Bone disease after renal transplantation

Kunzendorf, Ulrich; Krämer, Bernhard K.; Arns, Wolfgang; Braun, J.; Großmann, Jan; Pietruck, Frank; Schmidt‐Gayk, H.; Schwarz, Anke; Ziegler, Ekkehard; Sperschneider, H; Wüthrich, Rudolf P.; Nonnast-Daniel, B.; Schindler, Ralf; Renders, Lutz

doi:10.1093/ndt/gfm816

Cited by 38 publications

(24 citation statements)

References 94 publications

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“…This points to specific risk factors. Among these, preexisting renal osteodystrophy, hypogonadism, and metabolic acidosis undoubtedly play an important role (2). Post-transplant disturbances in phosphate homeostasis should be accounted for as well.…”

mentioning

confidence: 99%

Fibroblast Growth Factor-23 and Parathyroid Hormone Are Associated with Post-Transplant Bone Mineral Density Loss

Kanaan¹,

Claes²,

Devogelaer

et al. 2010

Clinical Journal of the American Society of Nephrology

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Background and objectives: Among the multiple factors contributing to bone mineral density (BMD) loss after renal transplantation, hypophosphatemia is increasingly recognized to play an important role. Hypophosphatemia occurs in up to 90% of the renal transplant recipients in the early post-transplant period and is caused by renal phosphate wasting. We hypothesized that a high pretransplant level of the recently described phosphaturic hormone fibroblast growth factor 23 (FGF-23) is a risk factor for accelerated BMD loss occurring within the first post-transplant year.Design, setting, participants, & measurements: We performed a two-center observational retrospective cohort study in 127 incident renal transplant recipients. Serum full-length FGF-23, parathyroid hormone (PTH), and parameters of mineral metabolism were determined at the time of transplantation. BMD was assessed by osteodensitometry at the time of transplantation and 1 year later.Results: A moderate decrease of BMD was observed during the first post-transplant year. High FGF-23 levels were associated with BMD loss at the lumbar spine and total hip region, whereas low PTH levels were associated with BMD loss at all three regions. Cumulative doses of prednisone and post-transplant serum phosphate level were not correlated with BMD changes.Conclusion: Our data indicate that patients with a high serum FGF-23 level and/or a low PTH level at the time of transplantation are at risk for increased BMD loss during the first post-transplant year.

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mentioning

confidence: 99%

Fibroblast Growth Factor-23 and Parathyroid Hormone Are Associated with Post-Transplant Bone Mineral Density Loss

Kanaan¹,

Claes²,

Devogelaer

et al. 2010

Clinical Journal of the American Society of Nephrology

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“…En el contexto de un paciente trasplantado renal, el estado nutricional, estado de inflamación y la exposición a esteroides representan riesgos para la persistencia o empeoramiento de las alteraciones del metabolismo mineral y óseo (62) .…”

Section: Enfermedad Mineral óSea Postrasplante Renalunclassified

“…Con el trasplante se remueve los estímulos metabólicos que llevan al hiperparatiroidismo secundario en pacientes con enfermedad renal, sin embargo, la producción excesiva de paratohormona persiste luego del trasplante llevando a hipersecreción de PTH con hipercalcemia (hiperparatiroidismo terciario) (62)(63)(64)(65) . En pacientes trasplantados renales se ha intentado reducir rápidamente las dosis de corticoides, por los múltiples efectos metabólicos que producen, reportándose reducción de los niveles de osteocalcina y deoxipiridinolina, sin incremento en la tasa de rechazos agudos de injerto.…”

Section: Enfermedad Mineral óSea Postrasplante Renalunclassified

Metabolismo mineral óseo en pacientes con enfermedad renal crónica: revisión sobre su fisiopatología y morbimortalidad

