Fibroblast growth factor 23 (FGF 23) and phosphocalcic metabolism in chronic kidney disease
Factor de crecimiento fibroblástico 23 (FGF 23) y metabolismo fosfocálcico en la enfermedad renal crónica
Pere Torguet Escudera, Pere Torguet-Escuderb, Bernat Guasch Aragayc, Bernat Guasch-Aragayb, Jordi Calabia Martinezd, Jordi Calabia-Martínezb, Nàdia Martin Alemanye, Nàdia Martín-Alemanyb, Isabel Garcia Mendezf, Isabel García-Méndezb, Gerard Maté Benitog, Gerard Maté-Benitob, Esther Clapés Sánchezh, Esther Clapés-Sánchezi, Monica Sabater Masdeuj, Mònica Sabater-Masdeuk, Jose Manuel Fernandez Reall, José M. Fernández-Realm, Martí Vallès Pratsc, Martí Vallès-Pratsn
a Nefrología, Hospt Dr. J.Trueta, Girona Girona, Spain,
b Servicio de Nefrología, Hospital Universitari Doctor Josep Trueta, Girona
c Nefrología, Hospt Dr J. Trueta, Girona, Girona, Spain,
d Nefrología, Hospt Dr. J. rueta, Girona, Girona, Spain,
e Nefrología, Hopst. Dr J. Trueta, Girona, Girona, Spain,
f Nefrología, Host. Dr J. Trueta, Girona, Girona, Spain,
g Nefrología, Hospt Dr J. Trueta, Girona, girona, Spain,
h Laboratorio Territorial de Girona, Hospt. Dr J. Trueta, Girona Girona, Spain,
i Laboratorio Territorial de Girona, Hospital Universitari Doctor Josep Trueta, Girona
j Departamento de diabetes,Endocrinología, y Nutrición. Instituto de Investigación Biomédica de Girona (IdIBGi), Hospt Dr J Trueta, Girona, Girona, Spain,
k Departamento de Diabetes, Endocrinología y Nutrición, Fundación Privada Instituto de Investigación Biomédica de Girona (IdIBGi), Girona,
l Endocrinología, Hospt. Dr J. Trueta, Girona, Girona, Spain,
m Servicio de Endocrinología, Hospital Universitari Doctor Josep Trueta, Girona,
n Servicio de Nefrología, Hospital Universitari Doctor Josep Trueta, Girona,
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Trueta, Girona Girona, Spain, " "etiqueta" => "<span class="elsevierStyleSup">h</span>" "identificador" => "affh" ] 8 => array:3 [ "entidad" => "Laboratorio Territorial de Girona, Hospital Universitari Doctor Josep Trueta, Girona " "etiqueta" => "<span class="elsevierStyleSup">i</span>" "identificador" => "affi" ] 9 => array:3 [ "entidad" => "Departamento de diabetes,Endocrinología, y Nutrición. Instituto de Investigación Biomédica de Girona (IdIBGi), Hospt Dr J Trueta, Girona, Girona, Spain, " "etiqueta" => "<span class="elsevierStyleSup">j</span>" "identificador" => "affj" ] 10 => array:3 [ "entidad" => "Departamento de Diabetes, Endocrinología y Nutrición, Fundación Privada Instituto de Investigación Biomédica de Girona (IdIBGi), Girona, " "etiqueta" => "<span class="elsevierStyleSup">k</span>" "identificador" => "affk" ] 11 => array:3 [ "entidad" => "Endocrinología, Hospt. Dr J. Trueta, Girona, Girona, Spain, " "etiqueta" => "<span class="elsevierStyleSup">l</span>" "identificador" => "affl" ] 12 => array:3 [ "entidad" => "Servicio de Endocrinología, Hospital Universitari Doctor Josep Trueta, Girona, " "etiqueta" => "<span class="elsevierStyleSup">m</span>" "identificador" => "affm" ] 13 => array:3 [ "entidad" => "Servicio de Nefrología, Hospital Universitari Doctor Josep Trueta, Girona, " "etiqueta" => "<span class="elsevierStyleSup">n</span>" "identificador" => "affn" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Factor de crecimiento fibroblástico 23 (FGF 23) y metabolismo fosfocálcico en la enfermedad renal crónica" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35246_en_t111180.jpg" "Alto" => 1669 "Ancho" => 1075 "Tamanyo" => 703192 ] ] "descripcion" => array:1 [ "en" => "Patient characteristics" ] ] ] "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION/OBJECTIVES </span></p><p class="elsevierStylePara"> </p><p class="elsevierStylePara">Our understanding of phosphocalcic metabolism in chronic renal failure has changed substantially in recent years. New advancements in the physiological and pathophysiological characteristics of this condition have pointed out new actors, facilitated earlier definitions of disease, provided several prognostic implications, suggested therapeutic interventions, and have replaced or at least modified many old paradigms.<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">Despite the decrease in nephron mass, a dysfunctional kidney is still capable of effectively eliminating phosphate (P), with phosphataemia increasing only in very advanced stages of disease. Fibroblast growth factor 23 (FGF 23) is a protein synthesised in the osteocytes that inhibits proximal reabsorption of P, promotes a decrease in 1,25 (OH)2 vit D3 (calcitriol) by inhibiting renal 1-α hydroxylase, and blocks the synthesis/release of intact parathyroid hormone (iPTH).