Regression of vascular calcification in a patient treated with cinacalcet: A case report
Regresión de la calcificación vascular en un paciente tratado con cinacalcet: informe de un caso
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Salgueira, A.I. Martínez, J.A. Milán" "autores" => array:3 [ 0 => array:4 [ "Iniciales" => "M." "apellidos" => "Salgueira" "email" => array:1 [ 0 => "msalgueira@yahoo.es" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:3 [ "Iniciales" => "A.I." "apellidos" => "Martínez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 2 => array:3 [ "Iniciales" => "J.A." 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(B) Anteroposterior X-ray of left hand in 2007" ] ] ] "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">The presence of vascular calcifications (VC) are traditionally associated with chronic kidney disease (CKD); nevertheless, until recently it had been considered a passive phenomenon with little clinical importance. Over the last decade various epidemiological studies identified vascular calcification as an independent risk factor of cardiovascular mortality, in both the general and uraemic populations.<span class="elsevierStyleSup">1-5</span></p><p class="elsevierStylePara">Although the aetiopathogenic mechanisms of VC are not accurately defined and the factors related to its appearance are multiple, mineral and bone disorders are key factors in this process. Hyperphosphataemia, treatment with vitamin D, calcium salt overdose, hypercalcaemia episodes, remodeling bone disorders, etc., are direct causes of the serious VC load in patients with kidney problems.<span class="elsevierStyleSup">1-6</span></p><p class="elsevierStylePara">To date, VC has been considered an irreversible process, and nephrologists’ efforts had been channelled to slow down its progression.<span class="elsevierStyleSup">6,7</span> Although regression is unlikely, the use of therapeutic alternatives recently available and proper control of hyperparathyroidism (SHPT) have generated expectations.</p><p class="elsevierStylePara">Calcification of the mammary artery detected in the mammography is proof of generalised atherosclerotic vascular disease (ASVD), in both general population and diabetic patients. A mammography is a highly sensitive diagnosis technique for calcification characterisation, including VC; furthermore, it may be a potentially useful tool for diagnosing VC in CKD women.<span class="elsevierStyleSup">8</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT</span><span class="elsevierStyleBold"></span></p><p class="elsevierStylePara">We present the case of a 48-year-old woman with chronic renal failure secondary to tubulointerstitial nephropathy. The patient had received long-term HD replacement treatment and undergone two kidney transplants with transplantectomies: the first one was due to acute humoral rejection and the second due to acute humoral and vascular rejection. She resumed haemodialysis in March 2005.</p><p class="elsevierStylePara">The intact-parathyroid hormone (iPTH) serum values were intermittently high. The patient had been treated previously with calcitriol for short periods of time, since it caused hypercalcaemia and hyperphosphataemia.</p><p class="elsevierStylePara">In January 2006, she presented serious SPTH, with notable increase in iPTH levels. The parathyroid ultrasound revealed an echo-rich pseudo-nodular structure in the posteriomedial area of the left thyroid lobe, compatible with parathyroid gland hypertrophy. A series of X-rays showed signs of hyperparathyroidism in the bones of both hands and wrists, with VC in radial and interdigital arteries. The mammography revealed multiple linear VC in both breasts (Figures: 1A, 2A, 3A and 4A; hand and mammary gland images in 2006).