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NDT Advance Access originally published online on June 9, 2006
Nephrology Dialysis Transplantation 2006 21(9):2664-2666; doi:10.1093/ndt/gfl306
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Teaching Point
(Section Editor: A. Meyrier)

A patient with unexplained hyperphosphataemia

Piero Stratta1, Caterina Canavese1, Marco Quaglia1, Elisa Lazzarich1, Veronica Morellini1, Maddalena Brustia1, Beatrice Bardone2 and Giorgio Bellomo2

1 Departments of Nephro-Urology, Nephrology and Transplantation and 2 Department of Biomedical Sciences, Laboratory of Chemistry and Clinical Research, Amedeo Avogadro University, Maggiore Hospital, Novara, Italy

Correspondence and offprint requests to: Prof. Piero Stratta, Transplantation and Nephrology, Department of Nephro-Urology, Amedeo Avogadro University, Novara, Ospedale Maggiore della Carità, Corso Mazzini 18, 28100 Novara, Italy. Email: strattanefro@hotmail.com

Keywords: monoclonal gammopathy; myeloma; paraproteinaemia; phosphate

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   Introduction
 
Hyperphosphataemia is not a common biochemical alteration outside the context of renal failure. In fact, phosphate homeostasis is mainly regulated by kidney function and parathyroid hormone (PTH) activity [1–4]. In the presence of normal renal function and normal PTH activity, serum phosphate values are tightly regulated within a reference range of 0.8–1.5 mmol/l (2.5–4.5 mg/dl). As phosphates are filtered by the glomerular barrier and excreted into the urine with a renal clearance of 15–20 ml/min, serum phosphate levels do increase early from the beginning of renal failure, reaching levels as high as 4–5 mmol/l in the case of end-stage renal failure . . . [Full Text of this Article]



   Case report
 


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   Teaching points
 

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