same dose. In vitro tests showed that Pi starvation increased the cellular accumulation of DOX in an irreversible manner and enhanced cytotoxicity and cell apoptosis by suppressing the expression of ABC transporters (P-glycoprotein (P-gp), BCRP, and MRP1) and the production of intracellular ATP. Our results are indicative of an alternative interventional therapy combining chemotherapy with embolization more effectively.

Rationale and objective: Data suggest that non-calcium-based binders, and specifically sevelamer, may lead to lower rates of death when compared with calcium-based binders in end-stage renal disease (ESRD) patients. However, the association between sevelamer use and mortality for those with non-dialysis-dependent chronic kidney disease (NDD-CKD) patients has been uncertain. Study design: Our research is presented in a prospective cohort study. Setting and participants: A total of 966 participants with NDD-CKD stages 4–5 were enrolled in the PECERA study from 12 centers in Spain. Exposure: The participants were treated with sevelamer. Outcome: This study yielded all-cause and cardiovascular mortality outcomes. Analytical approach: We conducted an association analysis between mortality and sevelamer use with time-dependent Cox proportional hazards models. Results: After a median follow-up of 29 months (IQR: 13–36 months), death occurred in 181 participants (19%), with cardiovascular (n = 95, 53%) being the leading cause of death. In a multivariable model, the adjusted hazard ratios (HRs) for patients under sevelamer treatment were 0.44 (95% CI, 0.22 to 0.88) and 0.37 (95% CI, 0.18 to 0.75) for all-cause and cardiovascular mortality, respectively, compared with those of untreated patients. Limitations: Some limitations include potential confusion via indication bias; causal statements about these associations cannot be made due to the observational nature of this study. Conclusions: In this prospective NDD-CKD cohort study, the administration of sevelamer was independently associated with lower all-cause and cardiovascular mortality, suggesting that non-calcium-based phosphate binders might be the first-line therapy for phosphate lowering in this population. Further interventional studies clarifying the risks and benefits of phosphate binders in NDD-CKD are warranted.

Aluminum phosphide (AlP) is widely used for protecting grains from pests. AlP releases toxic phosphine gas (PH3) while exposed to humidity. Poisoning with these tablets is dangerous and can cause death or serious injuries. Up to now, no definite antidote has been introduced for specific treatment of this poisoning. Sevelamer carbonate or sevelamer hydrochloride (Renagel) is a polymeric pharmaceutical prescribed for treating hyperphosphatemia in patients with chronic kidney disease. Sevelamer can bind with phosphate groups and act as an anion exchanger. Herein, sevelamer is repurposed as a potent antidote agent in phosphine gas poisoning. In vivo evaluation was conducted on male Sprague Dawley rats. The evaluation was conducted on three groups of animals: control, AlP-poisoned, and AlP-poisoned treated with sevelamer. Survival percentage, serum biomarkers level of organ injury, and ATP level were recorded. The results indicate a high survival rate in sevelamer-treated animals compared with the AlP-poisoned group (75% vs. 0% respectively, 48 h after poisoning). The analysis of serum markers of organ injury also showed that sevelamer could reduce toxicity and organ injury in poisoned animals. ATP level of separate organs showed that sevelamer treated groups were recovered. The results showed that sevelamer could be a potent antidote for managing aluminum phosphide poisoning. Moreover, a mechanism is suggested for the interaction of sevelamer with phosphine gas.

As the most efficient method to treat hepatocellular carcinoma in the immediate or advanced stage, transarterial chemoembolization (TACE) is coming into the era of microsphere (MP). Drug-eluting beads have shown their huge potential as an embolic agent and drug carrier for chemoembolization, but their sizes are strictly limited to be above 40 μm, which was considered to occlude vessels in a safe mode. microsphere smaller than 40 µm is easy to be washed out and transported to the normal liver lobe or other organs, causing severe adverse events and failed embolization. To determine whether sevelamer ultrafine particle (0.2–0.5 µm) is qualified as a safe and efficient embolic agent, we investigated the safety and therapeutic efficiency of transarterial sevelamer embolization (TASE) in the VX2 rabbit liver cancer model, aiming to challenge the “40 µm” rule on the selection criteria of the MP. In a four-arm study, blank bead (Callisphere, 100–300 µm), luminescent polystyrene microsphere (10, 100 µm), and sevelamer particle were transarterially administered to evaluate the threshold size of the MP size for intrahepatic or extrahepatic permeability. Another four-arm study was designed to clarify the safety and efficiency of preclinical transarterial sevelamer embolizationTASE tests over other techniques. Sham (saline), TASE, C-TACE, and D-TACE (n = 6) were compared in terms of serum chemistry, histopathology, and tumor necrosis ratio. In the first trials, the “40 µm” rule was detectable on the VX2 cancer model, but the regulation has no application to the new embolic agent as sevelamer ultrafine particles have not been found to leak out from the VX2 lesions, only found in the embolized vessels. Pathology proves that less viable tumor residue was found 2 weeks after the procedure, evidencing a better therapeutic outcome. No adverse events were found except for a short stress response. These results indicate that sevelamer is a safe and efficient embolic as an alternative to the current MP-based embolization therapy techniques.