</p><p class="elsevierStylePara">The patient was only treated with calcium carbonate initially. Later, oral calcitriol and sevelamer (800mg with main meals), a phosphate-binding agent (P), were added to the treatment and calcium carbonate dose was reduced. Figure 5 shows Ca, P and serum iPTH levels. Hyperphosphataemia was controlled after 2 months’ treatment and the Ca-P product was adequate; however, iPTH levels increased to 734pg/ml, so treatment was changed. Oral calcitriol was replaced with 30mg of oral cinacalcet once a day and intravenous alfacalcidol (2µg) was given immediately after haemodialysis. Calcium carbonate and sevelamer doses were not adjusted.</p><p class="elsevierStylePara">Two months later, the calcimimetic dose was reduced due to hypocalcaemia (7.6mg/dl). Intravenous vitamin D and calcium carbonate treatment was maintained, and the dialysate calcium changed from 2.5 to 3mEq/l.</p><p class="elsevierStylePara">During the following 6 months, all the parameter levels were maintained within the interval recommended by the KDOQI guidelines. In November 2006 excessive supression of iPTH (138pg/ml) and a potential hypercalcaemia (9.4mg/dl) were noticed, so treatment with calcium carbonate and alfacalcidol was suspended. In January 2007 treatment continued with sevelamer (800mg with main meals) and a minimum weekly dose of calcimimetic (30mg cinacalcet MMondays and Ffridays), resulting in good control of mineral and bone metabolism.</p><p class="elsevierStylePara">During this period, the X-ray series showed that the interdigital artery calcifications had disappeared, and the bone appeared better structured (Figures 1B and 2B; hand X-ray, 2007). The mammography also showed regression of the VC. Initial linear calcifications were replaced by irregular calcifications (Figures 3B and 4B; mammary glands in 2007).</p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">The metabolic mineral and bone disorder associated with CKD (MBD-CKD) is defined as a progressive multifactor systemic disorder, which includes a series of biochemical disorders, bone anomalies and abnormal extra-skeletal calcifications appearing in patients with CKD. Each of these complications results in serious clinical consequences that cause, in turn, increased morbimortality in uraemic patients.<span class="elsevierStyleSup">9</span></p><p class="elsevierStylePara">The presence of VC alters vascular function and structure, which are responsible for the appearance of potentially fatal cardiovascular events like ischaemic heart disease, heart failure, stroke and peripheral vascular disease (PVD). Clinical studies have demonstrated association between the presence of calcification in the arterial intima and/or media layers and a greater risk of cardiovascular and overall mortality.<span class="elsevierStyleSup">1-6</span></p><p class="elsevierStylePara">As a consequence, in recent years, the examination of patients to determine the presence of VC has become an essential part of nephrologists’ daily clinical practice. The aim of KDOQI guidelines and KDIGO proposals is to make an early diagnosis, and individualise treatments to prevent their appearance or reduce their progression, since once established, regression is highly unlikely.<span class="elsevierStyleSup">7,9-11</span><span class="elsevierStyleSup"> </span></p><p class="elsevierStylePara">Traditional treatments for SPTH and mineral and bone disorders (a diet low in P, calcium-based phosphate binders and vitamin D supplements) are insufficient for most patients and have often resulted in widespread VC. High concentrations of P, Ca and Ca-P product predispose to VC and increase the risk of adverse cardiovascular events.<span class="elsevierStyleSup">1-6,9-11</span> Therefore, the treatment should meet the clinical practice guideline criteria as far as possible to minimise adverse effects.</p><p class="elsevierStylePara">In our patient, use of cinacalcet in combination with vitamin D normalised the Ca, P, Ca-P product and iPTH levels, and managed to keep them within the recommended ranges.