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but it decreases progressively in the first year and remains practically stable at around 5-10&#37; thereafter&#46;<span class="elsevierStyleSup">2-5</span></p><p class="elsevierStylePara">Until the introduction of the management guidelines for mineral and bone metabolism disorders in patients with chronic kidney disease in 2003&#44;<span class="elsevierStyleSup">6</span> the series of patients compiled showed a higher incidence and prevalence of post-RT hypercalcemia&#46; In fact&#44; in 1973&#44; hypercalcemia prevalence above 30&#37; was reported one year after the RT&#44; which persisted practically unchanged 2 and 5 years after transplantation&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">Following the introduction of the guidelines and their clinical application&#44; there appeared to be a turning point in the prevalence of post-transplantation hypercalcemia&#46; This was the case when patients studied between 2004 and 2006 were compared to a hostoric control group of patients studied between 1989 and 2002&#44;<span class="elsevierStyleSup">1&#44;2</span> in which we observed a 41&#37; prevalence of hypercalcemia in the historic group&#44; while in the more recent group&#44; it had been reduced to 14&#37;&#46;</p><p class="elsevierStylePara">Nevertheless&#44; most studies on post-RT calcium metabolism were carried out prior to the introduction of cinacalcet for the treatment of secondary hyperparathyroidism &#40;HPT&#41; in dialysis patients&#46;</p><p class="elsevierStylePara">Cinacalcet was approved by the United States Food and Drug Administration in 2004 and by the European Medicines Agency in 2005 to treat secondary HPT in dialysis patients&#44; and subsequently&#44; to treat parathyroid carcinoma and primary HPT&#46; The efficacy of cinacalcet for controlling the parathyroid hormone &#40;PTH&#41; in dialysis patients has been widely demonstrated&#46;<span class="elsevierStyleSup">7-10</span></p><p class="elsevierStylePara">The better control of secondary HPT in dialysis patients after the introduction of cinacalcet probably has an effect on mineral and bone metabolism disorders after RT&#44; although few studies have been carried out in this regard&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CAUSES OF HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Studies from the era prior to the introduction of cinacalcet showed that high serum PTH values were the main predictor of post-transplantation hypercalcemia&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">The introduction of cinacalcet has resulted in a better control of secondary HPT&#44; and as such&#44; there has been a decrease in the percentage of patients who undergo RT with high serum PTH values&#46; However&#44; withdrawing cinacalcet after RT results in high PTH levels immediately after transplantation&#44; and consequently&#44; hypercalcemia in a high number of patients&#46;<span class="elsevierStyleSup">11</span></p><p class="elsevierStylePara">In a recent study&#44; although carried out on a small number of patients&#44; this was also observed and patients on treatment with cinacalcet before transplantation whose treatment was discontinued on the day of surgery displayed a higher hypercalcemia incidence &#40;corrected Ca &#62;10&#46;3mg&#47;dl&#41; three months after transplantation than those patients who had not received cinacalcet &#40;42&#46;9&#37; vs&#46; 11&#46;4&#37;&#41; &#46;<span class="elsevierStyleSup">12</span></p><p class="elsevierStylePara">In our experience&#44; when we compared patients who received cinacalcet at the time of RT and those who did not receive it&#44; we found a hypercalcemia proportion &#40;corrected Ca &#62; 10&#46;3mg&#47;dl&#41; of 26&#46;3&#37; 3 months after transplantation compared with 0&#37; hypercalcemia in the control group &#40;<span class="elsevierStyleItalic">P</span>&#61;&#46;01&#41;&#44; despite both groups displaying similar PTH and calcaemia values at the time of transplantation&#46;<span class="elsevierStyleSup">13</span></p><p class="elsevierStylePara">Studies subsequent to the introduction of cinacalcet showed that pre-transplantation PTH only influenced post-transplantation Ca values in patients who were not on treatment with cinacalcet&#44; while&#44; in patients who received cinacalcet prior to RT&#44; it was the cinacalcet dose that predicted the subsequent development of HPT and hypercalcemia&#44; being a marker for the severity of secondary HPT in these patients&#46;<span class="elsevierStyleSup">11&#44;12</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">PHYSIOPATHOLOGY</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The physiopathological mechanisms suggested as responsible for post-transplantation hypercalcemia are&#58;</p><p class="elsevierStylePara">- More tubular calcium reabsorption&#44; due to PTH action&#46; The results of different studies are disparate&#59; while some show a decrease in fractional calcium excretion&#44;<span class="elsevierStyleSup">1 </span>others refer to greater urinary calcium excretion&#46;<span class="elsevierStyleSup">3</span> It seems that the effect of PTH increasing tubular calcium reabsorption would be more evident in the long term and less evident immediately after transplantation&#46;<span class="elsevierStyleSup">1&#44;3</span></p><p class="elsevierStylePara">- More intestinal calcium absorption&#44; due to increased serum calcitriol caused by the increase in its synthesis due to PTH stimulation&#46; Serum