Objective: To ascertain the efficacy of Sevelamer Carbonate as a better phosphate binder for controlling mineral bone disease biochemical parameters in dialysis patients of a tertiary care centre compared to calcium acetate. Study Design: Prospective Quasi-experimental study. Place and duration of the study: Dialysis unit of Pakistan Emirates Military Hospital Rawalpindi Pakistan from Aug to Dec 2020. Methodology: The sample population comprised 91 patients undergoing maintenance thrice weekly haemodialysis patients treated with Sevelamer Carbonate or Calcium Acetate. CKD-MBD was assessed by serum calcium, phosphorus, ALP, albumin and PTH at the start of the study and then at the end of three months after being treated with phosphate binders. Results: Both Groups had reduced serum phosphorus significantly from baseline to 12 weeks but Sevelamer slightly more than calcium acetate. (Group-1 from 6.90±1.35 to 5.10±1.21, while Group-2 from 7.00±1.31 to 5.90±1.48). The mean Calcium x Phosphorus product was also significantly reduced (p<0.005), decreases after 12 weeks, with 50.0 ± 16.0 in the Sevelamer Hydrochloride Group and insignificantly reduced (52.20±5.20mg2/dl) in the calcium acetate Group. The mean serum calcium increased significantly in the calcium acetate Group from 9.55±0.47 to 10.50±0.90) p=0.003 but was unchanged in the Sevelamer hydrochloride Group (9.56±0.60 to 9.57±0.67; p=0.94). Conclusions: CKD-MBD and its sequelae need special medication, and early detection of biochemical abnormalities and timely intervention with phosphate lowering therapy can abridge the disease burden, thus revamping the quality of life and ultimately abatement of cardiovascular morbidity and mortality. [ABSTRACT FROM AUTHOR]

Chronic kidney disease is a public health problem. The purpose of this study was to compare the effects of sevelamer and calciumbased binders on mortality of hemodialysis patients. PubMed, EMBASE and Web of Science were searched for related articles published before May 14, 2020. We included six studies with 43330 participants, of which 21147 and 22183 received calciumbased phosphate binders and sevelamer, respectively. In the analysis of unadjusted data, sevelamer could lower cardiovascular mortality. When adjusted HRs was pooled, the cardiovascular mortality did not differ significantly in the sevelamer and calcium-based phosphate binders groups. Additionally, the all-cause mortality rate in sevelamer group was different from that in calcium-based phosphate binders group. However, sevelamer could not lower all-cause mortality in terms of the adjusted data. No significant difference was found in calcium and phosphorus between calcium-based phosphate binders and sevalmer. Sensitivity analysis showed that partial results of the study were inconsistent. There was no difference in the effect of sevelamer and calciumbased phosphate binders on the risk of all-cause mortality in patients with hemodialysis, after adjusting confounders. However, given the instability of the results, the results need to be further confirmed by a large sample and high quality RCTs. [ABSTRACT FROM AUTHOR]

The phosphorous balance is clinically important in increasing the long-term outcomes and preventing complications of end-stage renal disease. Sevelamer is a phosphate binder used widely to regulate hyperphosphatemia. On the other hand, gastrointestinal side effects increase with increasing sevelamer intake. A 29-year-old male with end-stage renal disease of IgA nephropathy on maintenance hemodialysis was admitted for diffuse alveolar bleeding and pneumonia. He presented with a low-grade fever and watery diarrhea tinged with blood. Initially, a Clostridioides difficile-associated diarrhea treatment was started with positive findings of Clostridioides difficile toxin and culture. Despite this, there was no improvement in the symptoms even with the appropriate antibiotic treatment. Computed tomography of the abdomen and pelvis revealed an occlusive mass in the rectum and secondary obstructive changes in the sigmoid colon. The initial suspicion was a malignancy or fungal infection. Sigmoidoscopy with a biopsy identified the mass as a lump of mucous material with the entire lumen covered with exudate. The subsequent histopathology examination revealed a colonic mucosal injury and characteristic ''fish scale"-like sevelamer crystals in the exudate. The diagnosis of a sevelamer-induced rectal ulcer was made. We report this case of a sevelamer-associated rectal ulcer of the sigmoid.