Phosphate Toxicity in CKD: The Killer among Us

Ritter, Cynthia S.; Slatopolsky, Eduardo

doi:10.2215/cjn.11901115

Cited by 110 publications

(124 citation statements)

References 140 publications

(103 reference statements)

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“…An increase by 1 mmol/L of serum phosphate from baseline to week 4 led to a decrease of T 50 -time by 145 (95% CI: –237 to –52) min. This result compares well with several other lines of research, which had identified hyperphosphatemia levels as the number one driver of vascular calcification in CKD patients (reviewed in Ritter et al [30]). In cell cultures high phosphate levels transform vascular smooth muscle cells into osteoblast-like cells [31], and cells from CKD patients lack inherent pathways to prevent calcification compared to healthy control cells [32].…”

Section: Discussionsupporting

confidence: 88%

Oral Sodium Bicarbonate Supplementation Does Not Affect Serum Calcification Propensity in Patients with Chronic Kidney Disease and Chronic Metabolic Acidosis

Aigner¹,

Cejka²,

Sliber³

et al. 2019

Kidney Blood Press Res

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Background: Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD) and metabolic acidosis might accelerate vascular calcification. The T₅₀ calcification inhibition test (T₅₀-test) is a global functional test analyzing the overall propensity of calcification in serum, and low T₅₀-time is associated with progressive aortic stiffening and with all-cause mortality in non-dialysis CKD, dialysis, and transplant patients. Low serum bicarbonate is associated with a short T₅₀-time and alkali supplementation could be a simple modifier of calcification propensity. The aim of this study was to investigate the short-term effect of oral sodium bicarbonate supplementation on T₅₀-time in CKD patients. Material and Methods: The SoBic-study is an ongoing randomized-controlled trial in CKD-G3 and G4 patients with chronic metabolic acidosis (serum HCO₃^– ≤21 mmol/L), in which patients are randomized to either achieve serum HCO₃^– levels of 24 ± 1 mmol/L (intervention group) or 20 ± 1 mmol/L (rescue group). The effect of bicarbonate treatment on T₅₀-time was assessed. Results: The study cohort consisted of 35 (14 female) patients aged 57 (±15) years, and 18 were randomized to the intervention group. The mean T₅₀-time was 275 (± 64) min. After 4 weeks, the mean change of T₅₀-time was 4 (±69) min in the intervention group and 18 min (±56) in the rescue group (β = –25; 95% CI: –71 to 22; p = 0.298). Moreover, change of serum bicarbonate in individual patients was not associated with change in T₅₀-time, analyzed by regression analysis. Change of serum phosphate had a significant impact on change of T₅₀-time (β = –145; 95% CI: –237 to –52). Conclusion: Oral sodium bicarbonate supplementation showed no effect on T₅₀-time in acidotic CKD patients.

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Section: Discussionsupporting

confidence: 88%

Oral Sodium Bicarbonate Supplementation Does Not Affect Serum Calcification Propensity in Patients with Chronic Kidney Disease and Chronic Metabolic Acidosis

Aigner¹,

Cejka²,

Sliber³

et al. 2019

Kidney Blood Press Res

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“…In previous studies, the phosphate was proved to be associated with CAC progression and the mortality in both general and CKD patients [14, 28–31]. In our study, the hyperphosphatemia was related to the CAC initiation in PD patients.…”

Section: Discussionsupporting

confidence: 62%

Hyperphosphatemia and hs-CRP Initiate the Coronary Artery Calcification in Peritoneal Dialysis Patients

Shang

Xie

Shang

et al. 2017

BioMed Research International

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Background. Coronary artery calcification (CAC) contributes to high risk of cardiocerebrovascular diseases in dialysis patients. However, the risk factors for CAC initiation in peritoneal dialysis (PD) patients are not known clearly. Methods. Adult patients with baseline CaCS = 0 and who were followed up for at least 3 years or until the conversion from absent to any measurable CAC detected were included in this observational cohort study. Binary logistic regression was performed to identify the risk factors for CAC initiation in PD patients. Results. 70 patients recruited to our study were split into a noninitiation group (n = 37) and an initiation group (n = 33) according to the conversion of any measurable CAC during their follow-up or not. In univariate analysis, systolic blood pressure, serum phosphorus, fibrinogen, hs-CRP, serum creatinine, and triglycerides were positively associated with the initiation of CAC, while the high density lipoprotein and nPCR did the opposite function. Multivariate analysis revealed that hyperphosphatemia and hs-CRP were the independent risk factors for CAC initiation after adjustments. Conclusions. Hyperphosphatemia and hs-CRP were the independent risk factors for CAC initiation in PD patients. These results suggested potential clinical strategies to prevent the initiation of CAC in PD patients.