calcitriol values gradually recover in most patients after RT and we have observed that this is in relation to the rapid and progressive decrease in serum FGF23 &#40;fibroblast growth factor 23&#41; values&#46;<span class="elsevierStyleSup">13</span> Nevertheless&#44; no study has shown differences in calcitriol values between patients with hypercalcemia and normocalcemia&#46;<span class="elsevierStyleSup">1&#44;2</span></p><p class="elsevierStylePara">- More bone calcium resorption&#44; mediated by the PTH&#46; This seems to be the mechanism involved particularly in recent RT&#46; In patients with hypercalcemia&#44; we observed significantly higher serum alkaline phosphatase values than in normocalcaemic patients&#44; which suggests an increased bone turnover&#46;<span class="elsevierStyleSup">1</span><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONSEQUENCES OF</span><span class="elsevierStyleBold">HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">- Effect on the kidney graft&#46; Hypercalcemia&#44; through a vasoconstriction mechanism may impair renal graft function&#44; both acutely and chronically&#46;<span class="elsevierStyleSup">3&#44;14 </span>It may also cause tubulointerstitial calcifications that may have a negative influence on long-term graft survival&#46;<span class="elsevierStyleSup">15</span></p><p class="elsevierStylePara">- Other effects<span class="elsevierStyleBold"><span class="elsevierStyleItalic">&#46;</span></span> Cases of pancreatitis have been reported in <br></br> renal transplant patients with hypercalcemia due to HPT&#44;<span class="elsevierStyleSup">16</span> and it has also been demonstrated that it increases the risk of soft tissue calcification and the development of vascular calcification&#46;<span class="elsevierStyleSup">17</span></p><p class="elsevierStylePara">Hypercalcemia is fundamentally the result of an increase in bone remodelling with increased calcium reabsorption&#44; and as such&#44; persistent hypercalcemia will indicate that there is an increased risk of bone disease deterioration in these patients&#46;<span class="elsevierStyleSup">16&#44;18</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">MANAGEMENT OF POST-TRANSPLANTATION HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">To manage hypercalcemia due to persistent HPT following RT&#44; the alternatives are&#58;</p><p class="elsevierStylePara">a&#41; Watchful waiting&#46; Initial action&#44; in the case of moderate hypercalcemia may be to monitor serum calcium and PTH values while waiting for them to normalise over time&#46; However&#44; when there is significant hypercalcemia &#40;&#62; 11mg&#47;dl&#41; and&#47;or it persists over time &#40;&#62; 1 year&#41;&#44; or it is symptomatic&#44; we should take a more proactive approach&#46;</p><p class="elsevierStylePara">In our opinion&#44; shared by others&#44;<span class="elsevierStyleSup">19</span> in the absence of symptoms or significant hypercalcemia&#44; it would be prudent to wait at least a year for spontaneous resolution&#44; although some authors advocate waiting only 3-6 months after RT before opting for parathyroidectomy&#46;<span class="elsevierStyleSup">20</span></p><p class="elsevierStylePara">b&#41; Parathyroidectomy&#46; Traditionally&#44; it was the only alternative for controlling hypercalcemia in these patients and it remains the best option for correcting hypercalcemia when compared with calcimimetics&#46;<span class="elsevierStyleSup">21</span> However&#44; 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A total parathyroidectomy with autotransplantation in the forearm results in quicker calcemia correction&#59; however&#44; there is a higher risk of hypocalcaemia&#46;&#160;</p><p class="elsevierStylePara">In patients with a functioning RT&#44; the recurrence rate appears to be similar for this technique and subtotal parathyroidectomy&#46;<span class="elsevierStyleSup">28</span></p><p class="elsevierStylePara">In the event of recurrence&#47;persistence&#44; it is sometimes difficult to discern whether this is due to a hyperplasia of the autotransplant or residual tissue in the cervical area&#46; In this case&#44; mibi scintigraphy may help us&#46;<span class="elsevierStyleSup">29</span></p><p class="elsevierStylePara">The gland autotransplanted in the forearm in the event of recurrence seems to be more accesible&#44;<span class="elsevierStyleSup">30</span> but&#44; in the case of significant hyperplasia &#40;also called parathyromatosis&#41; it usually spreads in the implant area and is normally very difficult to remove&#46;</p><p class="elsevierStylePara">This involves the removal of all the parathyroid glands except for the remainder of a well-vascularised gland the size of a normal gland&#46; 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If with the cervical ultrasound examination and&#47;or MIBI scintigraphy it is shown that there are one or two adenomatous glands&#44; some authors advocate removing only those pathological glands &#40;enlarged and&#47;or with increased uptake&#41;&#46;</p><p class="elsevierStylePara">With this technique&#44; the acute hypocalcaemia percentage is less than with the previous techniques and the percentage of persistent hypocalcaemia is almost nil&#46;<span class="elsevierStyleSup">16&#44;35</span> By contrast&#44; it appears to increase the risk of persistence&#47;recurrence of HPT&#44;<span class="elsevierStyleSup">28&#44;36</span> although there are also series that show good progression and low incidence of recurrence&#46;<span