</p><p class="elsevierStylePara">Different clinical studies carried out with cinacalcet have demonstrated its efficacy in achieving proper control of biochemical disorders associated with MBD-CKD, and that the combined treatment of cinacalcet and vitamin D enable reduction of the necessary vitamin D doses thereby reducing its side effects.<span class="elsevierStyleSup">12-15</span><span class="elsevierStyleSup"> </span>In this case, the combination of cinacalcet and intravenous vitamin D treatment enabled correct control of iPTH levels without determining the appearance of hypercalcaemia or hyperphosphoraemia. Hypercalcaemia and hyperphosphoraemia appear when only vitamin D is administered, due to greater intestinal absorption of Ca and P. However, Ca and P serum concentrations are reduced with cinacalcet, as this reduces the flow from the bone in response to PTH reduction, without an additional intestinal mineral source.<span class="elsevierStyleSup">16</span> The combined use of both drugs reduces the undesirable effects of vitamin D by mutually counteracting and increasing the inhibition of PTH secretion, thus achieving better control of the biochemical disorders associated with MBD-CKD.</p><p class="elsevierStylePara">Experimental trials performed on animals have demonstrated that the addition of calcimetics to treatment significatively reduces VC in rats treated with calcitriol and paricalcitol, moreover it may induce regression of extra-osseous calcification. Uraemic rats treated with calcimimetic agents presented a reduction in aortic wall thickness with an increase in calcium receptor expression on the vascular intima and reduction of VC.<span class="elsevierStyleSup">17-19</span> This protective effect of cinacalcet against VC has also been published in clinical cases of human patients with CDK and SPTH, as with the case in hand.<span class="elsevierStyleSup">20,21</span></p><p class="elsevierStylePara">Calcium-free binding agents like sevelamer delay development of calcifications and improve their appearance when compared with calcium salts; moreover, they have been associated with a reduction in mortality.<span class="elsevierStyleSup">22-24</span><span class="elsevierStyleSup"> </span>Nevertheless, many studies have shown that the ingestion of calcium salts and subsequent calcium accumulation in the body is associated with VC.<span class="elsevierStyleSup">1-6,24</span> In this case both binding agents were used. It is a proven fact that the use of cinacalcet is usually associated with an increase in the calcium carbonate dose.<span class="elsevierStyleSup">25,26</span> In this patient, calcium salts were necessary to control hypocalcaemia, initially induced by treatment with cinacalcet. One can see in the initial months that the patient presented a negative calcium balance, which we consider could have been decisive in VC regression in this case. Therefore, the therapeutic treatment used in this patient combining the synergic and antagonistic effects of the drugs used, was highly efficient in controlling SHPT and led to VC regression.</p><p class="elsevierStylePara">Regression is evident in the mammographies, where we see how linear calcification was replaced by smaller areas of patchy irregular calcification. The images show how clearly VC can be seen in the mammographies, enabling accurate follow-up of their evolution. This is therefore a useful economic and accessible technique for VC diagnosis and follow-up in women with CKD.<span class="elsevierStyleSup">8,27</span><span class="elsevierStyleSup"> </span>The presence of VC in a mammography is considered a cardiovascular risk marker in the general population, which is related to atherosclerosis and diabetes mellitus. However, for the uraemic population, a recently published study establishes the existence of histological correlation between CV presence in a mammography and calcification of the medial layer in arteries.<span class="elsevierStyleSup">28</span> Whereas calcification on the arterial intima is essentially related to atheromatosis and inflammation, medial artery calcification has a greater relation to CKD and associated metabolic disorders.