Analysis of serum phosphate control and phosphate binder utilization in incident hemodialysis patients

Farrand, Kimberly F; Copley, John B.; Heise, Jamie; Fridman, Moshe; Keith, Michael; Poole, Lynne

doi:10.2147/ijnrd.s58037

Cited by 5 publications

(2 citation statements)

References 28 publications

(36 reference statements)

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“…Current medical management of hyperphosphatemia with dietary phosphate restriction and oral phosphate binders often proves inadequate to consistently achieve serum phosphate concentration within the target range (22, 47–49). Additional strategies to optimize serum phosphate control are required because hyperphosphatemia is associated with poor clinical outcomes (8–14).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability

et al. 2018

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Hyperphosphatemia is common in patients with chronic kidney disease and is increasingly associated with poor clinical outcomes. Current management of hyperphosphatemia with dietary restriction and oral phosphate binders often proves inadequate. Tenapanor, a minimally absorbed, small-molecule inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3), acts locally in the gastrointestinal tract to inhibit sodium absorption. Because tenapanor also reduces intestinal phosphate absorption, it may have potential as a therapy for hyperphosphatemia. We investigated the mechanism by which tenapanor reduces gastrointestinal phosphate uptake, using in vivo studies in rodents and translational experiments on human small intestinal stem cell-derived enteroid monolayers to model ion transport physiology. We found that tenapanor produces its effect by modulating tight junctions, which increases transepithelial electrical resistance (TEER) and reduces permeability to phosphate, reducing paracellular phosphate absorption. NHE3-deficient monolayers mimicked the phosphate phenotype of tenapanor treatment, and tenapanor did not affect TEER or phosphate flux in the absence of NHE3. Tenapanor also prevents active transcellular phosphate absorption compensation by decreasing the expression of NaPi2b, the major active intestinal phosphate transporter. In healthy human volunteers, tenapanor (15 mg, given twice daily for 4 days) increased stool phosphorus and decreased urinary phosphorus excretion. We determined that tenapanor reduces intestinal phosphate absorption predominantly through reduction of passive paracellular phosphate flux, an effect mediated exclusively via on-target NHE3 inhibition.

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Section: Discussionmentioning

confidence: 99%

Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability

et al. 2018

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“…Beberapa strategi untuk membantu meningkatkan pengelolaan hiperfosfatemia pada pasien hemodialisis meliputi: modifikasi diet, optimasi dialisis, dan peningkatan penggunaan phosphate binders secara teratur [19].…”

Section: Hasil Uji Kadar Fosfatunclassified

Hubungan Kepatuhan Konsumsi Kalsium Karbonat terhadap Kadar Fosfat Pasien Gagal Ginjal dengan Hemodialisis

Ramadhani

2023

JSSCR

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Non-adherence to renal failure treatment increases the risk of disease complications, such as metabolic disorders of calcium and phosphate. Education is one of way to increase medication adherence. Education is one way to increase patient compliance in therapy. One way of conducting education is by giving leaflets. This study aims to determine the correlation between compliance with consumption of calcium carbonate and phosphate levels in patients with kidney failure on hemodialysis. This research were experimental and prospective study at PKU Muhammadiyah General Hospital, Yogyakarta City for 4 weeks using the one-group pretest posttest design to test patients' phosphate levels pre and post administation of leaflets increase adherence. Sample consisted of 70 kidney disease patients with hemodialysis were divided into 2 groups, each consisting of 35 patients. The intervention group were given education leaflets and checking phosphate levels, while the control group were not given leaflets. Data were obtained from medical records, questionnaire instruments and phosphate laboratory data. The level of patient adherence in taking calcium carbonate medication assessed by MMAS questionnaire and phosphate levels of patients. Data were analysis using the Wilcoxon test and Spearman test.The results of the analysis between adherence and phosphate levels showed no relationship between adherence and phosphate levels p=0.591 (p0.05). Overall, it can be concluded that there is no correlation between adherence to calcium carbonate consumption and phosphate levels

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An open-label phase 2 trial to assess the efficacy, safety and pharmacokinetics of lanthanum carbonate in hyperphosphatemic children and adolescents with chronic kidney disease undergoing dialysis

et al. 2022

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Background This study assessed the efficacy, tolerability and pharmacokinetics (PK) of lanthanum carbonate (LC) in hyperphosphatemic children and adolescents with chronic kidney disease (CKD) undergoing dialysis. Methods This was a three-part, multicenter, open-label study of LC (oral powder formulation) in patients 10 to < 18 years old with CKD undergoing dialysis. In part 1, the single-dose PK of LC (500 mg, ≤12 years old; 1000 mg, > 12 years old) were summarized. In part 2, patients received calcium carbonate (CC [chewable tablet formulation]) (1500–6500 mg [total daily dose]) followed by LC (powder formulation) (1500–3000 mg [total daily dose]), or LC only (1500–3000 mg [total daily dose]), each for 8 weeks. During part 3, patients received LC (1500–3000 mg [total daily dose]) for up to 6 months. The primary efficacy endpoint was the proportion of LC-treated patients achieving serum phosphorus control after 8 weeks during parts 2 and/or 3, defined as: ≤1.94 mmol/L, < 12 years old; ≤1.78 mmol/L, ≥12 years old. Secondary efficacy endpoints included: the proportion of patients who achieved serum phosphorus control after 8 weeks of treatment with CC followed by 8 weeks of treatment with LC (with a washout period between treatments). The safety of LC and CC was also evaluated. Results In part 1, 20 patients received a single dose of LC. In part 2, 53 and 51 patients were treated with CC and LC for 8 weeks, respectively. During part 3, 42 patients received LC for up to 6 months. Most patients were white and male. For the primary efficacy endpoint, 50% (17/34) of patients who received LC for 8 weeks during parts 2 and/or 3 achieved serum phosphorus control. After 8 weeks of treatment with CC, 58.8% of patients achieved serum phosphorus control; after a subsequent washout period and 8 weeks of treatment with LC, 70.6% of patients achieved serum phosphorus control. Tmax and t1/2 occurred within 3–8 h and ~ 19 h, respectively; however, variability was observed. LC and CC were generally well tolerated. Conclusions These data support the use of LC to manage hyperphosphatemia in pediatric patients with CKD undergoing dialysis. Trial registration ClinicalTrials.gov identifier: NCT01696279; EudraCT identifier: 2012–000171-17. Date of registration: 01/10/2012.

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Analysis of serum phosphate control and phosphate binder utilization in incident hemodialysis patients

Cited by 5 publications

References 28 publications

Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability

Inhibition of sodium/hydrogen exchanger 3 in the gastrointestinal tract by tenapanor reduces paracellular phosphate permeability

Hubungan Kepatuhan Konsumsi Kalsium Karbonat terhadap Kadar Fosfat Pasien Gagal Ginjal dengan Hemodialisis

An open-label phase 2 trial to assess the efficacy, safety and pharmacokinetics of lanthanum carbonate in hyperphosphatemic children and adolescents with chronic kidney disease undergoing dialysis

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