Serum level of fibroblast growth factor 23 in maintenance renal transplant patients

Fructuoso, Ana I. Sánchez; Maestro, M.L.; Pérez‐Flores, Isabel; Valero, Rosalía; Rafael, Sara; Veganzones, Silvia; Calvo, N.; Orden, Virginia de la; Flor, J. C. De la; Valga, Francisco; Vidaurreta, Marta; Fernández-Pérez, Cristina; Barrientos, Alberto

doi:10.1093/ndt/gfs409

Cited by 29 publications

(24 citation statements)

References 38 publications

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“…2 ) [25] . Further, FGF23 reductions were repeatedly observed at longer follow-up, approximating normal levels 1-3 years after transplantation [26][27][28] .…”

Section: Epidemiology Of Altered Vitamin D Metabolism In Ktrsmentioning

confidence: 82%

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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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“…2 ) [25] . Further, FGF23 reductions were repeatedly observed at longer follow-up, approximating normal levels 1-3 years after transplantation [26][27][28] .…”

Section: Epidemiology Of Altered Vitamin D Metabolism In Ktrsmentioning

confidence: 82%

“…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: 96%

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Cianciolo¹,

Galassi

Capelli³

et al. 2016

Am J Nephrol

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“…The difference might be due to methodological problems, issues of calibration and possibly racial differences, which need to be further explored. Another study of 279 long-term kidney transplant patients concluded that FGF23 concentrations remained increased a median of 7.1 years after transplantation even in patients with eGFR O60 ml/min per 1.73 m 2 (34). It is however difficult to interpret their FGF23 results due to inconsistencies as to which assay for measuring FGF23 was used, and the study did not include a control group.…”

Section: Discussionmentioning

confidence: 99%

Soluble Klotho and intact fibroblast growth factor 23 in long-term kidney transplant patients

Bleskestad

Thorsen

Jonsson

et al. 2015

European Journal of Endocrinology

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Background: Controversies exist whether disturbances in mineral and bone disorder (MBD) normalise or persist after kidney transplantation. We assessed markers of MBD in patients with well-functioning kidney transplants to minimise confounding by reduced transplant function. Methods: In this cross-sectional study, 40 patients aged R18 years who received a first kidney transplant more than 10 years ago were included. A well-functioning transplant was defined as an estimated glomerular filtration rate (eGFR) R45 ml/min per 1.73 m 2 .

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“…In CKD patients, FGF-23 levels are strongly associated with mortality, regardless of the phosphate concentration [41], and have been surmised to play a role in LVH, endothelial function, CAC and atherosclerosis [42]. In KTRs, high FGF-23 levels may persist for a long time, partly as consequence of steroid therapy and parathormone (PTH) [43]. In a study on 984 prevalent KTRs, elevated FGF-23 levels were independently associated with greater subsequent risks of mortality and allograft loss [44].…”

Section: Progression Risk Factorsmentioning

confidence: 99%

Importance of Vascular Calcification in Kidney Transplant Recipients

Cianciolo¹,

Capelli²,

Angelini³

et al. 2014

Am J Nephrol

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Background: Kidney transplantation is the treatment of choice for chronic kidney disease (CKD), but in kidney transplant recipients (KTRs) cardiovascular events are the first cause of death with a functioning graft, ranging from 36 to 55%. The impact of vascular calcification (VC) on morbidity and mortality of KTRs is not appreciated enough nowadays. Summary: This review summarizes 13 important studies on VC in KTRs, comparing the results with CKD and dialysis populations. We focused on VC evaluation and use of coronary artery calcification (CAC) and aorta calcification (AoC) scores. We also evaluated the influence of traditional and non-traditional progression risk factors. Key Messages: VC strongly predicts cardiovascular events and all-cause mortality in KTRs. VC assessment is important in KTRs and based essentially on multislice computed tomography or electron beam computed tomography recognition of lesions. Quantitative measurement of CAC and AoC scores is essential for a correct definition of the calcium burden before and after kidney transplant. Progression of CAC slows down but does not halt after kidney transplant. A variable association of both traditional and non-traditional risk factors is shown. There is a strong association between baseline CAC score and CAC progression. A significant improvement in secondary hyperparathyroidism after transplantation favorably affects the progression of CAC. Low 25(OH)D₃ levels are an independent determinant of CAC progression. Diabetes is a risk factor for the presence of CAC in KTRs, but has not been independently associated with CAC progression. The data published on the use of immunosuppressive drugs as progression factors are few and inconclusive.

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Serum level of fibroblast growth factor 23 in maintenance renal transplant patients

Cited by 29 publications

References 38 publications

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Vitamin D in Kidney Transplant Recipients: Mechanisms and Therapy

Soluble Klotho and intact fibroblast growth factor 23 in long-term kidney transplant patients

Importance of Vascular Calcification in Kidney Transplant Recipients

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