Determinants of bone mineral density in stable kidney transplant recipients

As transplantation osteoporosis results from alterations in the bone remodeling system, a review of normal bone remodeling is helpful to understanding the pathogenesis of this disease. The bone remodeling cycle is an orderly progression of events in which old, microdamaged bone is replaced by new, mechanically stronger bone. The complete remodeling cycle at each remodeling site requires approximately 3-6 months. Bone remodeling occurs by two main processes, resorption [1] followed by formation [2], which take place on both cancellous and cortical bone surfaces. Resorption begins with activation of macrophage precursors to form osteoclasts, giant multinucleated cells that excavate a cavity on the bone surface. Osteoclasts express receptors for receptor activator of receptor activator of nuclear factor-kappaB ligand (RANKL), which is produced by osteoblasts and osteocytes, and for calcitonin, prostaglandins (PGs), calcium, and vitronectin (integrin α 1 β 3 ). Approximately 0.05 mm 3 of bone tissue is resorbed by each osteoclast, leaving small resorption pits on the bone surface called Howship's lacunae in a process that takes approximately 2-3 weeks. A brief rest period called the reversal phase follows. Next, local mesenchymal bone marrow stem cells differentiate into osteoblasts that are attracted to the empty resorption pits where they accumulate as clusters of plump cuboidal cells along the bone surface. Osteoblasts produce the collagenous and noncollagenous proteins that constitute the matrix of the newly formed bone and are responsible for mineralization of the matrix or osteoid after a period of maturation that lasts approximately 20 days. Osteoblasts express receptors for several hormones (thyroid and parathyroid hormones, estrogens, vitamin D 3 ), cell adhesion molecules (integrins), and cytokines. RANKL, receptor activator of nuclear factor-kappaB (RANK), and osteoprotegerin (OPG) are three members of the tumor necrosis factor (TNF) ligand and receptor-signaling family that are final mediators of bone resorption [3,4]. RANKL is expressed in osteoblasts, osteocytes, and bone marrow stromal cells. When sufficient concentrations of macrophage colony stimulating factor (M-CSF) are present, RANKL binds to RANK, which is expressed on the surface of osteoclast lineage cells. This binding results in rapid differentiation of osteoclast precursors in bone marrow to mature osteoclasts, increased osteoclast activity, and reduced apoptosis of mature osteoclasts. RANKL is neutralized by binding to OPG, which is secreted by cells of the osteoblast lineage. Competitive binding of RANKL to either RANK or OPG regulates bone remodeling by increasing (RANK) or decreasing (OPG) osteoclastogenesis. Immunosuppressants exert their effects on bone remodeling by interacting with the RANK/RANKL/ OPG system [5].In healthy adults, declines in bone mass as a result of remodeling imbalance occur, but are small. When bone remodeling becomes "uncoupled," such that the rate of resorption exceeds the rate of formation, bone loss will occur...

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“…Bone resorption markers were elevated in half of the cohort [104]. Other studies have shown similar results [43,[105][106][107].…”

Section: Prevalence Of Osteoporosis In Kidney Transplant Recipientssupporting

confidence: 67%

Osteoporosis in Organ Transplant Patients

Stein

Shane

2013

Osteoporosis

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“…The prevalence of “osteopenia” and “osteoporosis” after renal transplant has been reported to range from 25% to 35% and 8% to 28%, respectively [ 55 – 57 ]. A cross-sectional analysis of 389 stable renal transplant recipients has showed that osteopenia or osteoporosis is more prevalent at the femoral neck than lumbar spine [ 58 ]. The main pathology of bone remodeling following transplantation is considered to include decreased bone formation and mineralization associated with persistent bone resorption [ 59 ].…”

Section: Different Types Of Transplantationmentioning

confidence: 99%

Current Status of Research on Osteoporosis after Solid Organ Transplantation: Pathogenesis and Management

Lan

Xie

Peng

et al. 2015

BioMed Research International

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Improved survival following organ transplantation has brought to the forefront some long-term complications, among which osteoporosis and associated fractures are the major ones that adversely affect the quality of life in recipients. The pathogenesis of osteoporosis in transplant recipients is complex and multifactorial which may be related to increased bone resorption, decreased bone formation, or both. Studies have shown that the preexisting underlying metabolic bone disorders and the use of immunosuppressive agents are the major risk factors for osteoporosis and fractures after organ transplantation. And rapid bone loss usually occurs in the first 6–12 months with a significant increase in fracture risk. This paper will provide an updated review on the possible pathogenesis of posttransplant osteoporosis and fractures, the natural history, and the current prevention and treatment strategies concerning different types of organ transplantation.

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“…Low BMI is a known risk factor for osteoporosis [21], and loss of BMD is a common complication that correlates with low body weight and low BMI in renal transplantation recipients [22]. Our previous study of renal transplant recipients indicated that body height, body weight, and BMI were positively correlated with lumbar BMD [14].…”

Section: Discussionmentioning

confidence: 99%

Inverse relationship of bone mineral density and serum level of N-terminal pro-B-type natriuretic peptide in peritoneal dialysis patients

Wang

Tsai

Lai

et al. 2016

Tzu Chi Medical Journal

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Objective:Chronic kidney disease is associated with decreased bone mineral density (BMD). In this study, the relationship between BMD and the fasting serum concentration of N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) was evaluated in peritoneal dialysis (PD) patients.Material and Methods:Fasting blood samples were obtained from 52 PD patients. BMD was measured by dual energy X-ray absorptiometry of the lumbar vertebrae (L2–L4). The serum NT-pro-BNP level was measured by an electrochemiluminescence immunoassay.Results:Ten patients (19.2%) had osteoporosis, 23 patients (44.2%) had osteopenia, and 19 patients had normal BMD. Increased serum NT-pro-BNP (p < 0.001), advanced age (p = 0.012), decreased body mass index (p = 0.006), body height (p = 0.018), and body weight (p = 0.004) were associated with lower lumbar T-scores, but sex, menopausal status, PD modality, diabetes mellitus, and hypertension were not. Multivariate forward stepwise linear regression analysis with adjustment for age, body height, body weight, body mass index, and log-NT-pro-BNP indicated that a high serum level of log-NT-pro-BNP (R2 change = 0.346; p < 0.001) and low body weight (R2 change = 0.208; p < 0.001) were significantly and independently associated with poor lumbar BMD.Conclusion:A high serum level of NT-pro-BNP and low body weight were associated with poor BMD in PD patients.

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Determinants of bone mineral density in stable kidney transplant recipients

Abstract: Significant bone loss in KTRs is most prevalent at the femoral neck. Identifying risk factors for specific sites may allow for earlier intervention prior to osteoporosis development.

Cited by 21 publications

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Osteoporosis in Organ Transplant Patients

Osteoporosis in Organ Transplant Patients

Current Status of Research on Osteoporosis after Solid Organ Transplantation: Pathogenesis and Management

Inverse relationship of bone mineral density and serum level of N-terminal pro-B-type natriuretic peptide in peritoneal dialysis patients

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