Phosphate management in chronic kidney disease

Bhan, Ishir

doi:10.1097/01.mnh.0000441155.47696.41

Cited by 6 publications

(6 citation statements)

References 36 publications

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“…Hyperphosphatemia is a well-recognized risk factor for renal osteodystrophy and cardiovascular mortality in people with ESKD. 2,8,11 Collectively this is called chronic kidney disease -mineral bone disorder (CKD-MBD). Treatment of hyperphosphatemia requires a combination of dietary phosphate restrictions, use of oral phosphate binder therapy to reduce intestinal phosphate absorption, vitamin D3 (calcitriol) supplementation and adequate dialysis prescription to promote removal of phosphate.…”

Section: Methods Of Phosphate Controlmentioning

confidence: 99%

“…16 However, there is a linear relationship between phosphate and protein intake. 2 In general, foods high in phosphate such as milk and meat are rich in protein. For each gram of protein, there is approximately 13-15 mg of phosphate.…”

Section: Dietary Phosphate Restrictionmentioning

confidence: 99%

“…The mainstay treatment of hyperphosphatemia is the use of oral phosphate binder medication. 2,20 Phosphate binders lower phosphate absorption in the intestines by binding to and sequestering phosphate in the gastrointestinal tract, forming insoluble products that are not readily absorbed. 21 The Dialysis Outcomes and Practice Patterns Study (DOPPS) involving 23,898 patients on HD at 923 facilities in 12 countries found that 88% of patients were prescribed phosphate binders and 12% were not.…”

Section: Phosphate Bindersmentioning

confidence: 99%

“…1 Hyperphosphatemia occurs in people with ESKD as a result of the kidneys' reduced ability to excrete an ingested phosphate load. 2,3 Hyperphosphatemia significantly lowers the serum calcium concentration, stimulating the release of parathyroid hormone (PTH), causing secondary hyperparathyroidism. 4 In ESKD, hyperphosphatemia also slows the activation of vitamin D impaired absorption of calcium from the gastrointestinal tract, resulting in reduced mobilization of calcium and phosphate from the bones, and causing metabolic bone disease.…”

Section: Introductionmentioning

confidence: 99%

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Effectiveness of educational or behavioral interventions on adherence to phosphate control in adults receiving hemodialysis: a systematic review

Milazi

Bonner

Douglas

2017

JBI Database of Systematic Reviews and Implementation Reports

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Overall, educational or behavioral interventions increase adherence to phosphate control. Studies in this systematic review revealed improved outcomes on serum phosphate levels, patient knowledge and adherence to phosphate control methods, CKD self-management behavior and perceived self-efficacy for CKD related to phosphate control. However, there is a lack of sufficient data on how some of the studies implemented their interventions, suggesting that further research is required. Successful strategies that improve and optimize long-term adherence to phosphate control still need to be formulated.

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Section: Methods Of Phosphate Controlmentioning

confidence: 99%

Section: Dietary Phosphate Restrictionmentioning

confidence: 99%

Section: Phosphate Bindersmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effectiveness of educational or behavioral interventions on adherence to phosphate control in adults receiving hemodialysis: a systematic review

Milazi

Bonner

Douglas

2017

JBI Database of Systematic Reviews and Implementation Reports

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“…Although the therapeutic armamentarium for treating hyperphosphatemia now includes a series of effective phosphate‐lowering drugs , the evidentiary basis whereupon treatment of hyperphosphatemia remains disconcertingly weak. We still lack well‐designed, large scale, placebo‐controlled clinical trials assessing whether reducing serum phosphate levels by phosphate binders may translate into better clinical outcomes.…”

mentioning

confidence: 99%

Phosphate Binders and Clinical Outcomes in Patients with Stage 5D Chronic Kidney Disease

Zoccali

Mallamaci

Cannata-Andía

2015

Seminars in Dialysis

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Knowledge informing the prescription and the choice of phosphate binders in end stage kidney disease (ESKD) patients has a weak evidentiary base. To date, no placebo-controlled trial based on meaningful clinical endpoints (death, cardiovascular events, bone fractures) has been performed to test the efficacy of these drugs. By the same token, we still lack solid proof that noncalcium binders afford better clinical outcomes as compared with calcium-based binders. Without proper trials, clinical decisions about the treatment of hyperphosphatemia rest on experience and contingent clinical judgment. The use of huge doses of calcium-based binders typically prescribed in the nineties now appears unwarranted. The relationship between phosphate and the risk of death is U shaped and moderate hyperphosphatemia carries just a mild-to-moderate risk excess and may not be seen as a compelling indication for the prescription of phosphate binders. Placebo-controlled randomized clinical trials assessing whether non-calcium and calcium-based binders reduce the risk of death and cardiovascular disease events in ESKD patients remain a public health priority.

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Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

Voelkl

Läng

Eckardt

et al. 2019

Cell. Mol. Life Sci.

131

202

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Medial vascular calcification has emerged as a putative key factor contributing to the excessive cardiovascular mortality of patients with chronic kidney disease (CKD). Hyperphosphatemia is considered a decisive determinant of vascular calcification in CKD. A critical role in initiation and progression of vascular calcification during elevated phosphate conditions is attributed to vascular smooth muscle cells (VSMCs), which are able to change their phenotype into osteo-/chondroblasts-like cells. These transdifferentiated VSMCs actively promote calcification in the medial layer of the arteries by producing a local pro-calcifying environment as well as nidus sites for precipitation of calcium and phosphate and growth of calcium phosphate crystals. Elevated extracellular phosphate induces osteo-/chondrogenic transdifferentiation of VSMCs through complex intracellular signaling pathways, which are still incompletely understood. The present review addresses critical intracellular pathways controlling osteo-/chondrogenic transdifferentiation of VSMCs and, thus, vascular calcification during hyperphosphatemia. Elucidating these pathways holds a significant promise to open novel therapeutic opportunities counteracting the progression of vascular calcification in CKD.

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Phosphate management in chronic kidney disease

Cited by 6 publications

References 36 publications

Effectiveness of educational or behavioral interventions on adherence to phosphate control in adults receiving hemodialysis: a systematic review

Effectiveness of educational or behavioral interventions on adherence to phosphate control in adults receiving hemodialysis: a systematic review

Phosphate Binders and Clinical Outcomes in Patients with Stage 5D Chronic Kidney Disease

Signaling pathways involved in vascular smooth muscle cell calcification during hyperphosphatemia

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