Paricalcitol supplementation during the first year after kidney transplantation does not affect calcification propensity score

Ussif, Amin; Pihlstrøm, Hege; Holdaas, Hallvard; Hartmann, Anders; Smerud, Knut; Åsberg, Anders

doi:10.1186/s12882-018-1000-8

Cited by 5 publications

(3 citation statements)

References 17 publications

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“…Thus, the decreased end product could improve bone health [82]. Vitamin D also alleviated secondary CPP formation in recipients of renal transplantation [83]. Based on the clinical trials above, vitamin D supplements improved the serum concentration of MGP and osteocalcin.…”

Section: Introductionmentioning

confidence: 99%

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Hou

Zheng

et al. 2019

Nutrients

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Vascular calcification is a critical complication in patients with chronic kidney disease (CKD) because it is predictive of cardiovascular events and mortality. In addition to the traditional mechanisms associated with endothelial dysfunction and the osteoblastic transformation of vascular smooth muscle cells (VSMCs), the regulation of calcification inhibitors, such as calciprotein particles (CPPs) and matrix vesicles plays a vital role in uremic vascular calcification in CKD patients because of the high prevalence of vitamin K deficiency. Vitamin K governs the gamma-carboxylation of matrix Gla protein (MGP) for inhibiting vascular calcification, and the vitamin D binding protein receptor is related to vitamin K gene expression. For patients with chronic kidney disease, adequate use of vitamin D supplements may play a role in vascular calcification through modulation of the calciprotein particles and matrix vesicles (MVs).

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Section: Introductionmentioning

confidence: 99%

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Hou

Zheng

et al. 2019

Nutrients

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“…Hyperphosphatemia is one of the main factors associated with a high calcification propensity. A few phosphate binders decreased calcification propensity in hemodialysis patients: sevelamer, calcium carbonate, sucroferric oxyhydroxide and modified-release nicotinamide combined with an oral phosphate binder [47][48][49]. The calcimimetic etelcalcetide was associated with a longer T50 in hemodialysis patients with secondary hyperparathyroidism [61], and spironolactone was associated with a slightly longer T50 in hemodialysis patients [60].…”

Section: Discussionmentioning

confidence: 99%

“…Neither trial evidenced an effect of oral NaHCO 3 supplementation on T50 [50,53]. In an RCT, the synthetic vitamin D analog paricalcitol had no effect on T50 (relative to placebo) during the first year post-transplantation [49]. A post-hoc analysis of an RCT looked at the impact of the bisphosphonate ibandronate on T50 in kidney transplant recipients.…”

Section: Other Treatmentsmentioning

confidence: 99%

Serum Calcification Propensity Represents a Good Biomarker of Vascular Calcification: A Systematic Review

Pluquet

Kamel

Choukroun

et al. 2022

Toxins

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Vascular calcification contributes to cardiovascular morbidity and mortality. A recently developed serum calcification propensity assay is based on the half-transformation time (T50) from primary calciprotein particles (CPPs) to secondary CPPs, reflecting the serum’s endogenous capacity to prevent calcium phosphate precipitation. We sought to identify and review the results of all published studies since the development of the T50-test by Pasch et al. in 2012 (whether performed in vitro, in animals or in the clinic) of serum calcification propensity. To this end, we searched PubMed, Elsevier EMBASE, the Cochrane Library and Google Scholar databases from 2012 onwards. At the end of the selection process, 57 studies were analyzed with regard to the study design, sample size, characteristics of the study population, the intervention and the main results concerning T50. In patients with primary aldosteronism, T50 is associated with the extent of vascular calcification in the abdominal aorta. In chronic kidney disease (CKD), T50 is associated with the severity and progression of coronary artery calcification. T50 is also associated with cardiovascular events and all-cause mortality in CKD patients, patients on dialysis and kidney transplant recipients and with cardiovascular mortality in patients on dialysis, kidney transplant recipients, patients with ischemic heart failure and reduced ejection fraction, and in the general population. Switching from acetate-acidified dialysate to citrate-acidified dialysate led to a longer T50, as did a higher dialysate magnesium concentration. Oral administration of magnesium (in CKD patients), phosphate binders, etelcalcetide and spironolactone (in hemodialysis patients) was associated with a lower serum calcification propensity. Serum calcification propensity is an overall marker of calcification associated with hard outcomes but is currently used in research projects only. This assay might be a valuable tool for screening serum calcification propensity in at-risk populations (such as CKD patients and hemodialyzed patients) and, in particular, for monitoring changes over time in T50.

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Cardiovascular calcifications in kidney transplant recipients

Podestà

Cucchiari

Ciceri

et al. 2021

Nephrology Dialysis Transplantation

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Vascular and valvular calcifications are highly prevalent in kidney transplant recipients and are associated with an increased risk of cardiovascular events, which represent the leading cause of long-term mortality in these patients. However, cardiovascular calcification has been traditionally considered as a condition mostly associated with advanced chronic kidney disease stages and dialysis, and comparatively fewer studies have assessed its impact after kidney transplantation. Despite partial or complete resolution of uremia-associated metabolic derangements, kidney transplant recipients are still exposed to several pro-calcifying stimuli that favour the progression of pre-existing vascular calcifications or their de novo development. Traditional risk factors, bone mineral disorders, inflammation, immunosuppressive drugs and deficiency of calcification inhibitors may all play a role, and strategies to correct or minimize their effects are urgently needed. The aim of this work is to provide an overview of established and putative mediators involved in the pathogenesis of cardiovascular calcification in kidney transplantation, and to describe the clinical and radiological features of these forms. We also discuss current evidence on preventive strategies to delay the progression of cardiovascular calcifications in kidney transplant recipients, as well as novel therapeutic candidates to potentially prevent their long-term deleterious effects.

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Paricalcitol supplementation during the first year after kidney transplantation does not affect calcification propensity score

Cited by 5 publications

References 17 publications

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Serum Calcification Propensity Represents a Good Biomarker of Vascular Calcification: A Systematic Review

Cardiovascular calcifications in kidney transplant recipients

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