<span class="elsevierStyleSup">2</span> FGF 23 requires klotho, a protein involved in the aging process, as a requisite cofactor that converts its potential receptor into a highly specific target.</p><p class="elsevierStylePara">In recent years, we have advanced our understanding that altered phosphocalcic metabolism explains a considerable part of the elevated cardiovascular risk of patients with renal failure, in the form of morphologically and functionally altered large vessels through vascular calcification, endothelial dysfunction, and arterial rigidity.<span class="elsevierStyleSup">3</span> While FGF 23 may only represent a marker for phosphate load, clear evidence exists that suggests a direct toxic action on the blood vessels.<span class="elsevierStyleSup">4</span></p><p class="elsevierStylePara">Although the available information is limited, we know that relative levels of FGF 23, calcium (Ca), P, iPTH, and several different metabolites of vitamin D<span class="elsevierStyleInf">3</span> (25 hydroxyvitamin D [25 OHD<span class="elsevierStyleInf">3</span>] and 1,25 dihydroxyvitamin D [1,25 OHD<span class="elsevierStyleInf">3</span>]) vary consistently as chronic kidney disease (CKD) progresses. The temporal evolution of the disease reflects the categorisation of the mutual influences that govern these parameters.</p><p class="elsevierStylePara">We elaborated a cross-sectional, descriptive, and analytical study of these parameters in a large sample of patients with all different stages of CKD.</p><p class="elsevierStylePara"> </p><p class="elsevierStylePara"> <span class="elsevierStyleBold">MATERIAL AND METHOD</span></p><p class="elsevierStylePara"> </p><p class="elsevierStylePara">We examined patients with CKD who were treated in our nephrological outpatient department within the last two years. We excluded all patients with rapidly progressing nephropathy or nephrotic syndrome and those receiving immunosuppressant treatment.</p><p class="elsevierStylePara">We evaluated renal function by calculating estimated glomerular filtration rate (eGFR) using the CKD-EPI formula.<span class="elsevierStyleSup">5</span> We staged renal failure using the five stages established by the K/DOQI giudelines.<span class="elsevierStyleSup">6</span> In stage five patients, we differentiated between predialysis situations (5a) and patients on renal replacement therapy (5b).</p><p class="elsevierStylePara">Blood samples were extracted and stored at -80 ºC until analysis. We measured Ca and P using standard procedures at our laboratory; iPTH was measured using ECLIA (electrochemiluminescence immunoassay, PTH Cobas<span class="elsevierStyleSup">®</span>, Roche), with a normal range of 15-65pg/ml; 25 OHD<span class="elsevierStyleInf">3</span> was also measured using ECLIA (vitamin D3 [25-OH] Cobas<span class="elsevierStyleSup">®</span>, Roche), with a normal range of 19.1-57.6ng/ml; 1,25 OHD<span class="elsevierStyleInf">3</span> was measured using radio-isotopes (DIAsource 1,25 [OH]2-VIT.D-RIA-CT<span class="elsevierStyleSup">®</span>), with a normal range of 18-78pg/ml. Intact FGF 23 was measured using a second-generation ELISA (Kainos Laboratories, Japan). FGF 23 refer to a control sample from 136 healthy individuals, receiving no treatment whatsoever, with similar age and sex distributions to the treatment sample, with a mean value of 29.23ng/l (standard deviation: 8.3ng/l).</p><p class="elsevierStylePara">We obtained informed consent from all patients, and the study was approved by the hospital ethics committee.</p><p class="elsevierStylePara">We performed a descriptive and analytical statistical analysis using parametric and non-parametric tests based on the distribution of each variable. We used Spearman’s correlation tests to evaluate the relationship between continuous variables. We used one-way ANOVA tests to compare each variable in the different stages of CKD, along with a Sheffe test. The bivariate relationships between 1,25 OHD<span class="elsevierStyleInf">3</span>, eGFR, and FGF 23 were modelled using a curvilinear regression model. The assumed relationship was modelled of the following equation: ln(y) = ln(b<span class="elsevierStyleInf">0</span>) + (b<span class="elsevierStyleInf">1</span> ln(x)). We then constructed a generalised linear model to analyse the relationships between the primary variable of interest (FGF 23) and all other explanatory variables; continuous variables that did not have a linear relationship with the primary variable of interest (phosphorous, 1,25 OHD<span class="elsevierStyleInf">3</span> and eGFR) were transformed in order to create a linear relationship. For all analyses, we considered a <span class="elsevierStyleItalic">P</span>-value <.05 to be statistically significant. We used SPSS statistical software, version 17, for all analyses (SPSS, Chicago, IL, USA).