MgCaCO<sub>3</sub> Versus CaCO<sub>3</sub> in Peritoneal Dialysis Patients – a Cross-over Pilot Trial

Evsanaa, Baigalmaa; Liu, Irene; Aliazardeh, Babak; Mahdavi, Sara; Bajwa, Gursarn; Gula, Jerry; Tam, Michelle; Sze, Elena; Roscoe, Janet; Tam, Paul; Sikaneta, Tabo

doi:10.3747/pdi.2013.00129

Cited by 9 publications

(4 citation statements)

References 7 publications

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“…An asymptomatic, albeit significant, increase in serum magnesium occurred in the CaMg group as well. Another small clinical trial in peritoneal dialysis patients showed that CaMg was somewhat less effective than calcium carbonate in controlling serum phosphate, and, more importantly, that diarrhea appeared to be a more common dose-limiting adverse effect with CaMg 62 …”

Section: Dietary Phosphate Restrictionmentioning

confidence: 99%

Strategies for Phosphate Control in Patients With CKD

Barreto

Massy

et al. 2019

Kidney International Reports

102

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Hyperphosphatemia is a common complication in patients with chronic kidney disease (CKD), particularly in those requiring renal replacement therapy. The importance of controlling serum phosphate has long been recognized based on observational epidemiological studies that linked increased phosphate levels to adverse outcomes and higher mortality risk. Experimental data further supported the role of phosphate in the development of bone and cardiovascular diseases. Recent advances in our understanding of the mechanisms involved in phosphate homeostasis have made it clear that the serum phosphate concentration depends on a complex interplay among the kidneys, intestinal tract, and bone, and is tightly regulated by a complex endocrine system. Moreover, the source of dietary phosphate and the use of phosphate-based additives in industrialized foods are additional factors that are of particular importance in CKD. Not surprisingly, the management of hyperphosphatemia is difficult, and, despite a multifaceted approach, it remains unsuccessful in many patients. An additional issue is the fact that the supposedly beneficial effect of phosphate lowering on hard clinical outcomes in interventional trials is a matter of ongoing debate. In this review, we discuss currently available treatment approaches for controlling hyperphosphatemia, including dietary phosphate restriction, reduction of intestinal phosphate absorption, phosphate removal by dialysis, and management of renal osteodystrophy, with particular focus on practical challenges and limitations, and on potential benefits and harms.

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Section: Dietary Phosphate Restrictionmentioning

confidence: 99%

Strategies for Phosphate Control in Patients With CKD

Barreto

Massy

et al. 2019

Kidney International Reports

102

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“…Of note, GI side effects were severe enough to limit effectiveness of MgCaCO 3 in only one study of 20 PD patients. Patients on MgCaCO 3 were only able to achieve 56% of the prescribed binder dose due to diarrhea as compared with 92% in the CaCO 3 group . Importantly, this was one of only two studies conducted in PD patients.…”

Section: Magnesium and Mineral Bone Disease In Dialysis Patientsmentioning

confidence: 90%

“…All other studies that used combination calcium‐magnesium binders have varied significantly with regard to calcium agent used (acetate vs carbonate), intervention allocation and comparator used (if any), outcomes studied (phosphate balance vs markers of systemic calcification), and reporting of side effects; all have generally included <50 patients . As a whole, these studies have demonstrated that phosphate binders consisting of calcium‐magnesium compounds were effective with respect to phosphate control, and that hypermagnesemia, if present, was generally mild and asymptomatic . Of note, GI side effects were severe enough to limit effectiveness of MgCaCO 3 in only one study of 20 PD patients.…”

Section: Magnesium and Mineral Bone Disease In Dialysis Patientsmentioning

confidence: 99%

Clinical aspects of magnesium physiology in patients on dialysis

Misra

Nessim

2017

Seminars in Dialysis

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Magnesium balance is infrequently discussed in the dialysis population, and the clinical consequences of derangements in magnesium homeostasis are incompletely understood. There is an association between hypomagnesemia and adverse outcomes including increases in cardiovascular disease and mortality, while elevated magnesium levels have also been linked with complications such as osteomalacia. In this review, we discuss the features of magnesium physiology relevant to dialysis patients and provide an updated summary of the literature linking magnesium derangements with bone disease, cardiovascular disease, sudden cardiac death, and mortality.

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“…Phosphate binders have proven effective in reducing serum phosphorus levels, but their use is often limited by adverse events (AEs) and/or heavy pill burden [ 9 ]. The reports that PD patients have poor control of serum phosphorus levels with existing phosphate binders [ 10 , 11 ] may indicate the involvement of subjective symptoms, such as abdominal fullness, diarrhea, and constipation. In fact, a study of Asian patients undergoing PD found that adherence to phosphate binder therapy was the only significant contributor to reduced serum phosphorus levels [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Tenapanor for peritoneal dialysis patients with hyperphosphatemia: a phase 3 trial

Nakayama,

Kobayashi,

Kusakabe

et al. 2023

Clin Exp Nephrol

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Background Tenapanor is a novel selective inhibitor of intestinal sodium/hydrogen exchanger 3 transporter. This is the first trial to assess the efficacy and safety of tenapanor in Japanese patients with hyperphosphatemia who are undergoing peritoneal dialysis. Methods This phase 3, open-label, multicenter, single-arm clinical trial targeted patients whose serum phosphorus was within 3.5–7.0 mg/dL with phosphate binders at screening. After phosphate binder washout, tenapanor was orally administered twice-daily, stepwise from 5 to 30 mg/dose for 16 weeks. The primary endpoint, mean change in serum phosphorus level, was evaluated at week 8. The 16-week treatment period was completed with tenapanor alone, and only one phosphate binder type was allowed for combined use after the primary endpoint. Results Of the 54 patients enrolled, 34 completed the study. At week 8, the primary endpoint, mean change in serum phosphorus level (last observation carried forward), was − 1.18 mg/dL (95% confidence interval: − 1.54, − 0.81 mg/dL) with tenapanor. From a baseline value of 7.65 mg/dL, serum phosphorus decreased to 6.14 and 5.44 mg/dL at weeks 8 and 16, respectively, and 46.3% and 76.5% of patients achieved serum phosphorus within 3.5–6.0 mg/dL at week 8 and week 16, respectively. The most common adverse event, diarrhea, occurred in 74.1% of patients; the severity of diarrhea was mild or moderate. Thus, the discontinuation percentage due to diarrhea was low at 5.6%. Conclusions Administration of tenapanor resulted in a sufficient reduction in serum phosphorus level at week 8 and was considered safe and tolerable. Trial registration NCT04766385.

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MgCaCO₃ Versus CaCO₃ in Peritoneal Dialysis Patients – a Cross-over Pilot Trial

Cited by 9 publications

References 7 publications

Strategies for Phosphate Control in Patients With CKD

Strategies for Phosphate Control in Patients With CKD

Clinical aspects of magnesium physiology in patients on dialysis

Tenapanor for peritoneal dialysis patients with hyperphosphatemia: a phase 3 trial

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MgCaCO3 Versus CaCO3 in Peritoneal Dialysis Patients – a Cross-over Pilot Trial

Cited by 9 publications

References 7 publications

Strategies for Phosphate Control in Patients With CKD

Strategies for Phosphate Control in Patients With CKD

Clinical aspects of magnesium physiology in patients on dialysis

Tenapanor for peritoneal dialysis patients with hyperphosphatemia: a phase 3 trial

Contact Info

Product

Resources

About

MgCaCO₃ Versus CaCO₃ in Peritoneal Dialysis Patients – a Cross-over Pilot Trial