Bone mineral density, bone turnover markers, and incident fractures in de novo kidney transplant recipients

Evenepoel, Pieter; Claes, Kathleen; Meijers, Björn; Laurent, Michaël; Bammens, Bert; Naesens, Maarten; Sprangers, Ben; Pottel, Hans; Cavalier, Étienne; Kuypers, Dirk

doi:10.1016/j.kint.2018.12.024

Cited by 74 publications

(72 citation statements)

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“…To date, only one retrospective study, total hip DXA measurement after KT was associated with increased fracture risk. In addition, a recent prospective study had similar findings [81,82]. Despite the insufficient evidence for KTRs, Vitamin D Deficiency in Renal Disease DOI: http://dx.doi.org /10.5772/intechopen.88928 KDIGO suggests the use of BMD testing in all stages of post-transplant CKD in KTRs with high risk for osteoporosis, if the measurement will have effect on treatment.…”

Section: Ptmbd: Bone Diseasementioning

confidence: 89%

Vitamin D Deficiency in Renal Disease

Filipov¹,

Dimitrov²

2020

Vitamin D Deficiency

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Vitamin D deficiency is highly prevalent in patients with renal disease. The abnormal vitamin D (VD) metabolism in chronic kidney disease (CKD) is a key factor for developing CKD-related mineral bone disease (CKD-MBD), which directly influences the survival of the CKD patients. The importance of VD is perhaps of greater value due to its pleiotropic effects that span beyond calcium-phosphorus metabolism (cancer protection, diabetes prevention, and renal protection). The aim of our chapter is to depict the clinical implications of VD deficiency in the setting of CKD, including VD pleiotropy in renal disease, and to propose the most adequate treatment suggested in the literature. Keywords: vitamin D deficiency, chronic kidney disease, mineral bone disease, vitamin D pleiotropy, vitamin D supplementationVitamin D Deficiency 2 the ratio between free and total 25VD remained unchained; therefore, total 25VD is the indicator of VD status in CKD [3].Generally, 25VD level has reverse association with parathyroid hormone (PTH) levels. In addition, higher 25VD is associated with higher calcium intestinal reabsorption. However, at 25VD ≥ 75 nmol/l, no reduction in PTH levels and no increase in calcium intestinal reabsorption occurs [4, 5]. Therefore, 25VD ≥ 75 nmol/l is regarded as a cut-off value for vitamin D sufficiency.No generally accepted definition for VD deficiency exists, as authors choose cut-off value either serum 25VD of 25 nmol/L [6] or serum 25VD of 50 nmol/L [7]. However, target levels of 75 nmol/L are recommended, taking into consideration the clinical importance of mild VD insufficiency (25VD between 50 and 74.9 nmol/L) [7,8].Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, present for more than 3 months, with implications for health [one of the following: estimated glomerular filtration rate (eGFR) less than 60 ml/ min/1.73 m 2 ,presence of proteinuria, structural abnormalities of the kidney detected on imaging, pathological findings detected on kidney biopsy, urine sediment pathology, electrolyte abnormalities due to tubular disorders, history of kidney transplantation] [9]. CKD patients are at increased risk for VD deficiency; therefore, they require VD screening [7]. Vitamin D metabolism in health and renal disease VD metabolism in healthy subjectsVD is synthesized predominantly endogenously (approx. to 90% of the total VD in human body). In the skin, the ultraviolet light transforms 7-dehydroxycholesterol (provitamin D) to pre-vitamin D, which under the influence of body temperature spontaneously isomerizes to cholecalciferol (vitamin D3). Approximately, 10% of total body VD is taken orally (vitamin D2, ergocalciferol, and cholecalciferol). VD is transported via VD-binding protein to the liver, where it is hydroxylated to 25VD. The next step in VD activation is hydroxylation of 25VD by the enzyme 1α-hydroxylase (CYP27B1) to 1,25VD, which is the active VD metabolite. The process occurs predominantly in the renal tubules. In addition, non-renal CYP27B1 was detected...

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Section: Ptmbd: Bone Diseasementioning

confidence: 89%

Vitamin D Deficiency in Renal Disease

Filipov¹,

Dimitrov²

2020

Vitamin D Deficiency

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“…Our present results showed that (i) respectively, 34.5% and 6.1% of the patients presented osteopenia and osteoporosis one month after kidney transplantation and (ii) 1% of the patients presented a fracture in the 24 months following kidney transplantation. Evenepoel et al have shown that over a median follow-up period of 5.2 years, 38 out of 518 (7.3%) de novo renal transplant recipients experienced a fragility fracture; this corresponds to an incidence rate of 14.2 fractures per 1000 person-years [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Association between Uremic Toxin Concentrations and Bone Mineral Density after Kidney Transplantation

Batteux

Bodeau

André

et al. 2020

Toxins

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Although uremic osteoporosis is a component of mineral and bone disorder in chronic kidney disease, uremic toxin (UT) concentrations in patients with end-stage kidney disease and bone mineral density (BMD) changes after kidney transplantation have not previously been described. We hypothesized that elevated UT concentrations at the time of transplantation could have a negative impact on bone during the early post-transplantation period. Hence, we sought to determine whether concentrations of UTs (trimethylamine-N-oxide, indoxylsulfate, p-cresylsulfate, p-cresylglucuronide, indole-3-acetic acid, hippuric acid, and 3-carboxy-4-methyl-5-propyl-furanpropionic acid) upon transplantation are predictive markers for (i) osteoporosis one month after transplantation, and (ii) a BMD decrease and the occurrence of fractures 12 and 24 months after kidney transplantation. Between 2012 and 2018, 310 kidney transplant recipients were included, and dual-energy X-ray absorptiometry was performed 1, 12, and 24 months after transplantation. The UT concentrations upon transplantation were determined by reverse-phase high-performance liquid chromatography. Indoxylsulfate concentrations upon transplantation were positively correlated with BMD one month after transplantation for the femoral neck but were not associated with osteoporosis status upon transplantation. Concentrations of the other UTs upon transplantation were not associated with osteoporosis or BMD one month after transplantation. None of the UT concentrations were associated with BMD changes and the occurrence of osteoporotic fractures 12 and 24 months after transplantation. Hence, UT concentrations at the time of kidney transplantation were not predictive markers of osteoporosis or fractures.

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“…2 To confirm these data in humans, we performed a post hoc analysis on data collected in the frame of prospective, observational studies in patients referred for kidney transplantation. 3 Patients receiving cinacalcet (cases, n ¼ 65) were randomly matched 3:1 on PTH levels to patients free of cinacalcet (controls, n ¼ 166). PTH, calcium, and phosphate levels were comparable, whereas bone-specific alkaline phosphatase, intact procollagen type I N-terminal propeptide, and tartrate-resistant acid phosphatase type 5b were significantly higher in cases versus controls (Figure 1).…”

Section: Clinical Evidence Of Direct Bone Effects Of Cinacalcetmentioning

confidence: 99%

“…Previous studies have also reported that nonadherence was associated with both DSA and graft survival. 2,3 Then, it is unclear whether it is nonadherence that leads to the development of DSA and TCMR, which then resulted in worse transplant outcomes.…”

Section: Clinical Evidence Of Direct Bone Effects Of Cinacalcetmentioning

confidence: 99%

“…Kidney transplant recipients infected with coronavirus have a significant risk of graft loss and death. [1][2][3] However, the psychosocial impact of the COVID-19 pandemic on graft and patient outcomes in non-COVID kidney transplant recipients is unclear. The federal and local governments have enforced confinement orders to mitigate the spread of infection, but these restrictions have also limited health care access to "essential visits" only.…”

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confidence: 99%

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