<span class="elsevierStyleSup">5</span> In this case, given that it is a young woman without additional cardiovascular risks, one might consider that the calcification present in the mammary glands was more related to CKD and mainly affected the medial layer. Were this the case, regression of the mammary calcifications observed could be justified by the correct control of MBD-CKD disorders, since this regression would be unlikely in other patients in whom the VC at the arterial intima and media layers converge due to the interaction of many other factors, thus making the desired regression difficult to achieve.</p><p class="elsevierStylePara">To conclude, this case has demonstrated that the use of the right treatment can lead to VC regression, and shows the potentially beneficial effect of the calcimimetic in its regression. </p><p class="elsevierStylePara"><a href="grande/10869_108_21698_en_f1_a_y_b_10869.jpg" class="elsevierStyleCrossRefs"><img src="10869_108_21698_en_f1_a_y_b_10869.jpg" alt="(A) Anteroposterior X-ray of left hand in 2006. (B) Anteroposterior X-ray of left hand in 2007"></img></a></p><p class="elsevierStylePara">Figure 1. (A) Anteroposterior X-ray of left hand in 2006. (B) Anteroposterior X-ray of left hand in 2007</p><p class="elsevierStylePara"><a href="grande/10869_108_21699_en_f2_a_y_b_10869.jpg" class="elsevierStyleCrossRefs"><img src="10869_108_21699_en_f2_a_y_b_10869.jpg" alt="(A) Anteroposterior X-ray of right hand in 2006. (B) Anteroposterior X-ray of right hand in 2007"></img></a></p><p class="elsevierStylePara">Figure 2. (A) Anteroposterior X-ray of right hand in 2006. (B) Anteroposterior X-ray of right hand in 2007</p><p class="elsevierStylePara"><a href="grande/10869_108_21700_en_f3_a_y_b_10869.jpg" class="elsevierStyleCrossRefs"><img src="10869_108_21700_en_f3_a_y_b_10869.jpg" alt="(A) Anteroposterior X-ray of mammary gland in 2006. (B) Anteroposterior X-ray of mammary gland in 2007"></img></a></p><p class="elsevierStylePara">Figure 3. (A) Anteroposterior X-ray of mammary gland in 2006. (B) Anteroposterior X-ray of mammary gland in 2007</p><p class="elsevierStylePara"><a href="grande/10869_108_21701_en_f4_a_y_b_10869.jpg" class="elsevierStyleCrossRefs"><img src="10869_108_21701_en_f4_a_y_b_10869.jpg" alt="(A) Craniocaudal breast X-ray in 2006. (B) Craniocaudal breast X-ray in 2007"></img></a></p><p class="elsevierStylePara">Figure 4. (A) Craniocaudal breast X-ray in 2006. (B) Craniocaudal breast X-ray in 2007</p><p class="elsevierStylePara"><a href="grande/10869_108_21702_en_f5_10869.jpg" class="elsevierStyleCrossRefs"><img src="10869_108_21702_en_f5_10869.jpg" alt="Evolution of Ca, P and serum iPTH levels"></img></a></p><p class="elsevierStylePara">Figure 5. Evolution of Ca, P and serum iPTH levels</p>" "pdfFichero" => "P1-E524-S3342-A10869-EN.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "es" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec440671" "palabras" => array:1 [ 0 => "Insuficiencia renal crónica" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec440676" "palabras" => array:1 [ 0 => "Hiperparatiroidismo secundario" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec440679" "palabras" => array:1 [ 0 => "Mamografía" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec440681" "palabras" => array:1 [ 0 => "Cinacalcet" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec440683" "palabras" => array:1 [ 0 => "Calcificación vascular" ] ] ] "en" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec440674" "palabras" => array:1 [ 0 => "Chronic kidney disease" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec440678" "palabras" => array:1 [ 0 => "Secondary hyperparathyroidism" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec440680" "palabras" => array:1 [ 0 => "Mammography" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec440682" "palabras" => array:1 [ 0 => "Cinacalcet" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec440684" "palabras" => array:1 [ 0 => "Vascular calcification" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:1 [ "resumen" => "<p class="elsevierStylePara">The purpose of this case report is to describe the regression of vascular calcifications (VC) in a patient with secondary hyperparathyroidism (SHPT) after having added cinacalcet to her treatment. We present the clinical case of a 48-year-old woman with chronic renal failure secondary to tubulointerstitial disease. She was being treated with long-term haemodialysis (HD) and underwent two kidney transplants with transplantectomies. The patient presented with severe SHPT caused by parathyroid gland hypertrophy. The radiology test showed signs of VC in the radial and interdigital arteries, and VC in a linear arrangement were observed in both breasts on the mammography. Cinacalcet was added to her treatment with vitamin D derivatives and phosphate-binding agents, which resulted in a good control of mineral metabolism. The radiology test showed that the calcification in the interdigital artery had disappeared and that the bone appeared to be more structured. The mammography also showed regression of the VC. To conclude, cinacalcet may have potential for regression of VC in patients with SHPT.</p>" ] "es" => array:1 [ "resumen" => "<p class="elsevierStylePara">El propósito de este informe de caso es describir la regresión de las calcificaciones vasculares (CV) en una paciente con hiperparatiroidismo secundario (HPTS) tras añadir cinacalcet a su tratamiento. Presentamos un caso clínico de una mujer de 48 años de edad con insuficiencia renal crónica secundaria a nefropatía túbulo-intersticial, tratada con hemodiálisis (HD) de larga duración y sometida a dos trasplantes renales con trasplantectomías. La paciente presentaba HPTS grave causado por la hipertrofia de la glándula paratiroidea; la radiología mostró signos de CV en las arterias radiales e interdigitales y la mamografía, CV lineales múltiples en ambas mamas. Se añadió cinacalcet al tratamiento previo con derivados de la vitamina D y agentes quelantes del fósforo, lo que dio como resultado un buen control del metabolismo mineral. La radiología mostró que las calcificaciones de la arteria interdigital habían desaparecido y que el hueso presentaba un aspecto más estructurado. La mamografía también mostró una regresión de las CV. En conclusión, cinacalcet puede tener potencial para la regresión de las CV en pacientes con HPTS.</p>" ] ] "multimedia" => array:5 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10869_108_21698_en_f1_a_y_b_10869.jpg" "Alto" => 243 "Ancho" => 600 "Tamanyo" => 108899 ] ] "descripcion" => array:1 [ "en" => "(A) Anteroposterior X-ray of left hand in 2006. (B) Anteroposterior X-ray of left hand in 2007" ] ] 1 => array:8 [ "identificador" => "fig2" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10869_108_21699_en_f2_a_y_b_10869.jpg" "Alto" => 255 "Ancho" => 600 "Tamanyo" => 105767 ] ] "descripcion" => array:1 [ "en" => "(A) Anteroposterior X-ray of right hand in 2006. (B) Anteroposterior X-ray of right hand in 2007" ] ] 2 => array:8 [ "identificador" => "fig3" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10869_108_21700_en_f3_a_y_b_10869.jpg" "Alto" => 202 "Ancho" => 600 "Tamanyo" => 105442 ] ] "descripcion" => array:1 [ "en" => "(A) Anteroposterior X-ray of mammary gland in 2006. (B) Anteroposterior X-ray of mammary gland in 2007" ] ] 3 => array:8 [ "identificador" => "fig4" "etiqueta" => "Fig. 4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10869_108_21701_en_f4_a_y_b_10869.jpg" "Alto" => 472 "Ancho" => 600 "Tamanyo" => 184962 ] ] "descripcion" => array:1 [ "en" => "(A) Craniocaudal breast X-ray in 2006. (B) Craniocaudal breast X-ray in 2007" ] ] 4 => array:8 [ "identificador" => "fig5" "etiqueta" => "Fig. 5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "10869_108_21702_en_f5_10869.jpg" "Alto" => 356 "Ancho" => 600 "Tamanyo" => 117526 ] ] "descripcion" => array:1 [ "en" => "Evolution of Ca, P and serum iPTH levels" ] ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:28 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Block GA, Hulbert-Shearon TE, Levin NW, Port FK. Association of serum phosphorus and Ca x phosphate product with mortality risk in chronic hemodialysis patients: a national study. 