10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Prevalence of Musculoskeletal Manifestations in Adult Kidney Transplant’s Recipients: A Systematic Review

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background and Objectives: The musculoskeletal (MSK) manifestations in the kidney transplant recipient (KTxR) could lead to decreased quality of life and increased morbidity and mortality. However, the prevalence of these MSK manifestations is still not well-recognized. This review aimed to investigate the prevalence and outcomes of MSK manifestations in KTxR in the last two decades. Materials and Methods: Research was performed in EBSCO, EMBASE, CINAHL, PubMed/MEDLINE, Cochrane, Google Scholar, PsycINFO, Scopus, Science Direct, and Web of Science electronic databases were searched during the years 2000–2020. Results: The PRISMA flow diagram revealed the search procedure and that 502 articles were retrieved from the initial search and a total of 26 articles were included for the final report in this review. Twelve studies reported bone loss, seven studies reported a bone pain syndrome (BPS) or cyclosporine-induced pain syndrome (CIPS), and seven studies reported hyperuricemia (HU) and gout. The prevalence of MSK manifestations in this review reported as follow: BPS/CIPS ranged from 0.82% to 20.7%, while bone loss ranged from 14% to 88%, and the prevalence of gout reported in three studies as 7.6%, 8.0%, and 22.37%, while HU ranged from 38% to 44.2%. Conclusions: The post-transplantation period is associated with profound MSK abnormalities of mineral metabolism and bone loss mainly caused by corticosteroid therapy, which confer an increased fracture risk. Cyclosporine (CyA) and tacrolimus were responsible for CIPS, while HU or gout was attributable to CyA. Late diagnosis or treatment of post-transplant bone disease is associated with lower quality of life among recipients

          Related collections

          Most cited references88

          • Record: found
          • Abstract: found
          • Article: not found

          Glucocorticoid-induced osteoporosis: pathophysiology and therapy.

          Glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. Fractures, which are often asymptomatic, may occur in as many as 30-50% of patients receiving chronic glucocorticoid therapy. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Fractures tend to occur at higher BMD levels than in women with postmenopausal osteoporosis. In human subjects, the early rapid decline in BMD is followed by a slower progressive decline in BMD. Glucocorticoids have direct and indirect effects on the skeleton. The primary effects are on osteoblasts and osteocytes. Glucocorticoids impair the replication, differentiation and function of osteoblasts and induce the apoptosis of mature osteoblasts and osteocytes. These effects lead to a suppression of bone formation, a central feature in the pathogenesis of GIO. Glucocorticoids also favor osteoclastogenesis and as a consequence increase bone resorption. Bisphosphonates are effective in the prevention and treatment of GIO. Anabolic therapeutic strategies are under investigation.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Effects of uric acid-lowering therapy on renal outcomes: a systematic review and meta-analysis.

            Non-randomized studies suggest an association between serum uric acid levels and progression of chronic kidney disease (CKD). The aim of this systematic review is to summarize evidence from randomized controlled trials (RCTs) concerning the benefits and risks of uric acid-lowering therapy on renal outcomes. Medline, Excerpta Medical Database and Cochrane Central Register of Controlled Trials were searched with English language restriction for RCTs comparing the effect of uric acid-lowering therapy with placebo/no treatment on renal outcomes. Treatment effects were summarized using random-effects meta-analysis. Eight trials (476 participants) evaluating allopurinol treatment were eligible for inclusion. There was substantial heterogeneity in baseline kidney function, cause of CKD and duration of follow-up across these studies. In five trials, there was no significant difference in change in glomerular filtration rate from baseline between the allopurinol and control arms [mean difference (MD) 3.1 mL/min/1.73 m2, 95% confidence intervals (CI) -0.9, 7.1; heterogeneity χ2=1.9, I2=0%, P=0.75]. In three trials, allopurinol treatment abrogated increases in serum creatinine from baseline (MD -0.4 mg/dL, 95% CI -0.8, -0.0 mg/dL; heterogeneity χ2=3, I2=34%, P=0.22). Allopurinol had no effect on proteinuria and blood pressure. Data for effects of allopurinol therapy on progression to end-stage kidney disease and death were scant. Allopurinol had uncertain effects on the risks of adverse events. Uric acid-lowering therapy with allopurinol may retard the progression of CKD. However, adequately powered randomized trials are required to evaluate the benefits and risks of uric acid-lowering therapy in CKD.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Mechanisms of glucocorticoid action in bone.

              Glucocorticoids cause profound effects on bone cell replication, differentiation, and function. Glucocorticoids increase bone resorption by stimulating osteoclastogenesis by increasing the expression of RANK ligand and decreasing the expression of its decoy receptor, osteoprotegerin. In accordance with the increase in bone resorption, glucocorticoids stimulate the expression of collagenase 3 by posttranscriptional mechanisms. The most significant effect of glucocorticoids in bone is an inhibition of bone formation. This is because of a decrease in the number of osteoblasts and their function. The decrease in cell number is secondary to a decrease in osteoblastic cell replication and differentiation, and an increase in the apoptosis of mature osteoblasts. Glucocorticoids decrease osteoblastic function directly and indirectly through the modulation of growth factor expression, receptor binding, or binding protein levels. Clinically, patients with glucocorticoid-induced osteoporosis (GIOP) develop bone loss in the first few months of glucocorticoid exposure, and modest doses of glucocorticoids increase the risk of fractures of the spine and hip. Bisphosphonates inhibit bone resorption and prevent and revert the bone loss that follows glucocorticoid exposure. Anabolic agents, such as parathyroid hormone, stimulate bone formation and can increase bone mass in GIOP.
                Bookmark

                Author and article information

                Journal
                Medicina (Kaunas)
                Medicina (Kaunas)
                medicina
                Medicina
                MDPI
                1010-660X
                1648-9144
                23 May 2021
                June 2021
                : 57
                : 6
                : 525
                Affiliations
                [1 ]College of Medicine and Medical Sciences, Arabian Gulf University (AGU), 323 Manama, Bahrain; kanzalkinooz@ 123456hotmail.com (K.W.G.); hjahrami@ 123456health.gov.bh (H.A.J.)
                [2 ]Department of Internal Medicine, University Medical Center (UMC), King Abdullah Medical City (KAMC), 323 Manama, Bahrain
                [3 ]Ministry of Health, 410 Manama, Bahrain
                Author notes
                [* ]Correspondence: adla.hassan@ 123456gmail.com (A.B.H.); amgadeem@ 123456agu.edu.bh (A.E.E.-A.)
                Author information
                https://orcid.org/0000-0002-1992-3740
                https://orcid.org/0000-0001-8990-1320
                Article
                medicina-57-00525
                10.3390/medicina57060525
                8224589
                34071098
                cc1167b5-1011-4d36-b430-3efa2209a8f9
                © 2021 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                : 03 April 2021
                : 21 May 2021
                Categories
                Review

                bone pain,cya-induced pain syndrome,renal transplant,osteoporosis,musculoskeletal,hyperuricemia

                Comments

                Comment on this article