Parathyroid hormone and phosphorus overload in uremia: impact on cardiovascular system

Custódio, Melani Ribeiro; Koike, Márcia Kiyomi; Neves, Kátia R.; Reis, Luciene M. dos; Graciolli, Fabiana G.; Neves, Camila Zander; Batista, Daniella G.; Magalhães, Andrea Olivares; Hawlitschek, Philippe; Oliveira, Ivone B.; Dominguez, Wagner V.; Moysés, Rosa Maria Affonso; Jorgetti, Vanda

doi:10.1093/ndt/gfr447

Cited by 63 publications

(58 citation statements)

References 29 publications

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“…Admittedly, hyperphosphatemia and hypocalcemia both could trigger secondary elevation of PTH. It has been reported that pronounced PTH levels were associated with myocardial hypertrophy and fibrosis, as well as higher coronary lesion scores in 5/6 nephrectomy mice [20]. Likewise, a close association between PTH and LVH has also been reported in patients [21].…”

Section: Discussionmentioning

confidence: 96%

Elevated Cardiac Markers in Chronic Kidney Disease as a Consequence of Hyperphosphatemia-Induced Cardiac Myocyte Injury

Wang

Qin

et al. 2014

Med Sci Monit

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BackgroundElevated cardiac markers (CMs) and hyperphosphatemia are commonly encountered in patients with chronic kidney diseases (CKD), but the causal relationship between them has not been established.Material/MethodsWe enrolled 151 patients with different kidney functions in a cross-sectional study to explore the relationship of serum phosphorus with CMs, including cardiac troponin T (cTnT), myoglobin (MYO), creatine kinase-MB (CK-MB), and brain natriuretic peptide (BNP). Then, the effect of reducing phosphorus levels on CMs by taking phosphate binder for 3 months was prospectively observed in 64 hemodialysis patients. Finally, human cardiomyocytes were exposed to different concentrations of inorganic phosphorus to examine its underlying mechanism.Results1) Serum phosphorus and CMs gradually increased as the glomerular filtration rate declined in CKD patients (p<0.01). 2) Elevation of CMs was much greater and cardiac structure and function were worse in CKD patients who had higher serum phosphorus concentrations (p<0.05). 3) Serum phosphorus level positively correlated with cTnT, MYO, and BNP in CKD patients (p<0.001). 4) In hemodialysis patients, the reduction of cTnT, MYO, and CK-MB was synchronous with the pharmacologically-induced decline of serum phosphorus level. However, levels of serum Fibroblast growth factor 23 (FGF23) had no statistical decrease. 5) Simulated hyperphosphatemia inhibited proliferation of human cardiomyocytes in a time- and concentration-dependent manner.ConclusionsHyperphosphatemia may induce myocardial damage in CKD patients, possibly through triggering apoptosis of human cardiomyocytes, and this could account for the elevated cardiac markers in CKD patients.

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Section: Discussionmentioning

confidence: 96%

Elevated Cardiac Markers in Chronic Kidney Disease as a Consequence of Hyperphosphatemia-Induced Cardiac Myocyte Injury

Wang

Qin

et al. 2014

Med Sci Monit

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“…foram capazes de demonstrar o efeito direto do Pi no coração, incluindo hipertrofia miocárdica, hiperplasia de cardiomiócitos e fibrose intersticial, na ausência de mudanças na concentração sérica de PTH. 43,44 Outra forma de demonstrar o papel do Pi como indutor de doença cardiovascular é investigar se a redução de seus níveis interfere positivamente no desenvolvimento dessa condição. Nesse interim, estudos in vivo, que utilizaram modelos animais de DRC em camundongos knock-out para apolipoproteína E (ApoE -/-) e para receptor LDL (LDLR -/-) demonstraram que a redução do Pi sérico pode diminuir a progressão de calcificação vascular.…”

Section: Mecanismos De Lesão Cardiovascular Pelo Fosfato -Lições De Eunclassified

Papel Do Fosfato Na Doença Cardiovascular: Marcador Ou Causador De Lesão?

Almeida¹,

Cancela

Moises

et al. 2015

Rev. Med. UFPR

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RESUMOO fosfato (Pi) é um mineral essencial que participa de diversos processos metabólicos, como produção de energia e sinalização intracelular, além de ser um importante constituinte de diversos elementos celulares. A homeostase do Pi, estritamente regulada pelo paratormônio, pela vitamina D e pelo fator de crescimento fibroblástico -23, sofre um grande desequilíbrio com a perda da função renal, culminando com o desenvolvimento de hiperfosfatemia. Nessa revisão abordaremos a fisiologia do Pi e o seu desequilíbrio causado pela disfunção renal, que se revela através do desenvolvimento da sobrecarga de Pi e da própria hiperfosfatemia. Discutiremos ainda as principais evidências clínicas e experimentais que apontam para o Pi como o mais novo vilão das doenças cardiovasculares tanto na população renal crônica quanto na geral. As estratégias terapêuticas devem ser voltadas sobretudo para a redução da ingestão de Pi, que encontra-se aumentada nos dias atuais devido a presença de conservantes à base desse elemento utilizados nos alimentos industrializados. Estudos populacionais são urgentemente necessários para testar de modo mais amplo os possíveis efeitos benéficos do controle da sobrecarga de Pi sobre o sistema cardiovascular.Palavras chave: Fosfato; Doença Cardiovascular ABSTRACT Phosphate is an essential intracellular mineral that plays its role in a variety of metabolic pathways, like energy production and intracellular synthetis, apart from being and important block to various intracellular elements. Homeostasis of Pi, strictly regulated by parathormone, vitamin D and fibroblast growth factor 23, suffers greatly by the decline of renal function, as seen when phosphate overload and hyperphosphatemia takes its place. We will discuss the major clinical and experimental evidence that points to Pi as the newest villain of cardiovascular disease in the chronic renal disease population, as well as the population in general. Therapeutic strategies should be directed mainly in the reduction of Pi intake, that finds itself increased nowadays due to the presence of food preservatives based on this element in industrialized food. Populational studies are urgently needed to test in a more broad way the possible benefic effects of Pi overload control on cardiovascular system.

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“…Lo que sí es cierto es que está estrechamente asociado al entramado de alteraciones metabólicas y biológicas que acompañan a la ERC 7,8 , entre las que destaca la enfermedad mineral ósea renal. Dicha entidad implica alteraciones en el metabolismo del calcio, el fósforo 9 , la vitamina D 10,11 , el FGF23-Klotto y la hormona paratiroidea 12 (PTH). A ellos hay que añadir alteraciones biológicas como disfunciones en la producción de inhibidores de la calcificación por las células musculares lisas, inflamación crónica 13 , etc.…”

Section: Introductionunclassified

Sesión de hemodiálisis: la tormenta perfecta para la calcificación vascular

et al. 2015

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Parathyroid hormone and phosphorus overload in uremia: impact on cardiovascular system

Abstract: In uremia, PTH and phosphorus overload are both independently associated with major changes related to the cardiac remodeling process, emphasizing the need for a better control of these factors in chronic kidney disease.

Cited by 63 publications

References 29 publications

Elevated Cardiac Markers in Chronic Kidney Disease as a Consequence of Hyperphosphatemia-Induced Cardiac Myocyte Injury

Elevated Cardiac Markers in Chronic Kidney Disease as a Consequence of Hyperphosphatemia-Induced Cardiac Myocyte Injury

Papel Do Fosfato Na Doença Cardiovascular: Marcador Ou Causador De Lesão?

Sesión de hemodiálisis: la tormenta perfecta para la calcificación vascular

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