class="elsevierStyleSup">16&#44;35&#44;37</span></p><p class="elsevierStylePara">c&#41; Calcimimetics&#46; Since 2006&#44; calcimimetics have been employed as an alternative treatment for hypercalcemia secondary to persistent secondary HPT &#40;also called tertiary HPT&#41; in patients with a functioning RT&#46;<span class="elsevierStyleSup">38-46</span>&#160;<span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">In all published studies&#44; the appropriate control of calcemia was confirmed with an improvement in serum PTH and phosphatemia&#46;</p><p class="elsevierStylePara">In the majority of these studies&#44; effects on renal function were not reported&#44; although in some exceptional cases a slight deterioration in renal function after three months<span class="elsevierStyleSup">44</span> or after one year on treatment with cinacalcet<span class="elsevierStyleSup">41</span> was reported&#44; although in this latest study&#44; patients with a deterioritation in renal function were included prior to starting cinacalcet&#44; which was reversible in all cases after medication was discontinued&#46;<span class="elsevierStyleSup">41</span></p><p class="elsevierStylePara">Although the cause of this occasional deterioration in renal function is not clear&#44; it has been suggested that it could be related to a decrease in PTH values&#44; as with parathyroidectomy&#46;<span class="elsevierStyleSup">23&#44;47 </span>This has already been described in previous experimental studies that suggested that PTH plays a role in the regulation of renal perfusion and mesangial cell function&#46;<span class="elsevierStyleSup">48&#44;49</span></p><p class="elsevierStylePara">Another possibility that has been suggested is that the deterioration in renal function could be related to hypercalciuria secondary to the decrease in PTH&#59; nevertheless&#44; in most studies of patients being treated with cinacalcet we did not observe significant hypercalciuria and developments of renal tubular calcification was not observed in any case&#46;<span class="elsevierStyleSup">50</span></p><p class="elsevierStylePara">Recently&#44; a retrospective study comparing the use of calcimimetics with parathyroidectomy and medical observation without any surgery in renal transplant patients with stable renal function and tertiary HPT observed a higher rate of acute renal failure and a deterioration of the renal graft in the group of patients who did not receive treatment for their tertiary HPT&#46;<span class="elsevierStyleSup">22 </span></p><p class="elsevierStylePara">Cinacalcet is a safe therapeutic option for treating hypercalcemia in patients receiving a RT&#59; nevertheless&#44; recurrence of HPT is observed after the withdrawal of calcimimetics&#46;<span class="elsevierStyleSup">38&#44;43</span></p><p class="elsevierStylePara">Currently&#44; there is no marker that could indicate the suitable time point to withdraw cinacalcet treatment&#46;</p><p class="elsevierStylePara">Considering that it is a group of patients that is often treated with multiple drugs and that maintaining this medication for an indefinite period incurs a high economic cost&#44; it is necessary to carry out studies that allow us to find a marker that helps us know at what time we can withdraw calcimimetic treatment without the risk of recurrence of HPT and the resulting development of hypercalcemia&#46;</p><p class="elsevierStylePara">After all&#44; in our opinion&#44; treatment with calcimimetics must be tested for the management of hypercalcemia after renal transplantation before performing a parathyroidectomy</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">PROPOSAL FOR MANAGING POST TRANSPLANTATION HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Upon reviewing the literature and taking into account accumulated clinical experience&#44; we offer a proposal for managing hypercalcemia after renal transplantation&#44; set out schematically in the form of an algorithm &#40;Figure 1&#41;&#46;</p><p class="elsevierStylePara">We propose beginning treatment with cinacalcet in all patients with Cac &#62; 11mg&#47;dl and in those with Cac between 10&#46;5 and 11mg&#47;dl for more than 6 months&#44; in all cases with PTH &#62; 120pg&#47;ml&#46; The starting dose will be 30mg&#47;day of cinacalcet&#44; which will be maintained for 6 months&#46;</p><p class="elsevierStylePara">In the event that the patient responds to the initial dose of 30mg&#47;day &#40;Cac &#60; 10&#46;2mg&#47;dl 6 months after treatment&#41;&#44; we propose maintaining the same dose for another 6 months &#40;1 year total&#41; and&#44; if there is good control&#44; discontinuing the medication&#44; with a new test after 6 months&#44; and if calcaemia increases again above 10&#46;2mg&#47;dl we would recommence treatment with cinacalcet&#46;</p><p class="elsevierStylePara">If&#44; on the contrary&#44; with an initial dose of 30mg&#47;day calcaemia remains high &#40;Cac &#62; 10&#46;2mg&#47;dl after 6 months&#41;&#44; we would increase the dose to 60mg&#47;dl&#46; If by increasing the dose we are able to control calcaemia&#44; we could consider decreasing the dose again to 30mg&#47;day after 6 months and maintaining this regimen for at least another 6 months&#46; If calcaemia is controlled in this way&#44; we could consider withdrawing the drug&#46;</p><p class="elsevierStylePara">In the event that the patient has Cac &#62; 10&#46;5mg&#47;dl for more than 12 months despite an increased dose of cinacalcet&#44; the most suitable course of action would probably be to