Mineral and bone disorders in chronic kidney disease and end-stage renal disease patients: new insights into vitamin D receptor activation

Bover, Jordi; Cozzolino, Mario

doi:10.1038/kisup.2011.28

Cited by 35 publications

(24 citation statements)

References 107 publications

(160 reference statements)

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“…The extra-renal expression of CYP27B1, CYP24A1 and vitamin D receptor (VDR) is considered the cornerstone of vitamin D's pleiotropic effects [13] . VDR is a ubiquitous nuclear receptor, with a major genomic regulatory effect, currently considered a crucial modulator of the human genome.…”

Section: Vitamin D System: Pathophysiologymentioning

confidence: 99%

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: Vitamin D System: Pathophysiologymentioning

confidence: 99%

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Cianciolo¹,

Galassi

Capelli³

et al. 2016

Am J Nephrol

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“…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. The bone response to PTH might also be enhanced by gluco corticoid treatment, as shown in vitro.…”

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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“…Progressive loss of kidney function is linked to a reduction in the production of vitamin D and to a disturbance in serum calcium and phosphorus balance that have been associated with poor CKD outcome and to increased risk for CVD events and mortality [74].…”

Section: Other Markersmentioning

confidence: 99%

Cardiovascular Risk Factors in End-Stage Renal Disease Patients: The Impact of Conventional Dialysis versus Online-Hemodiafiltration

Coimbra¹,

Faria²,

Miranda³

et al. 2018

Aspects in Dialysis

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End-stage renal disease (ESRD) patients present high incidence of cardiovascular (CV) events, which are the most common causes of death in these patients. The occurrence of CV events appears as a consequence of the high prevalence of traditional and nontraditional CV risk factors. Online-hemodiafiltration (OL-HDF) was introduced as a better alternative to conventional dialysis, as it was proposed to be more biocompatible, to increase dialysis efficacy, to reduce the inflammatory response to treatment and to improve patient's quality of life, contributing to reduce CV and all-cause mortality risk in ESRD. However, data in literature, comparing the effect of OL-HDF with conventional dialysis for clinical CV outcome and all-cause mortality, yielded controversy about those benefits of OL-HFD over standard hemodialysis. A review of the traditional CV risk factors (e.g., arterial hypertension, diabetes mellitus, dyslipidemia, obesity, smoking and advanced age), non-traditional risk factors (e.g., anemia, oxidative stress, hyperphosphatemia, endothelial dysfunction, left ventricular hypertrophy, insulin resistance, high levels of lipoprotein(a) and inflammation) and potential renocardiovascular biomarkers, in the setting of ESRD, is presented. The impact of conventional hemodialysis and OL-HDF on CV risk factors and on the outcome of ESRD patients is also addressed.

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Mineral and bone disorders in chronic kidney disease and end-stage renal disease patients: new insights into vitamin D receptor activation

Cited by 35 publications

References 107 publications

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Phosphate and FGF-23 homeostasis after kidney transplantation

Cardiovascular Risk Factors in End-Stage Renal Disease Patients: The Impact of Conventional Dialysis versus Online-Hemodiafiltration

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