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Achieving NKF-K/DOQI bone metabolism and disease treatment goals with cinacalcet HCl. Kidney Int 2005;67:760-71. <a href="http://www.ncbi.nlm.nih.gov/pubmed/15673327" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 16 => array:3 [ "identificador" => "bib17" "etiqueta" => "17" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "López I, Mendoza FJ, Aguilera-Tejero E, Pérez J, Guerrero F, Martín D, et al.\u{A0}The effect of calcitriol, paricalcitol, and a calcimimetic on extraosseous calcifications in uremic rats. 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Kidney Int 2009;75(1):60-71. <a href="http://www.ncbi.nlm.nih.gov/pubmed/19092814" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 19 => array:3 [ "identificador" => "bib20" "etiqueta" => "20" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Zerbi S, Ruggiero P, Pedrini LA. Massive soft tissue calcifications and cinacalcet. J Clin Endocrinol Metab 2008;93(4):1121-2. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18390810" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 20 => array:3 [ "identificador" => "bib21" "etiqueta" => "21" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Aladrén Regidor MJ. Cinacalcet reduces vascular and soft tissue calcification in secondary hyperparathiroidism (SHPT) in hemodialysis patients. 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Kidney Int 2002;62(1):245-52. <a href="http://www.ncbi.nlm.nih.gov/pubmed/12081584" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 23 => array:3 [ "identificador" => "bib24" "etiqueta" => "24" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Block GA, Spiegel DM, Ehrlich J, Mehta R, Lindbergh J, Driesbach A, et al. Effects of sevelamer and calcium on coronary artery calcification in patients new to hemodialysis. Kidney Int 2005;68:1815-24. <a href="http://www.ncbi.nlm.nih.gov/pubmed/16164659" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 24 => array:3 [ "identificador" => "bib25" "etiqueta" => "25" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Arenas MD, Rebollo P, Álvarez Ude F, Prieto L, Gil MT, Malek T, et al.\u{A0}¿Es el cinacalcet un tratamiento coste-efectivo en el hiperparatiroidismo secundario severo en pacientes en hemodiálisis? Nefrologia 2008;28(5):511-6. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18816209" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 25 => array:3 [ "identificador" => "bib26" "etiqueta" => "26" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Segura Torres P, Borrego Utiel FJ, Sánchez Perales MC, García Cortés MJ, Bienchy Baldán MM, Pérez Bañasco V. Análisis de eficacia y de los factores que influyen en la respuesta del hiperparatiroidismo secundario de pacientes en hemodiálisis a cinacalcet. Nefrologia 2010;30(4):443-51. <a href="http://www.ncbi.nlm.nih.gov/pubmed/20651886" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:1 [ "itemHostRev" => array:3 [ "pii" => "S073510970901732X" "estado" => "S300" "issn" => "07351097" ] ] ] ] ] ] ] 26 => array:3 [ "identificador" => "bib27" "etiqueta" => "27" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Canabal A, Sabaté J, Salgueira M, Palma A. Cardiovascular risk in women with chronic renal failure: mammographic study of vascular calcifications. Radiologia 2008;50:54-60. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18275790" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] 27 => array:3 [ "identificador" => "bib28" "etiqueta" => "28" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Duhn V, D¿Orsi ET, Johnson S, D¿Orsi DJ, Adams ML, O¿Neill WC. Breast arterial calcification: a marker of medial vascular calcification in chronic kidney disease. Clin J Am Soc Nephrol 2011;6:377-82.