consider a parathyroidectomy&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11888&#95;16025&#95;52966&#95;en&#95;f11&#46;11888&#46;jpg" class="elsevierStyleCrossRefs"><img src="11888_16025_52966_en_f11.11888.jpg" alt="Proposal managing of hypercalcemia after renal transplantation&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Proposal managing of hypercalcemia after renal transplantation&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">La hipercalcemia postrasplante debida a la persistencia del hiperparatiroidismo &#40;HPT&#41; secundario tiene una prevalencia elevada en los primeros 3 meses postrasplante&#44; que va disminuyendo a lo largo del primer a&#241;o&#44; aunque en torno al 5-10&#160;&#37; de los trasplantados renales persiste en el tiempo&#46; La mayor resorci&#243;n &#243;sea y la mayor reabsorci&#243;n tubular de calcio debido a la acci&#243;n de la hormona paratiroidea &#40;PTH&#41; parecen ser los mecanismos principalmente implicados en la hipercalcemia&#46; La PTH en el momento del trasplante renal &#40;TR&#41; es el factor que determina el desarrollo de hipercalcemia pos-TR&#44; aunque a veces se encuentre enmascarada en los pacientes bien controlados con tratamiento m&#233;dico&#46; Cada vez m&#225;s los pacientes en di&#225;lisis reciben cinacalcet como tratamiento del HPT secundario&#46; La retirada del calcimim&#233;tico en el momento del trasplante renal da lugar a una mayor prevalencia de hipercalcemia e hiperparatiroidismo en estos pacientes&#46; En los pacientes con PTH bien controlada con cinacalcet antes del trasplante&#44; existe una relaci&#243;n directa entre la dosis y el desarrollo posterior de hipercalcemia&#44; probablemente porque indica la presencia de un HPT secundario m&#225;s severo&#46; La hipercalcemia puede tener efectos delet&#233;reos sobre el injerto renal dando lugar a calcificaci&#243;n tubulointersticial&#46; La hipercalcemia persistente es una marcador de aumento del riesgo de empeoramiento de la patolog&#237;a &#243;sea de estos pacientes&#46; Hoy en d&#237;a&#44; la primera opci&#243;n de tratamiento la constituye el cinacalcet&#44; y ante la ausencia de respuesta se valorar&#225; la realizaci&#243;n de una paratiroidectom&#237;a&#46; En esta revisi&#243;n proponemos un&#160;algoritmo de manejo de la hipercalcemia pos-TR&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Post-transplant hypercalcemia due to persistent secondary hyperparathyroidism &#40;HPT&#41; has a high prevalence in the first 3 months after surgery and decreases during the first year&#44; but it persists over time in around 5-10&#37; of renal transplant patients&#46; The increased bone resorption and tubular reabsorption of calcium due to the action of the parathyroid hormone &#40;PTH&#41; appear to be the main mechanisms involved in hypercalcemia&#46; At the time of the renal transplantation &#40;RT&#41;&#44; PTH is the factor that determines the development of post-RT hypercalcemia&#44; although it is sometimes masked in patients who are well controlled with medical treatment&#46; The number of dialysis patients receiving treatment with cinacalcet for secondary HPT is increasing&#46; The withdrawal of the calcimimetic at the time of renal transplantation results in a higher prevalence of hypercalcaemia and hyperparathyroidism in these patients&#46; In patients with PTH well controlled with cinacalcet before transplantation&#44; there is a direct relationship between the dose and the subsequent development of hypercalcemia&#44; probably because it indicates the presence of a more severe secondary HPT&#46; Hypercalcemia may have deleterious effects on the renal graft&#44; resulting in tubulointerstitial calcification&#46; Persistent hypercalcemia is a marker of an increased risk of bone disease deterioration in these patients&#46; Nowadays&#44; the first treatment option is cinacalcet and if there is no response&#44; we consider performing a parathyroidectomy&#46; In this review&#44; we propose an algorithm for management of post-RT hypercalcemia&#46;<span class="elsevierStyleItalic"></span></p>"
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Management of hypercalcemia after renal transplantation
Manejo de la hipercalcemia tras el trasplante renal
Jose-Vicente Torregrosaa, José V. Torregrosab, Xoana Barrosb
a Servicio de Nefrología y Trasplante Renal, Hospital Clínic de Barcelona, Barcelona, Spain,
b Servicio de Nefrología y Trasplante Renal, Hospital Clínic de Barcelona, España,
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but it decreases progressively in the first year and remains practically stable at around 5-10&#37; thereafter&#46;<span class="elsevierStyleSup">2-5</span></p><p class="elsevierStylePara">Until the introduction of the management guidelines for mineral and bone metabolism disorders in patients with chronic kidney disease in 2003&#44;<span class="elsevierStyleSup">6</span> the series of patients compiled showed a higher incidence and prevalence of post-RT hypercalcemia&#46; In fact&#44; in 1973&#44; hypercalcemia prevalence above 30&#37; was reported one year after the RT&#44; which persisted practically unchanged 2 and 5 years after transplantation&#46;<span class="elsevierStyleSup">5</span></p><p class="elsevierStylePara">Following the introduction of the guidelines and their clinical application&#44; there appeared to be a turning point in the prevalence of post-transplantation hypercalcemia&#46; This was the case when patients studied between 2004 and 2006 were compared to a hostoric control