</p><p class="elsevierStylePara"> </p><p class="elsevierStylePara"><span class="elsevierStyleBold">RESULTS</span></p><p class="elsevierStylePara"> </p><p class="elsevierStylePara">We evaluated a total of 251 patients with CKD ranging from stage 1 to stage 5. Their demographical, clinical, and laboratory variables, along with renal pathology and current treatment for phosphocalcic metabolism, are described in Table 1. We obtained reference values for FGF 23 from a sample of 26 healthy individuals.</p><p class="elsevierStylePara">Table 2 shows the results of the different phosphocalcic metabolism parameters during each stage of CKD.</p><p class="elsevierStylePara">FGF 23 levels increased progressively with the stage of CKD (Figure 1), with a statistically significant difference observed when comparing stage 4 patients with stage 1 patients. FGF 23 levels in the healthy reference population were consistently lower.</p><p class="elsevierStylePara">iPTH showed a similar behaviour to FGF 23, with progressively higher values at more advanced stages of CKD and a significant difference reached in stage 4.</p><p class="elsevierStylePara">1,25 OHD<span class="elsevierStyleInf">3</span> decreased consistently, but the high level of variation prevented any statistically significant differences until stage 4 CKD.</p><p class="elsevierStylePara">We did not observe variations in Ca or 25 OHD<span class="elsevierStyleInf">3</span> over the spectrum of renal dysfunction. Ca was consistently normal and 25 OHD<span class="elsevierStyleInf">3</span> was consistently low.</p><p class="elsevierStylePara">P levels did not vary until stage 4, where values were higher than in stage 1.</p><p class="elsevierStylePara">FGF 23 levels were positively correlated with P levels (Figure 2) and iPTH levels (Figure 3), and negatively correlated with glomerular filtration rate (GFR) (Figure 4) and 1,25 vit D<span class="elsevierStyleInf">3</span> (Figure 5).</p><p class="elsevierStylePara">In the multivariate analysis, P, iPTH, and GFR independently explained 55% of the variation in FGF 23 levels (Table 3).</p><p class="elsevierStylePara">Few patients were on active medication regimens (phosphate binders and vitamin D-based); most had stage 5 CKD (Table 1), and their exclusion from the analysis had no influence of study results.</p><p class="elsevierStylePara"> </p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"> </span></p><p class="elsevierStylePara">FGF 23 has been described as an independent progression marker for chronic renal failure, as well as in diabetic patients.<span class="elsevierStyleSup">7</span> It is consistently associated with cardiovascular risk factors, such as left ventricular hypertrophy, atherosclerosis, and vascular dysfunction.<span class="elsevierStyleSup">8</span> Elevated levels are correlated with coronary damage and myocardial dysfunction.<span class="elsevierStyleSup">9</span> In the incident and prevalent population of patients on haemodialysis,<span class="elsevierStyleSup">10</span> these values express the risk of general morbidity/mortality, regardless of other measures of phosphocalcic metabolism. In a large, recent study, FGF 23 was demonstrated to be a strong predictor of mortality in CKD patients.<span class="elsevierStyleSup">11</span></p><p class="elsevierStylePara">According to the medical literature, FGF 23 levels increase progressively as CKD advances, to the point that patients on renal replacement therapy have levels 20 times higher. In the largest study published to date involving 3879 CKD patients of stages ranging from 2 to 4, FGF 23 reached a significant increase once GFR dropped 57.8ml/min/1.73m<span class="elsevierStyleSup">2</span> as compared to a healthy control population.<span class="elsevierStyleSup">12</span> When compared to stage 1 CKD, these differences become significant once stage 4 is reached,<span class="elsevierStyleSup">13</span> as occurred in our study, or stage 3.<span class="elsevierStyleSup">14</span> In other studies, increases have been observed in even earlier stages of CKD.<span class="elsevierStyleSup">15</span> In these phases, the nephron mass is already reduced, and the elevated levels of FGF 23 facilitate increased urine excretion of P.<span class="elsevierStyleSup">16</span> In any case, these early increases impact not only P load, but also the complex relationships between FGF 23 and klotho protein. If chronic renal failure is a state of deficient klotho expression, it will yield a relative resistance to FGF 23, which it turn will increase FGF 23 levels,<span class="elsevierStyleSup">17</span> although in contrast, it has also been described that elevated levels of FGF 23 decrease the expression of klotho.