Bernuy

Gonzáles

2015

Rev Peru Med Exp Salud Publica

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RESUMENLa enfermedad mineral ósea (EMO) es un término amplio que incluye a las alteraciones séricas del calcio, fósforo, vitamina D, paratohormona, anormalidades en el crecimiento, mineralización ósea y/o a las calcificaciones extraesqueléticas que acompañan al paciente con enfermedad renal crónica (ERC). Está presente en casi la totalidad de pacientes en diálisis y con el trasplante renal puede no siempre mejorar. Se han identificado nuevos factores y hormonas; como klotho y factor de crecimiento de fibroblastos-23 (FGF-23) que interactúan con la vitamina D y con la paratohormona en el manejo renal del calcio y fósforo. Ciertos reportes indican que son marcadores precoces del desarrollo de EMO, incluso cuando la función renal está levemente disminuida y los niveles de paratohormona son normales. La EMO ha sido asociada con mayor mortalidad, principalmente por su vinculación con la calcificación vascular. Este proceso conlleva a un incremento de eventos cardiovasculares que constituyen la principal causa de morbimortalidad en pacientes con ERC, sobre todo aquellos que se encuentran en diálisis, independientemente de la modalidad que los pacientes sigan. La forma de presentación de la EMO puede ser de alto o bajo recambio. Aunque no está completamente definido qué es lo que determina que se exprese una en particular, se ha encontrado que la enfermedad de bajo recambio se relaciona con malnutrición, uso inadecuado de calcitriol y diálisis ineficiente. El conocimiento de la EMO es relevante por su asociación con las complicaciones mencionadas y porque constituye un parámetro para evaluar la terapia instalada. Palabras clave: Hormona paratiroidea; Deficiencia de vitamina B; Enfermedad renal crónica; Trastornos del metabolismo del calcio (fuente: DeCS BIREME). BONE MINERAL METABOLISM IN PATIENTS WITH CHRONIC KIDNEY DISEASE: REVIEW OF ITS PATHOPHYSIOLOGY AND MORBIMORTALITY ABSTRACTMineral Bone Disorder (MBD) is a broad term that includes abnormal serum calcium, phosphorus, vitamin D, parathyroid hormone, growth abnormalities, bone mineralization and/or extraskeletal calcifications in patients with chronic kidney disease (CKD ). It is present in almost all patients on dialysis and may not always improve with a kidney transplant. New factors and hormones have been identified, such as Klotho and fibroblast growth factor-23 (FGF-23) that interact with vitamin D and the parathyroid hormone in the renal management of calcium and phosphorus. Some reports indicate that they are early markers of the development of MBD, even when kidney function is slightly decreased and parathyroid hormone levels are normal. MBD has been associated with higher mortality, mainly because of its link with vascular calcification. This process leads to an increase in cardiovascular events which are the leading cause of morbidity and mortality in CKD patients, especially those who are on dialysis, regardless of the modality that the patients follow. The presentation of the BMD can be of high or low turnover. Although it is not completely defined wha...

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“…[1][2][3] Vitamin D is mainly involved in phosphocalcic metabolism regulation, but it also p l a y s a n i m p o r t a n t r o l e i n t h e prevention of cardiovascular risk, infectious and autoimmune diseases, and CKD progression. 2,4,5 Undoubtedly, factors determining such cardiovascular and bone risk increase are present in the pre-dialysis period and further increase during renal replacement therapy with dialysis or a kidney transplant. 4,[6][7][8][9] S o m e s t u d i e s c o n d u c t e d i n children with CKD showed that vitamin D administration reduced proteinuria and kidney disease progression.…”

Section: Introductionmentioning

confidence: 99%

High prevalence of vitamin D deficiency among children with chronic kidney disease and kidney transplant

et al. 2017

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Bone disease after renal transplantation

Cited by 38 publications

References 94 publications

Fibroblast Growth Factor-23 and Parathyroid Hormone Are Associated with Post-Transplant Bone Mineral Density Loss

Fibroblast Growth Factor-23 and Parathyroid Hormone Are Associated with Post-Transplant Bone Mineral Density Loss

Metabolismo mineral óseo en pacientes con enfermedad renal crónica: revisión sobre su fisiopatología y morbimortalidad

High prevalence of vitamin D deficiency among children with chronic kidney disease and kidney transplant

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