group of patients studied between 1989 and 2002&#44;<span class="elsevierStyleSup">1&#44;2</span> in which we observed a 41&#37; prevalence of hypercalcemia in the historic group&#44; while in the more recent group&#44; it had been reduced to 14&#37;&#46;</p><p class="elsevierStylePara">Nevertheless&#44; most studies on post-RT calcium metabolism were carried out prior to the introduction of cinacalcet for the treatment of secondary hyperparathyroidism &#40;HPT&#41; in dialysis patients&#46;</p><p class="elsevierStylePara">Cinacalcet was approved by the United States Food and Drug Administration in 2004 and by the European Medicines Agency in 2005 to treat secondary HPT in dialysis patients&#44; and subsequently&#44; to treat parathyroid carcinoma and primary HPT&#46; The efficacy of cinacalcet for controlling the parathyroid hormone &#40;PTH&#41; in dialysis patients has been widely demonstrated&#46;<span class="elsevierStyleSup">7-10</span></p><p class="elsevierStylePara">The better control of secondary HPT in dialysis patients after the introduction of cinacalcet probably has an effect on mineral and bone metabolism disorders after RT&#44; although few studies have been carried out in this regard&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CAUSES OF HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Studies from the era prior to the introduction of cinacalcet showed that high serum PTH values were the main predictor of post-transplantation hypercalcemia&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara">The introduction of cinacalcet has resulted in a better control of secondary HPT&#44; and as such&#44; there has been a decrease in the percentage of patients who undergo RT with high serum PTH values&#46; However&#44; withdrawing cinacalcet after RT results in high PTH levels immediately after transplantation&#44; and consequently&#44; hypercalcemia in a high number of patients&#46;<span class="elsevierStyleSup">11</span></p><p class="elsevierStylePara">In a recent study&#44; although carried out on a small number of patients&#44; this was also observed and patients on treatment with cinacalcet before transplantation whose treatment was discontinued on the day of surgery displayed a higher hypercalcemia incidence &#40;corrected Ca &#62;10&#46;3mg&#47;dl&#41; three months after transplantation than those patients who had not received cinacalcet &#40;42&#46;9&#37; vs&#46; 11&#46;4&#37;&#41; &#46;<span class="elsevierStyleSup">12</span></p><p class="elsevierStylePara">In our experience&#44; when we compared patients who received cinacalcet at the time of RT and those who did not receive it&#44; we found a hypercalcemia proportion &#40;corrected Ca &#62; 10&#46;3mg&#47;dl&#41; of 26&#46;3&#37; 3 months after transplantation compared with 0&#37; hypercalcemia in the control group &#40;<span class="elsevierStyleItalic">P</span>&#61;&#46;01&#41;&#44; despite both groups displaying similar PTH and calcaemia values at the time of transplantation&#46;<span class="elsevierStyleSup">13</span></p><p class="elsevierStylePara">Studies subsequent to the introduction of cinacalcet showed that pre-transplantation PTH only influenced post-transplantation Ca values in patients who were not on treatment with cinacalcet&#44; while&#44; in patients who received cinacalcet prior to RT&#44; it was the cinacalcet dose that predicted the subsequent development of HPT and hypercalcemia&#44; being a marker for the severity of secondary HPT in these patients&#46;<span class="elsevierStyleSup">11&#44;12</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">PHYSIOPATHOLOGY</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The physiopathological mechanisms suggested as responsible for post-transplantation hypercalcemia are&#58;</p><p class="elsevierStylePara">- More tubular calcium reabsorption&#44; due to PTH action&#46; The results of different studies are disparate&#59; while some show a decrease in fractional calcium excretion&#44;<span class="elsevierStyleSup">1 </span>others refer to greater urinary calcium excretion&#46;<span class="elsevierStyleSup">3</span> It seems that the effect of PTH increasing tubular calcium reabsorption would be more evident in the long term and less evident immediately after transplantation&#46;<span class="elsevierStyleSup">1&#44;3</span></p><p class="elsevierStylePara">- More intestinal calcium absorption&#44; due to increased serum calcitriol caused by the increase in its synthesis due to PTH stimulation&#46; Serum calcitriol values gradually recover in most patients after RT and we have observed that this is in relation to the rapid and progressive decrease in serum FGF23 &#40;fibroblast growth factor 23&#41; values&#46;<span class="elsevierStyleSup">13</span> Nevertheless&#44; no study has shown differences in calcitriol values between patients with hypercalcemia and normocalcemia&#46;<span class="elsevierStyleSup">1&#44;2</span></p><p class="elsevierStylePara">- More bone calcium resorption&#44; mediated by the PTH&#46; This seems to be the mechanism involved particularly in recent RT&#46; In patients with hypercalcemia&#44; we observed significantly higher serum alkaline phosphatase values than in normocalcaemic patients&#44; which suggests an increased bone turnover&#46;<span class="elsevierStyleSup">1</span><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONSEQUENCES OF</span><span class="elsevierStyleBold">HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">- Effect on the kidney graft&#46; Hypercalcemia&#44; through a