Persistence of Bone and Mineral Disorders 2 Years After Successful Kidney Transplantation

Neves, Camila Zander; Reis, Luciene M. dos; Batista, Daniella G.; Custódio, Melani Ribeiro; Graciolli, Fabiana G.; Martin, Rita de Cássia T.; Neves, Kátia R.; Dominguez, Wagner V.; Moysés, Rosa Maria Affonso; Jorgetti, Vanda

doi:10.1097/tp.0b013e3182985468

Cited by 38 publications

(43 citation statements)

References 36 publications

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“…Few studies have reported histological patterns of PTBD, describing a considerable prevalence of adynamic bone disease (5-50%), and high bone turnover (25-50%) [46][47][48] . More recent investigations observed a 48% rate of delayed mineralization, a 26% rate of low bone turnover, a 26% rate of high turnover and a 12% rate of mixed uremic bone disease 2 years after transplantation [36] .…”

Section: Ptbd: Epidemiology and Mechanismsmentioning

confidence: 93%

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Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Cianciolo¹,

Galassi

Capelli³

et al. 2016

Am J Nephrol

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Chronic kidney disease-mineral and bone disorder (CKD-MBD) is common in kidney transplant recipients (KTRs), where secondary hyperparathyroidism (HPTH) and post-transplantation bone disease (PTBD) are potential effectors of both graft and vascular aging. Reduced 25(OH)D levels are highly prevalent in KTRs. Experimental and clinical evidence support the direct involvement of deranged vitamin D metabolism in CKD-MBD among KTRs. This review analyzes the pathophysiology of vitamin D derangement in KTRs and its fall out on patient and graft outcome, highlighting the roles of both nutritional and active vitamin D compounds to treat PTBD, cardiovascular disease (CVD) and graft dysfunction. Fibroblast growth factor-23-parathyroid hormone (PTH)-vitamin D axis, immunosuppressive therapy and previous bone status have been associated with PTBD. Although several studies reported reduced PTH levels in KTRs receiving nutritional vitamin D, its effects on bone mineral density (BMD) remain controversial. Active vitamin D reduced PTH levels and increased BMD after transplantation, but paricalcitol treatment was not accompanied by benefits on osteopenia. Vitamin D is considered protective against CVD due to the widespread pleiotropic effects, but data among KTRs remain scanty. Although vitamin deficiency is associated with lower glomerular filtration rate (GFR) and faster estimated GFR decline and data on the anti-proteinuric effects of vitamin D receptor activation (VDRA) in KTRs sound encouraging, reports on related improvement on graft survival are still lacking. Clinical data support the efficacy of VDRA against HPTH and show promising evidence of VDRA's effect in counteracting post-transplant proteinuria. New insights are mandatory to establish if the improvement of surrogate outcomes will translate into better patient and graft outcome.

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Section: Ptbd: Epidemiology and Mechanismsmentioning

confidence: 93%

“…3 ). The cumulative prednisone dose was inversely correlated with 1,25(OH) 2 D 3 levels 2 years after transplantation [30] , and low 1,25(OH)D levels could also be favored by higher FGF23 concentrations induced by steroid therapy [27,[36][37][38] .…”

Section: Epidemiology Of Altered Vitamin D Metabolism In Ktrsmentioning

confidence: 99%

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Cianciolo¹,

Galassi

Capelli³

et al. 2016

Am J Nephrol

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“…Preexisting renal osteodystrophy is a risk factor for fracture and adverse outcomes post-transplantation (14). The prevalence of histologic patterns of post-transplantation bone disease is not well defined, because there have been very few bone biopsy studies in kidney transplant recipients.…”

Section: Evolution Of Preexisting Renal Osteodystrophymentioning

confidence: 99%

Bone Disease after Kidney Transplantation

Bouquegneau

Salam

Delanaye

et al. 2016

CJASN

126

109

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Bone and mineral disorders occur frequently in kidney transplant recipients and are associated with a high risk of fracture, morbidity, and mortality. There is a broad spectrum of often overlapping bone diseases seen after transplantation, including osteoporosis as well as persisting high-or low-turnover bone disease. The pathophysiology underlying bone disorders after transplantation results from a complex interplay of factors, including preexisting renal osteodystrophy and bone loss related to a variety of causes, such as immunosuppression and alterations in the parathyroid hormone-vitamin D-fibroblast growth factor 23 axis as well as changes in mineral metabolism. Management is complex, because noninvasive tools, such as imaging and bone biomarkers, do not have sufficient sensitivity and specificity to detect these abnormalities in bone structure and function, whereas bone biopsy is not a widely available diagnostic tool. In this review, we focus on recent data that highlight improvements in our understanding of the prevalence, pathophysiology, and diagnostic and therapeutic strategies of mineral and bone disorders in kidney transplant recipients.

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“…98 Persistent hyperparathyroidism after kidney transplantation is associated with hypercalcaemia and hypophosphataemia, which may be effectively corrected with cinacalcet-a calcimimetic. 107 Histomorphometric studies performed 2 years after transplantation revealed mineralization defects as well as higher osteoid, osteoblastic, resorption, and osteoclastic surfaces, indicative of persistent hyperparathyroidism that can be attributed at least in part to hypovitaminosis D. 107 Hyporesponsiveness of the bone to PTH in patients with CKD is caused by phosphate loading, decreased calcitriol, antagonistic PTH fragments, downregulation of PTH receptors, and decreased pulsatile secretion of PTH. 108 Some of the bone abnormalities induced by persistent hyperparathyroidism after kidney transplantation might, therefore, be explained by the removal of skeletal resistance to PTH, as most of the aforementioned factors are restored and elicit an important bone response to PTH.…”

Section: Kidney Transplantationmentioning

confidence: 99%

Phosphate and FGF-23 homeostasis after kidney transplantation

Baia

Heilberg²,

Navis

et al. 2015

Nat Rev Nephrol

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Dysregulated phosphate metabolism is a common consequence of chronic kidney disease, and is characterized by a high circulating level of fibroblast growth factor (FGF)-23, hyperparathyroidism, and hyperphosphataemia. Kidney transplantation can elicit specific alterations to phosphate metabolism that evolve over time, ranging from severe hypophosphataemia (<0.5 mmol/l) to hyperphosphataemia (>1.50 mmol/l) and high FGF-23 levels. The majority of renal transplant recipients develop hypophosphataemia during the first 3 months after transplantation as a consequence of relatively slow adaptation of FGF-23 and parathyroid hormone levels to restored renal function, and the influence of immunosuppressive drugs. By 3-12 months after transplantation, phosphate homeostasis is at least partially restored in the majority of recipients, which is paralleled by a substantially reduced risk of cardiovascular-associated morbidity and mortality compared with the pre-transplantation setting. Many renal transplant recipients, however, exhibit persistent abnormalities in phosphate homeostasis, which is often due to multifactorial causes, and may contribute to adverse outcomes on the cardiovascular system, kidney, and bone. Dietary and pharmacologic interventions might improve phosphate homeostasis in renal transplant recipients, but additional insight into the pathophysiology of transplantation-associated abnormalities in phosphate homeostasis is needed to further optimize disease management and improve prognosis for renal transplant recipients.

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Persistence of Bone and Mineral Disorders 2 Years After Successful Kidney Transplantation

Cited by 38 publications

References 36 publications

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Bone Disease after Kidney Transplantation

Phosphate and FGF-23 homeostasis after kidney transplantation

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