<span class="elsevierStyleSup">18</span></p><p class="elsevierStylePara">It has also been well demonstrated that iPTH levels increase in parallel to FGF 23 levels.<span class="elsevierStyleSup">19</span> Experimental evidence has indicated that iPTH levels increase slightly later than FGF 23 levels, with further support from recent studies.<span class="elsevierStyleSup">20</span> Undoubtedly, the pathogenesis of hyperparathyroidism secondary to FGF 23 plays an important role along with alterations to Ca sensors and vitamin D receptors. FGF 23 activated by klotho inhibits the synthesis of PTH. In a similar manner to the conditions produced in the kidney, the parathyroid glands express less klotho in patients with renal failure, such that secondary hyperparathyroidism can be considered as a state of resistance to FGF 23.<span class="elsevierStyleSup">21</span> We also know that certain levels of PTH are needed to facilitate the action of FGF 23 in the bones and kidneys.<span class="elsevierStyleSup">22</span> Elevated levels of FGF 23 can also prevent the success of treatments for secondary hyperparathyroidism.<span class="elsevierStyleSup">23</span></p><p class="elsevierStylePara">Progressive decreases in 1,25 OHD<span class="elsevierStyleInf">3</span> levels, such as we have observed, have been amply described in the medical literature.<span class="elsevierStyleSup">24</span> The inhibitory effect of FGF 23 on 1-α hydroxylase appears to predominate over the stimulatory effect of increased PTH levels. According to our results, it does not appear likely that decreases in 1,25 OHD<span class="elsevierStyleInf">3</span> can be explained by decreased levels of substrate, 25 OHD<span class="elsevierStyleInf">3</span>, since this molecule is found in reduced levels at an earlier point in time, as a generalised effect of CKD. Although studies have found no correlation between the levels of these two forms of vitamin D,<span class="elsevierStyleSup">25</span> others have observed the opposite.<span class="elsevierStyleSup">26</span> It has also been suggested that FGF 23 toxicity might be partially mediated by deficits of 25 and/or 1,25 vit D<span class="elsevierStyleInf">3</span>.<span class="elsevierStyleSup">27</span> In our study, 25 vit D<span class="elsevierStyleInf">3</span> levels were low at all times, with no progressive decreases such as were observed in the study by Craver.<span class="elsevierStyleSup">28</span> We performed a simultaneous measurement of 25 vit D<span class="elsevierStyleInf">3</span> using a single sampling kit. While we cannot deny that our values may be inappropriately low, we can conclude with complete confidence that these values do not decrease as renal failure progresses. One reason for which we can make this affirmation is the fact that a higher percentage of our study patients with diabetes were in the first stages of renal failure (in the group of patients with GFR>60ml/min/1.73m<span class="elsevierStyleSup">2</span>, the percentage of diabetics was 57.4%; in the group with GFR=30-60ml/min/1.73m<span class="elsevierStyleSup">2</span>, 29.6%; and in the group with GFR<30ml/min/1.73m<span class="elsevierStyleSup">2</span>, 13%). It has been shown that diabetes patients have a greater propensity for 25 vit D<span class="elsevierStyleInf">3</span> deficit.<span class="elsevierStyleSup">29</span></p><p class="elsevierStylePara">The late increase in phosphataemia that we observed in our study is a universally recognised phenomenon.<span class="elsevierStyleSup">30</span></p><p class="elsevierStylePara">While the univariate analysis indicated that increases in FGF 23 were parallel to the decreases in 1,25 vit D<span class="elsevierStyleInf">3</span> (r=-0.40; <span class="elsevierStyleItalic">P</span><.001), the multivariate analysis showed that FGF 23 levels are not independently correlated with 1,25 vit D<span class="elsevierStyleInf">3</span> levels. Previous studies have described several physiological and pathophysiological connections between the levels of these two substances, some direct and others related to other processes. 1,25 OHD<span class="elsevierStyleInf">3</span> stimulates osteocyte synthesis of FGF 23,<span class="elsevierStyleSup">31</span> a mirror image, and closes the self-controlling feedback loop of FGF 23 that inhibits the synthesis of 1,25 OHD<span class="elsevierStyleInf">3</span> by the kidney. In any case, the treatment of hyperparathyroidism with calcitriol and its analogues improves mortality/morbidity profiles, despite the paradoxical increase it produces in FGF 23 levels.