vasoconstriction mechanism may impair renal graft function&#44; both acutely and chronically&#46;<span class="elsevierStyleSup">3&#44;14 </span>It may also cause tubulointerstitial calcifications that may have a negative influence on long-term graft survival&#46;<span class="elsevierStyleSup">15</span></p><p class="elsevierStylePara">- Other effects<span class="elsevierStyleBold"><span class="elsevierStyleItalic">&#46;</span></span> Cases of pancreatitis have been reported in <br></br> renal transplant patients with hypercalcemia due to HPT&#44;<span class="elsevierStyleSup">16</span> and it has also been demonstrated that it increases the risk of soft tissue calcification and the development of vascular calcification&#46;<span class="elsevierStyleSup">17</span></p><p class="elsevierStylePara">Hypercalcemia is fundamentally the result of an increase in bone remodelling with increased calcium reabsorption&#44; and as such&#44; persistent hypercalcemia will indicate that there is an increased risk of bone disease deterioration in these patients&#46;<span class="elsevierStyleSup">16&#44;18</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">MANAGEMENT OF POST-TRANSPLANTATION HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">To manage hypercalcemia due to persistent HPT following RT&#44; the alternatives are&#58;</p><p class="elsevierStylePara">a&#41; Watchful waiting&#46; Initial action&#44; in the case of moderate hypercalcemia may be to monitor serum calcium and PTH values while waiting for them to normalise over time&#46; However&#44; when there is significant hypercalcemia &#40;&#62; 11mg&#47;dl&#41; and&#47;or it persists over time &#40;&#62; 1 year&#41;&#44; or it is symptomatic&#44; we should take a more proactive approach&#46;</p><p class="elsevierStylePara">In our opinion&#44; shared by others&#44;<span class="elsevierStyleSup">19</span> in the absence of symptoms or significant hypercalcemia&#44; it would be prudent to wait at least a year for spontaneous resolution&#44; although some authors advocate waiting only 3-6 months after RT before opting for parathyroidectomy&#46;<span class="elsevierStyleSup">20</span></p><p class="elsevierStylePara">b&#41; Parathyroidectomy&#46; Traditionally&#44; it was the only alternative for controlling hypercalcemia in these patients and it remains the best option for correcting hypercalcemia when compared with calcimimetics&#46;<span class="elsevierStyleSup">21</span> However&#44; it carries an increased risk of acute and chronic hypocalcaemia&#44;<span class="elsevierStyleSup">22</span> as well as a high rate of persistence or recurrence of HPT&#44; depending on the technique used&#46;</p><p class="elsevierStylePara">Parathyroidectomy is not without risks&#58;</p><p class="elsevierStylePara">- Hungry bone syndrome&#44; which results in severe hypocalcaemia following surgery&#44; with symptoms ranging from paraesthesias to marked tetany&#44; which is sometimes difficult to control&#44; requiring high doses of calcium and vitamin D supplements&#46;</p><p class="elsevierStylePara">- Local surgical complications&#58; surgical wound infections&#44; recurrent nerve palsy &#40;reported in 1&#37; of surgeries with subsequent progressive recovery&#41;&#46;</p><p class="elsevierStylePara">- Deterioration in renal function&#46; Some studies have reported a deterioration in renal function following parathyroidectomy&#44;<span class="elsevierStyleSup">21&#44;23-26</span> while others have not reported it&#46;<span class="elsevierStyleSup">19&#44;22</span> The deterioration in renal function is independent of the type of parathyroidectomy and it appears that patients who experience a deterioration in renal function already have deterioration prior to parathyroidectomy&#46;<span class="elsevierStyleSup">27</span></p><p class="elsevierStylePara">The surgical options are&#58;</p><p class="elsevierStylePara">- <span class="elsevierStyleBold">Total parathyroidectomy with autotransplantation in the forearm</span>&#46; A total parathyroidectomy with autotransplantation in the forearm results in quicker calcemia correction&#59; however&#44; there is a higher risk of hypocalcaemia&#46;&#160;</p><p class="elsevierStylePara">In patients with a functioning RT&#44; the recurrence rate appears to be similar for this technique and subtotal parathyroidectomy&#46;<span class="elsevierStyleSup">28</span></p><p class="elsevierStylePara">In the event of recurrence&#47;persistence&#44; it is sometimes difficult to discern whether this is due to a hyperplasia of the autotransplant or residual tissue in the cervical area&#46; In this case&#44; mibi scintigraphy may help us&#46;<span class="elsevierStyleSup">29</span></p><p class="elsevierStylePara">The gland autotransplanted in the forearm in the event of recurrence seems to be more accesible&#44;<span class="elsevierStyleSup">30</span> but&#44; in the case of significant hyperplasia &#40;also called parathyromatosis&#41; it usually spreads in the implant area and is normally very difficult to remove&#46;</p><p class="elsevierStylePara">This involves the removal of all the parathyroid glands except for the remainder of a well-vascularised gland the size of a normal gland&#46; The remainder of the gland that is left should have a normal macroscopic appearance or that of a simple diffuse hyperplasia&#46;</p><p class="elsevierStylePara">- Many authors advocate this technique as they consider it to be the least aggressive one&#46;<span class="elsevierStyleSup">28</span><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">- Total