\u{A0} <a href="http://www.ncbi.nlm.nih.gov/pubmed/21258037" target="_blank">[Pubmed]</a>" "contribucion" => array:1 [ 0 => null ] "host" => array:1 [ 0 => null ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/20132514/0000003100000005/v0_201502091634/X201325141105248X/v0_201502091634/en/main.assets" "Apartado" => array:4 [ "identificador" => "35422" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Case Reports" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/20132514/0000003100000005/v0_201502091634/X201325141105248X/v0_201502091634/en/P1-E524-S3342-A10869-EN.pdf?idApp=UINPBA000064&text.app=https://revistanefrologia.com/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X201325141105248X?idApp=UINPBA000064" ]
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| 2023 June | 46 | 27 | 73 |
| 2023 May | 57 | 34 | 91 |
| 2023 April | 46 | 16 | 62 |
| 2023 March | 55 | 23 | 78 |
| 2023 February | 38 | 26 | 64 |
| 2023 January | 46 | 20 | 66 |
| 2022 December | 51 | 27 | 78 |
| 2022 November | 64 | 44 | 108 |
| 2022 October | 47 | 52 | 99 |
| 2022 September | 38 | 27 | 65 |
| 2022 August | 43 | 39 | 82 |
| 2022 July | 41 | 52 | 93 |
| 2022 June | 40 | 32 | 72 |
| 2022 May | 38 | 31 | 69 |
| 2022 April | 46 | 43 | 89 |
| 2022 March | 55 | 47 | 102 |
| 2022 February | 46 | 28 | 74 |
| 2022 January | 35 | 31 | 66 |
| 2021 December | 31 | 33 | 64 |
| 2021 November | 36 | 36 | 72 |
| 2021 October | 37 | 37 | 74 |
| 2021 September | 54 | 37 | 91 |
| 2021 August | 52 | 32 | 84 |
| 2021 July | 36 | 36 | 72 |
| 2021 June | 64 | 21 | 85 |
| 2021 May | 40 | 36 | 76 |
| 2021 April | 64 | 29 | 93 |
| 2021 March | 59 | 36 | 95 |
| 2021 February | 60 | 20 | 80 |
| 2021 January | 50 | 27 | 77 |
| 2020 December | 46 | 15 | 61 |
| 2020 November | 36 | 7 | 43 |
| 2020 October | 23 | 22 | 45 |
| 2020 September | 28 | 12 | 40 |
| 2020 August | 39 | 24 | 63 |
| 2020 July | 46 | 8 | 54 |
| 2020 June | 40 | 21 | 61 |
| 2020 May | 43 | 20 | 63 |
| 2020 April | 40 | 25 | 65 |
| 2020 March | 40 | 15 | 55 |
| 2020 February | 46 | 27 | 73 |
| 2020 January | 66 | 28 | 94 |
| 2019 December | 61 | 30 | 91 |
| 2019 November | 36 | 32 | 68 |
| 2019 October | 34 | 14 | 48 |
| 2019 September | 51 | 25 | 76 |
| 2019 August | 26 | 13 | 39 |
| 2019 July | 55 | 26 | 81 |
| 2019 June | 44 | 17 | 61 |
| 2019 May | 44 | 22 | 66 |
| 2019 April | 100 | 46 | 146 |
| 2019 March | 29 | 21 | 50 |
| 2019 February | 30 | 22 | 52 |
| 2019 January | 48 | 15 | 63 |
| 2018 December | 91 | 42 | 133 |
| 2018 November | 128 | 23 | 151 |
| 2018 October | 102 | 24 | 126 |
| 2018 September | 89 | 17 | 106 |
| 2018 August | 62 | 19 | 81 |
| 2018 July | 83 | 14 | 97 |
| 2018 June | 53 | 14 | 67 |
| 2018 May | 69 | 17 | 86 |
| 2018 April | 48 | 6 | 54 |
| 2018 March | 62 | 6 | 68 |
| 2018 February | 44 | 9 | 53 |
| 2018 January | 40 | 5 | 45 |
| 2017 December | 55 | 7 | 62 |
| 2017 November | 73 | 7 | 80 |
| 2017 October | 70 | 11 | 81 |
| 2017 September | 40 | 8 | 48 |
| 2017 August | 45 | 9 | 54 |
| 2017 July | 39 | 5 | 44 |
| 2017 June | 54 | 11 | 65 |
| 2017 May | 59 | 11 | 70 |
| 2017 April | 59 | 17 | 76 |
| 2017 March | 61 | 10 | 71 |
| 2017 February | 128 | 16 | 144 |
| 2017 January | 58 | 12 | 70 |
| 2016 December | 81 | 9 | 90 |
| 2016 November | 111 | 16 | 127 |
| 2016 October | 190 | 12 | 202 |
| 2016 September | 193 | 1 | 194 |
| 2016 August | 200 | 10 | 210 |
| 2016 July | 154 | 11 | 165 |
| 2016 June | 155 | 0 | 155 |
| 2016 May | 129 | 0 | 129 |
| 2016 April | 123 | 0 | 123 |
| 2016 March | 108 | 0 | 108 |
| 2016 February | 137 | 0 | 137 |
| 2016 January | 109 | 0 | 109 |
| 2015 December | 138 | 0 | 138 |
| 2015 November | 102 | 0 | 102 |
| 2015 October | 112 | 0 | 112 |
| 2015 September | 86 | 0 | 86 |
| 2015 August | 65 | 0 | 65 |
| 2015 July | 92 | 0 | 92 |
| 2015 June | 42 | 0 | 42 |
| 2015 May | 46 | 0 | 46 |
| 2015 April | 8 | 0 | 8 |
Show all