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“…19,20 There is evidence that this is associated with low levels of [25OHD] S , 21,22 impairment in the renal production of [1,25(…”

Section: Discussionmentioning

confidence: 99%

The Calcium/Phosphorus Homeostasis in Chronic Kidney Disease: From Clinical Epidemiology to Pathophysiology

2017

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RESUMOIntrodução: O propósito do presente trabalho consistiu em descrever alguns dos mecanismos fisiopatológicos envolvidos nas perturbações do metabolismo fosfo-cálcico na doença renal crónica a partir de um processo simples de filtragem de dados e de alguns conceitos básicos de teoria de sistemas. Material e Métodos: Foram estudados os valores (um conjunto por doente, obtido numa única colheita de sangue) de creatinina, cál-cio, fósforo, paratormona, 25-hidroxivitamina D e 1,25-dihidroxivitamina D num grupo de 2507 doentes com doença renal crónica não sujeitos a substituição renal. As variáveis foram emparelhadas e tratadas, primeiro por um processo de média deslizante e depois por distribuição por classes de frequência. Os resultados obtidos foram interpretados à luz do conceito de ansa de retro-controlo contendo dois ramos de sinais opostos cuja intersecção define o 'ponto operacional' do sistema. Este ponto desloca-se ao longo da evolução da doença e o sentido do deslocamento indica qual dos dois fatores (a calcémia ou a concentração de paratormona, por exemplo) está a afetar primariamente o sistema. Resultados: Esta análise mostrou que a evolução das relações entre as variáveis observadas seguiu um padrão monótono, bifásico ou trifásico. Discussão: À medida que a doença renal crónica progride ocorrem alterações na regulação do metabolismo fosfo-cálcico, passando por diferentes fases. Numa fase mais avançada há uma perda do controlo das glândulas paratiróides pela calcémia e pela fosfatémia. A sensibilidade à ação inibitória da 1,25-dihidroxivitamina D diminui progressivamente mas nunca desaparece. Conclusão: A metodologia utilizada na análise de uma base de dados clínicos permitiu ilustrar mecanismos fisiopatológicos subjacentes. Palavras-chave: Cálcio; Fósforo; Hiperparatiroidismo; Homeostase; Insuficiência Renal Crónica ABSTRACT Introduction: A simple data filtering process together with some basic concepts of control theory applied to electronically stored clinical data were used to identify some of the pathophysiological mechanisms underlying the perturbations of the calcium/phosphorus homeostasis in chronic kidney disease. Material and Methods:Retrospective data (a set per patient of serum single value concentrations of creatinine, calcium, phosphorus, parathormone, 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D) from 2507 patients with stable chronic kidney disease not on renal replacement therapy were studied. The variables were paired and subjected sequentially to a moving average and partioned into frequency classes. The plots were interpreted using the concept of a feedback loop comprising two branches of opposite sign and of set point of the loop. The set point for each pair of variables is displaced in the course of the disease and this displacement indicates which of the two factors involved (the serum concentrations of calcium or parathormone, for example) is primarily affected.Results: This analysis showed that in the course of the development of chronic kidney disease the relationships bet...

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Phosphate Toxicity in CKD: The Killer among Us

Cited by 110 publications

References 140 publications

Oral Sodium Bicarbonate Supplementation Does Not Affect Serum Calcification Propensity in Patients with Chronic Kidney Disease and Chronic Metabolic Acidosis

Oral Sodium Bicarbonate Supplementation Does Not Affect Serum Calcification Propensity in Patients with Chronic Kidney Disease and Chronic Metabolic Acidosis

Hyperphosphatemia and hs-CRP Initiate the Coronary Artery Calcification in Peritoneal Dialysis Patients

The Calcium/Phosphorus Homeostasis in Chronic Kidney Disease: From Clinical Epidemiology to Pathophysiology

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