parathyroidectomy without autotransplantation&#46; This is an effective alternative in terms of improving bone pain and it is probably the technique in which we observe the lowest number of recurrences&#47;relapses of HPT&#46;<span class="elsevierStyleSup">31-34</span></p><p class="elsevierStylePara">In contrast&#44; most of these patients usually require calcium and vitamin D supplements indefinitely in order to avoid hypocalcaemia and osteomalacia&#44; respectively&#46;</p><p class="elsevierStylePara">- Selective parathyroidectomy&#46; This involves performing a parathyroidectomy on only one or two parathyroid glands&#46; If with the cervical ultrasound examination and&#47;or MIBI scintigraphy it is shown that there are one or two adenomatous glands&#44; some authors advocate removing only those pathological glands &#40;enlarged and&#47;or with increased uptake&#41;&#46;</p><p class="elsevierStylePara">With this technique&#44; the acute hypocalcaemia percentage is less than with the previous techniques and the percentage of persistent hypocalcaemia is almost nil&#46;<span class="elsevierStyleSup">16&#44;35</span> By contrast&#44; it appears to increase the risk of persistence&#47;recurrence of HPT&#44;<span class="elsevierStyleSup">28&#44;36</span> although there are also series that show good progression and low incidence of recurrence&#46;<span class="elsevierStyleSup">16&#44;35&#44;37</span></p><p class="elsevierStylePara">c&#41; Calcimimetics&#46; Since 2006&#44; calcimimetics have been employed as an alternative treatment for hypercalcemia secondary to persistent secondary HPT &#40;also called tertiary HPT&#41; in patients with a functioning RT&#46;<span class="elsevierStyleSup">38-46</span>&#160;<span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">In all published studies&#44; the appropriate control of calcemia was confirmed with an improvement in serum PTH and phosphatemia&#46;</p><p class="elsevierStylePara">In the majority of these studies&#44; effects on renal function were not reported&#44; although in some exceptional cases a slight deterioration in renal function after three months<span class="elsevierStyleSup">44</span> or after one year on treatment with cinacalcet<span class="elsevierStyleSup">41</span> was reported&#44; although in this latest study&#44; patients with a deterioritation in renal function were included prior to starting cinacalcet&#44; which was reversible in all cases after medication was discontinued&#46;<span class="elsevierStyleSup">41</span></p><p class="elsevierStylePara">Although the cause of this occasional deterioration in renal function is not clear&#44; it has been suggested that it could be related to a decrease in PTH values&#44; as with parathyroidectomy&#46;<span class="elsevierStyleSup">23&#44;47 </span>This has already been described in previous experimental studies that suggested that PTH plays a role in the regulation of renal perfusion and mesangial cell function&#46;<span class="elsevierStyleSup">48&#44;49</span></p><p class="elsevierStylePara">Another possibility that has been suggested is that the deterioration in renal function could be related to hypercalciuria secondary to the decrease in PTH&#59; nevertheless&#44; in most studies of patients being treated with cinacalcet we did not observe significant hypercalciuria and developments of renal tubular calcification was not observed in any case&#46;<span class="elsevierStyleSup">50</span></p><p class="elsevierStylePara">Recently&#44; a retrospective study comparing the use of calcimimetics with parathyroidectomy and medical observation without any surgery in renal transplant patients with stable renal function and tertiary HPT observed a higher rate of acute renal failure and a deterioration of the renal graft in the group of patients who did not receive treatment for their tertiary HPT&#46;<span class="elsevierStyleSup">22 </span></p><p class="elsevierStylePara">Cinacalcet is a safe therapeutic option for treating hypercalcemia in patients receiving a RT&#59; nevertheless&#44; recurrence of HPT is observed after the withdrawal of calcimimetics&#46;<span class="elsevierStyleSup">38&#44;43</span></p><p class="elsevierStylePara">Currently&#44; there is no marker that could indicate the suitable time point to withdraw cinacalcet treatment&#46;</p><p class="elsevierStylePara">Considering that it is a group of patients that is often treated with multiple drugs and that maintaining this medication for an indefinite period incurs a high economic cost&#44; it is necessary to carry out studies that allow us to find a marker that helps us know at what time we can withdraw calcimimetic treatment without the risk of recurrence of HPT and the resulting development of hypercalcemia&#46;</p><p class="elsevierStylePara">After all&#44; in our opinion&#44; treatment with calcimimetics must be tested for the management of hypercalcemia after renal transplantation before performing a parathyroidectomy</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">PROPOSAL FOR MANAGING POST TRANSPLANTATION HYPERCALCEMIA</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Upon reviewing the literature and taking into account accumulated clinical experience&#44; we offer a proposal for managing hypercalcemia after renal transplantation&#44; set out schematically in the form of an algorithm &#40;Figure 1&#41;&#46;</p><p class="elsevierStylePara">We propose beginning treatment with cinacalcet in all patients with Cac &#62; 11mg&#47;dl and in those with Cac between 