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      Hypophosphatemic osteomalacia: an unusual clinical presentation of multiple myeloma

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          Abstract

          An unusual case of a 75-year-old man is presented who had multiple stress fractures due to adult onset hypophosphatemic osteomalacia, which was the result of Fanconi syndrome, with light chain cast proximal tubulopathy due to multiple myeloma. A 75-year-old man presented with diffuse pain and muscle weakness. He had multiple stress fractures, low serum phosphate, decreased renal tubular reabsorption of phosphate, and normal PTH and FGF23, indicating adult onset hypophosphatemic osteomalacia. Phosphate supplements with calcitriol resulted in clinical recovery and healing of stress fractures. Because of proteinuria, a renal biopsy was performed that revealed Fanconi syndrome with light chain cast proximal tubulopathy and light kappa chains were found in serum and urine. A bone biopsy confirmed the diagnosis of multiple myeloma, and treatment with chemotherapy resulted in cytological and clinical recovery.

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          Most cited references12

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          Multiple myeloma.

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            The pathogenesis and diagnosis of acute kidney injury in multiple myeloma.

            Renal failure remains a principal cause of morbidity for patients with multiple myeloma. Once reversible factors such as hypercalcemia have been corrected, the most common cause of severe renal failure in these patients is a tubulointerstitial pathology that results from the very high circulating concentrations of monoclonal immunoglobulin free light chains. These endogenous proteins can result in isolated proximal tubule cell cytotoxicity, tubulointerstitial nephritis and cast nephropathy (myeloma kidney). Less frequently, high levels of free light chains can lead to immunoglobulin light chain amyloidosis and light chain deposition disease, although these conditions are usually associated with insidious progression of renal failure rather than acute kidney injury. Unless there is rapid intervention, progressive and irreversible damage occurs, particularly interstitial fibrosis and tubular atrophy. Despite advances in our understanding of the pathogenesis of these processes there has been a gap in translating these achievements into improved patient outcomes. The International Kidney and Monoclonal Gammopathy Research Group was formed to address this need. In this Review, we discuss the mechanisms of disease and diagnostic approaches to patients with acute kidney injury complicating multiple myeloma.
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              The pathogenesis of the bone disease of multiple myeloma.

              Multiple myeloma is a fatal hematologic malignancy associated with clonal expansion of malignant plasma cells within the bone marrow and the development of a destructive osteolytic bone disease. The principal cellular mechanisms involved in the development of myeloma bone disease are an increase in osteoclastic bone resorption, and a reduction in bone formation. Myeloma cells are found in close association with sites of active bone resorption, and the interactions between myeloma cells and other cells within the specialized bone marrow microenvironment are essential, both for tumor growth and the development of myeloma bone disease. This review discusses the many different factors which have been implicated in myeloma bone disease, including the evidence for their role in myeloma and subsequent therapeutic implications.
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                Author and article information

                Contributors
                margotreyskens@gmail.com
                kristiensleurs@hotmail.com
                Luc.Verresen@zol.be
                mia.janssen@zol.be
                j@vdbergh.org
                00 31 43 3875026 , piet.geusens@scarlet.be
                Journal
                Osteoporos Int
                Osteoporos Int
                Osteoporosis International
                Springer London (London )
                0937-941X
                1433-2965
                24 April 2015
                24 April 2015
                2015
                : 26
                : 7
                : 2039-2042
                Affiliations
                [ ]University Hasselt, Diepenbeek, Belgium
                [ ]ZOL, Genk, Belgium
                [ ]Limburg Oncologic Center, Hasselt, Belgium
                [ ]Department of Internal Medicine, VieCuri Medical Centre, PO Box 1926, 5900 BX Venlo, The Netherlands
                [ ]Department of Internal Medicine, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre (MUMC), PO Box 616, 6200 MD Maastricht, The Netherlands
                [ ]Biomedical Research Centre, Hasselt University, Agoralaan – gebouw D, 3590 Diepenbeek, Belgium
                [ ]Department of Internal Medicine, Subdivision Rheumatology, CAPHRI, Maastricht University Medical Centre (MUMC), PO Box 616, 6200 MD Maastricht, The Netherlands
                [ ]Department of Medicine, Subdivision of Rheumatology, Academic Hospital azM, P. Debyelaan 25, Postbus 5800, 6202 AZ Maastricht, The Netherlands
                Article
                3090
                10.1007/s00198-015-3090-5
                4483244
                25906239
                2be59b4f-80fa-4ee9-83f9-06cb96c50b3e
                © The Author(s) 2015

                Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

                History
                : 27 November 2014
                : 25 February 2015
                Categories
                Case Report
                Custom metadata
                © International Osteoporosis Foundation and National Osteoporosis Foundation 2015

                Orthopedics
                fanconi syndrome,multiple myeloma,myeloma cast nephropathy,osteomalacia,stress fracture

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