<span class="elsevierStyleSup">32</span> Perhaps the increased expression of klotho caused by administering 1,25 vit D<span class="elsevierStyleInf">3</span> plays an important role in this phenomenon.<span class="elsevierStyleSup">33</span> This expression may also increase as a result of blocking the synthesis or activity of angiotensin II.<span class="elsevierStyleSup">34</span> Regardless, the simultaneous use of phosphate binders could diminish the increases in FGF 23 by impeding intestinal absorption of P.<span class="elsevierStyleSup">35</span> Very favourable results have been described with the use of sevelamer,<span class="elsevierStyleSup">36</span> and more recently, with lanthanum.<span class="elsevierStyleSup">37</span> In addition, the combination of cinacalcet and low doses of vitamin D has been shown to be especially useful in modulating increases in FGF 23.<span class="elsevierStyleSup">38</span> Although still not available, long-lasting PTH analogues could, as the expression of renal P transporters (NPT2a/NPT2c) decreases, prevent increases in FGF 23.<span class="elsevierStyleSup">39</span></p><p class="elsevierStylePara">We do not believe that the few patients treated with vitamin D-based and/or phosphate binders, particularly in those on dialysis treatment, may have affected the validity of our data.</p><p class="elsevierStylePara">The previously available information regarding phosphocalcic metabolism in the progression of CKD should be supplemented with data regarding FGF 23. The traditional trade-off hypothesis that establishes hypocalcaemia and P load as the first drivers of decreased 1,25 vit D<span class="elsevierStyleInf">3</span> levels and increased iPTH levels has been modified by the new information regarding FGF 23, which is now establishing itself the primary actor in these procceses.<span class="elsevierStyleSup">40</span></p><p class="elsevierStylePara">In the coming years, clinical practice guidelines will probably define a time for starting treatment with phosphate binders a good deal before the appearance of hyperphosphataemia, based on FGF 23 levels or increased urine excretion of P.<span class="elsevierStyleSup">41</span> The treatment of altered phosphocalcic metabolism in renal failure goes far beyond bone health and directly improves cardiovascular mortality and morbidity profiles.<span class="elsevierStyleSup">42</span></p><p class="elsevierStylePara">We should mention the lack of information regarding urine excretion of P as the most important limitation in our study.</p><p class="elsevierStylePara">To conclude, changes to the paradigm of this condition that have been brought on by new information regarding the physiological and pathophysiological role of FGF 23, which is found in elevated and active levels starting in very early phases of CKD, may oblige us to adopt new attitudes and earlier treatment strategies, all in an attempt to slow the progressive advancement of renal failure and to minimise its impact as a cardiovascular risk factor.</p><p class="elsevierStylePara"> </p><p class="elsevierStylePara"><span class="elsevierStyleBold">Acknowledgements</span></p><p class="elsevierStylePara"> </p><p class="elsevierStylePara">We would like to thank our research fellows Àngels López and Mirta Solà for their collaboration.</p><p class="elsevierStylePara"> </p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"> </p><p class="elsevierStylePara">The authors have no conflicts of interest to declare.</p><p class="elsevierStylePara"><a href="grande/11180_16025_35246_en_t111180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35246_en_t111180.jpg" alt="Patient characteristics"></img></a></p><p class="elsevierStylePara">Table 1. Patient characteristics</p><p class="elsevierStylePara"><a href="grande/11180_16025_35247_en_t211180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35247_en_t211180.jpg" alt="Results according to CKD-EPI glomerular filtration rate"></img></a></p><p class="elsevierStylePara">Table 2. Results according to CKD-EPI glomerular filtration rate</p><p class="elsevierStylePara"><a href="grande/11180_16025_35248_en_t311180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35248_en_t311180.jpg" alt="Factors associated with fibroblast growth factor 23. Multivariate analysis"></img></a></p><p class="elsevierStylePara">Table 3. Factors associated with fibroblast growth factor 23. Multivariate analysis</p><p class="elsevierStylePara"><a href="grande/11180_16025_35249_en_f111180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35249_en_f111180.jpg" alt="Levels of fibroblast growth factor 23 based on stage of chronic kidney disease"></img></a></p><p class="elsevierStylePara">Figure 1. Levels of fibroblast growth factor 23 based on stage of chronic kidney disease</p><p class="elsevierStylePara"><a