10&#46;5 and 11mg&#47;dl for more than 6 months&#44; in all cases with PTH &#62; 120pg&#47;ml&#46; The starting dose will be 30mg&#47;day of cinacalcet&#44; which will be maintained for 6 months&#46;</p><p class="elsevierStylePara">In the event that the patient responds to the initial dose of 30mg&#47;day &#40;Cac &#60; 10&#46;2mg&#47;dl 6 months after treatment&#41;&#44; we propose maintaining the same dose for another 6 months &#40;1 year total&#41; and&#44; if there is good control&#44; discontinuing the medication&#44; with a new test after 6 months&#44; and if calcaemia increases again above 10&#46;2mg&#47;dl we would recommence treatment with cinacalcet&#46;</p><p class="elsevierStylePara">If&#44; on the contrary&#44; with an initial dose of 30mg&#47;day calcaemia remains high &#40;Cac &#62; 10&#46;2mg&#47;dl after 6 months&#41;&#44; we would increase the dose to 60mg&#47;dl&#46; If by increasing the dose we are able to control calcaemia&#44; we could consider decreasing the dose again to 30mg&#47;day after 6 months and maintaining this regimen for at least another 6 months&#46; If calcaemia is controlled in this way&#44; we could consider withdrawing the drug&#46;</p><p class="elsevierStylePara">In the event that the patient has Cac &#62; 10&#46;5mg&#47;dl for more than 12 months despite an increased dose of cinacalcet&#44; the most suitable course of action would probably be to consider a parathyroidectomy&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11888&#95;16025&#95;52966&#95;en&#95;f11&#46;11888&#46;jpg" class="elsevierStyleCrossRefs"><img src="11888_16025_52966_en_f11.11888.jpg" alt="Proposal managing of hypercalcemia after renal transplantation&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Proposal managing of hypercalcemia after renal transplantation&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">La hipercalcemia postrasplante debida a la persistencia del hiperparatiroidismo &#40;HPT&#41; secundario tiene una prevalencia elevada en los primeros 3 meses postrasplante&#44; que va disminuyendo a lo largo del primer a&#241;o&#44; aunque en torno al 5-10&#160;&#37; de los trasplantados renales persiste en el tiempo&#46; La mayor resorci&#243;n &#243;sea y la mayor reabsorci&#243;n tubular de calcio debido a la acci&#243;n de la hormona paratiroidea &#40;PTH&#41; parecen ser los mecanismos principalmente implicados en la hipercalcemia&#46; La PTH en el momento del trasplante renal &#40;TR&#41; es el factor que determina el desarrollo de hipercalcemia pos-TR&#44; aunque a veces se encuentre enmascarada en los pacientes bien controlados con tratamiento m&#233;dico&#46; Cada vez m&#225;s los pacientes en di&#225;lisis reciben cinacalcet como tratamiento del HPT secundario&#46; La retirada del calcimim&#233;tico en el momento del trasplante renal da lugar a una mayor prevalencia de hipercalcemia e hiperparatiroidismo en estos pacientes&#46; En los pacientes con PTH bien controlada con cinacalcet antes del trasplante&#44; existe una relaci&#243;n directa entre la dosis y el desarrollo posterior de hipercalcemia&#44; probablemente porque indica la presencia de un HPT secundario m&#225;s severo&#46; La hipercalcemia puede tener efectos delet&#233;reos sobre el injerto renal dando lugar a calcificaci&#243;n tubulointersticial&#46; La hipercalcemia persistente es una marcador de aumento del riesgo de empeoramiento de la patolog&#237;a &#243;sea de estos pacientes&#46; Hoy en d&#237;a&#44; la primera opci&#243;n de tratamiento la constituye el cinacalcet&#44; y ante la ausencia de respuesta se valorar&#225; la realizaci&#243;n de una paratiroidectom&#237;a&#46; En esta revisi&#243;n proponemos un&#160;algoritmo de manejo de la hipercalcemia pos-TR&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Post-transplant hypercalcemia due to persistent secondary hyperparathyroidism &#40;HPT&#41; has a high prevalence in the first 3 months after surgery and decreases during the first year&#44; but it persists over time in around 5-10&#37; of renal transplant patients&#46; The increased bone resorption and tubular reabsorption of calcium due to the action of the parathyroid hormone &#40;PTH&#41; appear to be the main mechanisms involved in hypercalcemia&#46; At the time of the renal transplantation &#40;RT&#41;&#44; PTH is the factor that determines the development of post-RT hypercalcemia&#44; although it is sometimes masked in patients who are well controlled with medical treatment&#46; The number of dialysis patients receiving treatment with cinacalcet for secondary HPT is increasing&#46; The withdrawal of the calcimimetic at the time of renal transplantation results in a higher prevalence of hypercalcaemia and hyperparathyroidism in these patients&#46; In patients with PTH well controlled with cinacalcet before transplantation&#44; there is a direct relationship between the dose and the subsequent development of hypercalcemia&#44; probably because it indicates the presence of a more severe secondary HPT&#46; Hypercalcemia may have deleterious effects on the renal graft&#44; resulting in tubulointerstitial calcification&#46; Persistent hypercalcemia is a marker of an increased risk of bone disease deterioration in these patients&#46; Nowadays&#44; the first treatment option is cinacalcet and if there is no response&#44; we consider performing a parathyroidectomy&#46; In this review&#44; we propose an algorithm for management of post-RT hypercalcemia&#46;<span class="elsevierStyleItalic"></span></p>"
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