href="grande/11180_16025_35250_en_f211180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35250_en_f211180.jpg" alt="Association between serum levels of fibroblast growth factor 23 and serum phosphorous levels"></img></a></p><p class="elsevierStylePara">Figure 2. Association between serum levels of fibroblast growth factor 23 and serum phosphorous levels</p><p class="elsevierStylePara"><a href="grande/11180_16025_35251_en_f311180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35251_en_f311180.jpg" alt="Association between serum levels of fibroblast growth factor 23 and serum levels of intact parathyroid hormone"></img></a></p><p class="elsevierStylePara">Figure 3. Association between serum levels of fibroblast growth factor 23 and serum levels of intact parathyroid hormone</p><p class="elsevierStylePara"><a href="grande/11180_16025_35252_en_f411180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35252_en_f411180.jpg" alt="Association between serum levels of fibroblast growth factor 23 and estimated glomerular filtration rate"></img></a></p><p class="elsevierStylePara">Figure 4. Association between serum levels of fibroblast growth factor 23 and estimated glomerular filtration rate</p><p class="elsevierStylePara"><a href="grande/11180_16025_35253_en_f511180.jpg" class="elsevierStyleCrossRefs"><img src="11180_16025_35253_en_f511180.jpg" alt="Association between serum levels of fibroblast growth factor 23 and serum levels of 1,25 OHD3"></img></a></p><p class="elsevierStylePara">Figure 5. Association between serum levels of fibroblast growth factor 23 and serum levels of 1,25 OHD3</p>" "pdfFichero" => "P1-E543-S3677-A11180-EN.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "es" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437647" "palabras" => array:1 [ 0 => "Enfermedad renal crónica (ERC)" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437649" "palabras" => array:1 [ 0 => "Paratohormona (PTH)" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437651" "palabras" => array:1 [ 0 => "Vitamina D (vit D)" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437653" "palabras" => array:1 [ 0 => "Fosfato (P)" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437655" "palabras" => array:1 [ 0 => "Factor de crecimiento fibroblástico 23 (FGF 23)" ] ] ] "en" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437648" "palabras" => array:1 [ 0 => "Chronic kidney disease (CKD)" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437650" "palabras" => array:1 [ 0 => "Parathyroid hormone (PTH)" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437652" "palabras" => array:1 [ 0 => "Vitamin D (vit D)" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437654" "palabras" => array:1 [ 0 => "Phosphate (P)" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437656" "palabras" => array:1 [ 0 => "Fibroblast growth factor 23 (FGF 23)" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "es" => array:1 [ "resumen" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Introducción y objetivos: </span>A pesar de disponer de una información limitada, el conocimiento de los niveles relativos del factor de crecimiento fibrobástico<span class="elsevierStyleItalic"> </span>23 (FGF 23), fosfato (P), calcio (Ca), paratohormona intacta (PTHi) y 25/1,25 vitamina D<span class="elsevierStyleInf">3</span> en cada momento evolutivo de la insuficiencia renal crónica ha aportado datos para sustituir o al menos modificar antiguos paradigmas. Se definen estadios más precoces, se señalan amplias implicaciones pronósticas y se sugieren nuevas intervenciones terapéuticas. Planteamos un estudio transversal-descriptivo y analítico de estos parámetros en una amplia muestra de enfermos distribuidos en todo el espectro de la enfermedad renal crónica. <span class="elsevierStyleBold">Material y métodos: </span>Evaluamos los niveles de FGF 23 con un ELISA de segunda generación que mide molécula intacta (Kainos Laboratories, Japón) en un diseño transversal de una población adulta con todos los estadios de la enfermedad renal crónica basados en CKD-EPI junto a niveles de Ca, P, paratohormona y metabolitos de la vitamina D. <span class="elsevierStyleBold">Resultados: </span>Estudiamos a 251 enfermos (146 hombres y 77 mujeres) con una edad promedio de 62,5 (desviación estándar [DE]: 11,5) años, siendo el 43% de ellos diabéticos. Los niveles de FGF 23 aumentan progresivamente; este cambio es significativo en el estadio 4 en relación con el 1 (110,61 vs. 31,32 ng/l). La PTHi muestra un comportamiento similar. La 1,25 vitamina D baja progresivamente hasta llegar en el estadio 4 a un cambio significativo. Los niveles de Ca no se modifican. Los niveles de 25 vitamina D<span class="elsevierStyleInf">3</span> son bajos en todo momento sin tender a un descenso progresivo. Los niveles de P no se modificaron hasta su aumento en el estadio 4. En el análisis multivariante, los niveles de FGF 23 se correlacionan negativamente con el filtrado glomerular (FG) y positivamente con la PTHi y el P. <span class="elsevierStyleBold">Conclusiones: </span>A lo largo de la enfermedad renal crónica, los incrementos de FGF 23 y PTHi podrían ser los más precoces, seguidos del descenso de 1,25 dihidroxivitamina D<span class="elsevierStyleInf">3</span> (1,25 OHD<span class="elsevierStyleInf">3</span>) y del incremento del P. El Ca y la 25 hidroxivitamina D<span class="elsevierStyleInf">3</span> no se modifican. Los niveles de FGF 23 muestran una sólida relación con el FG estimado, PTHi, 1,25 OHD<span class="elsevierStyleInf">3</span> y P.</p>" ] "en" => array:1 [ "resumen" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Background and Objectives: </span>The ample information available in relation to FGF 23, calcium, phosphorus, PTH, and 25/1,25 vitamin D has allowed us to define consistent values for each variable in each stage of chronic kidney disease (CKD). These values can define early stages, prognostic issues, and new treatment targets. We describe a cross-sectional study of these parameters in patients with different stages of CKD. <span class="elsevierStyleBold">Method: </span>We measured FGF 23 by ELISA (intact molecule, Kainos Laboratory, Japan), calcium, phosphorus, PTH and vit D by standard methods. <span class="elsevierStyleBold">Results: </span>We examined 251 patients, 146 of which were men, with a mean age of 62.5 (11.5) years and 43% prevalence of type II DM. Levels of FGF 23 rose progressively, in a very significant manner, in correlation with the evolution of CKD, especially in stage 4 as compared to stage 1 (110.61ng/L vs 31.32ng/L). The same happened with iPTH values. Additionally, levels of 1,25 vitamin D decreased in a similar manner. Calcium values did not change. 25 vit D3 levels were low at all times and showed no tendency for a steady decline. Phosphorus rose in stage 4 CKD. Levels of FGF 23 were negatively correlated with renal function indicators and positively correlated with PTH and P. <span class="elsevierStyleBold">Conclusions: </span>During the evolution of CKD, changes of FGF 23 and PTH would be the earliest markers. Calcium and 25 vit D3 do not vary with changes in the progression of CKD. Values of FGF 23 show an important correlation with PTH, 1,25 vit D3, P and estimated glomerular filtration rate.</p>" ] ] "multimedia" => array:8 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35246_en_t111180.jpg" "Alto" => 1669 "Ancho" => 1075 "Tamanyo" => 703192 ] ] "descripcion" => array:1 [ "en" => "Patient characteristics" ] ] 1 => array:8 [ "identificador" => "fig2" "etiqueta" => "Tab. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35247_en_t211180.jpg" "Alto" => 515 "Ancho" => 2184 "Tamanyo" => 409608 ] ] "descripcion" => array:1 [ "en" => "Results according to CKD-EPI glomerular filtration rate" ] ] 2 => array:8 [ "identificador" => "fig3" "etiqueta" => "Tab. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35248_en_t311180.jpg" "Alto" => 424 "Ancho" => 2184 "Tamanyo" => 283240 ] ] "descripcion" => array:1 [ "en" => "Factors associated with fibroblast growth factor 23. Multivariate analysis" ] ] 3 => array:8 [ "identificador" => "fig4" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35249_en_f111180.jpg" "Alto" => 824 "Ancho" => 1014 "Tamanyo" => 159304 ] ] "descripcion" => array:1 [ "en" => "Levels of fibroblast growth factor 23 based on stage of chronic kidney disease" ] ] 4 => array:8 [ "identificador" => "fig5" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35250_en_f211180.jpg" "Alto" => 840 "Ancho" => 1014 "Tamanyo" => 152445 ] ] "descripcion" => array:1 [ "en" => "Association between serum levels of fibroblast growth factor 23 and serum phosphorous levels" ] ] 5 => array:8 [ "identificador" => "fig6" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35251_en_f311180.jpg" "Alto" => 904 "Ancho" => 1014 "Tamanyo" => 175097 ] ] "descripcion" => array:1 [ "en" => "Association between serum levels of fibroblast growth factor 23 and serum levels of intact parathyroid hormone" ] ] 6 => array:8 [ "identificador" => "fig7" "etiqueta" => "Fig. 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35252_en_f411180.jpg" "Alto" => 878 "Ancho" => 1010 "Tamanyo" => 171122 ] ] "descripcion" => array:1 [ "en" => "Association between serum levels of fibroblast growth factor 23 and estimated glomerular filtration rate" ] ] 7 => array:8 [ "identificador" => "fig8" "etiqueta" => "Fig. 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11180_16025_35253_en_f511180.jpg" "Alto" => 900 "Ancho" => 1014 "Tamanyo" => 187689 ] ] "descripcion" => array:1 [ "en" => "Association between serum levels of fibroblast growth factor 23 and serum levels of 1,25 OHD3" ] ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:42 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Wolf M. 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Effects of cinacalcet and concurrent low dose vitamin D on FGF 23 levels in ESRD (ACHIEVE Study). Clin J Am Soc Nephrol 2010;5:110-6. <a href="http://www.ncbi.nlm.nih.gov/pubmed/19965548" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 38 => array:3 [ "identificador" => "bib39" "etiqueta" => "39" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Nagai S, Okazaki M, Segawa H, Bergwitz C, Dean T, Potts JT Jr, et al. Acute down-regulation of sodium-dependent phosphate transporter NPT2a involves\u{A0} predominantly the cAMP/PKA pathaway as revealed by signaling-selective parathyroid hormone analogs. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 5 | 8 | 13 |
| 2024 October | 47 | 61 | 108 |
| 2024 September | 44 | 67 | 111 |
| 2024 August | 62 | 109 | 171 |
| 2024 July | 46 | 51 | 97 |
| 2024 June | 71 | 67 | 138 |
| 2024 May | 86 | 61 | 147 |
| 2024 April | 69 | 72 | 141 |
| 2024 March | 57 | 45 | 102 |
| 2024 February | 53 | 50 | 103 |
| 2024 January | 47 | 36 | 83 |
| 2023 December | 38 | 56 | 94 |
| 2023 November | 45 | 40 | 85 |
| 2023 October | 64 | 46 | 110 |
| 2023 September | 49 | 46 | 95 |
| 2023 August | 52 | 28 | 80 |
| 2023 July | 61 | 51 | 112 |
| 2023 June | 73 | 35 | 108 |
| 2023 May | 84 | 62 | 146 |
| 2023 April | 36 | 58 | 94 |
| 2023 March | 83 | 48 | 131 |
| 2023 February | 43 | 29 | 72 |
| 2023 January | 36 | 35 | 71 |
| 2022 December | 82 | 47 | 129 |
| 2022 November | 76 | 33 | 109 |
| 2022 October | 97 | 99 | 196 |
| 2022 September | 59 | 30 | 89 |
| 2022 August | 51 | 48 | 99 |
| 2022 July | 50 | 51 | 101 |
| 2022 June | 61 | 45 | 106 |
| 2022 May | 39 | 28 | 67 |
| 2022 April | 57 | 49 | 106 |
| 2022 March | 51 | 52 | 103 |
| 2022 February | 32 | 46 | 78 |
| 2022 January | 44 | 26 | 70 |
| 2021 December | 45 | 52 | 97 |
| 2021 November | 50 | 48 | 98 |
| 2021 October | 52 | 58 | 110 |
| 2021 September | 44 | 76 | 120 |
| 2021 August | 28 | 56 | 84 |
| 2021 July | 47 | 64 | 111 |
| 2021 June | 37 | 23 | 60 |
| 2021 May | 52 | 40 | 92 |
| 2021 April | 117 | 67 | 184 |
| 2021 March | 79 | 28 | 107 |
| 2021 February | 52 | 25 | 77 |
| 2021 January | 53 | 19 | 72 |
| 2020 December | 35 | 20 | 55 |
| 2020 November | 43 | 16 | 59 |
| 2020 October | 50 | 9 | 59 |
| 2020 September | 27 | 4 | 31 |
| 2020 August | 44 | 11 | 55 |
| 2020 July | 31 | 8 | 39 |
| 2020 June | 51 | 13 | 64 |
| 2020 May | 49 | 15 | 64 |
| 2020 April | 47 | 14 | 61 |
| 2020 March | 52 | 14 | 66 |
| 2020 February | 52 | 15 | 67 |
| 2020 January | 69 | 26 | 95 |
| 2019 December | 71 | 26 | 97 |
| 2019 November | 51 | 21 | 72 |
| 2019 October | 50 | 9 | 59 |
| 2019 September | 33 | 29 | 62 |
| 2019 August | 55 | 14 | 69 |
| 2019 July | 60 | 24 | 84 |
| 2019 June | 70 | 16 | 86 |
| 2019 May | 58 | 13 | 71 |
| 2019 April | 126 | 19 | 145 |
| 2019 March | 44 | 17 | 61 |
| 2019 February | 39 | 17 | 56 |
| 2019 January | 40 | 20 | 60 |
| 2018 December | 108 | 30 | 138 |
| 2018 November | 104 | 18 | 122 |
| 2018 October | 102 | 16 | 118 |
| 2018 September | 70 | 16 | 86 |
| 2018 August | 68 | 15 | 83 |
| 2018 July | 50 | 15 | 65 |
| 2018 June | 73 | 8 | 81 |
| 2018 May | 57 | 8 | 65 |
| 2018 April | 77 | 12 | 89 |
| 2018 March | 75 | 9 | 84 |
| 2018 February | 49 | 8 | 57 |
| 2018 January | 50 | 7 | 57 |
| 2017 December | 49 | 11 | 60 |
| 2017 November | 64 | 9 | 73 |
| 2017 October | 42 | 4 | 46 |
| 2017 September | 41 | 16 | 57 |
| 2017 August | 40 | 44 | 84 |
| 2017 July | 41 | 22 | 63 |
| 2017 June | 48 | 21 | 69 |
| 2017 May | 48 | 30 | 78 |
| 2017 April | 45 | 24 | 69 |
| 2017 March | 37 | 26 | 63 |
| 2017 February | 56 | 18 | 74 |
| 2017 January | 28 | 14 | 42 |
| 2016 December | 85 | 9 | 94 |
| 2016 November | 113 | 14 | 127 |
| 2016 October | 167 | 10 | 177 |
| 2016 September | 273 | 7 | 280 |
| 2016 August | 326 | 12 | 338 |
| 2016 July | 278 | 16 | 294 |
| 2016 June | 157 | 0 | 157 |
| 2016 May | 198 | 0 | 198 |
| 2016 April | 182 | 0 | 182 |
| 2016 March | 111 | 0 | 111 |
| 2016 February | 135 | 0 | 135 |
| 2016 January | 125 | 0 | 125 |
| 2015 December | 153 | 0 | 153 |
| 2015 November | 117 | 0 | 117 |
| 2015 October | 124 | 0 | 124 |
| 2015 September | 127 | 0 | 127 |
| 2015 August | 92 | 0 | 92 |
| 2015 July | 72 | 0 | 72 |
| 2015 June | 36 | 0 | 36 |
| 2015 May | 59 | 0 | 59 |
| 2015 April | 5 | 0 | 5 |
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