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Research Article| Volume 13, ISSUE 1, P183-207, March 1993

Assessment of Hyperphosphatemia and Hypophosphatemia

  • Bourke Edmund
    Correspondence
    Address reprint requests to: Edmund Bourke, MD VAMC, Department of Medicine, 800 Poly Place, Room 970, Brooklyn, NY 11209.
    Affiliations
    Department of Medicine, Veterans Administration Medical Center, Brooklyn; and Department of Medicine, State University of New York, Health Science Center, Brooklyn, New York
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  • Yanagawa Norimoto
    Affiliations
    UCLA/San Fernando Valley Program, San Fernando; and Department of Veteran’s Affairs, Olive View Medical Center, Sepulveda Veteran’s Administration Medical Center, Sepulveda, California
    Search for articles by this author
      This paper is only available as a PDF. To read, Please Download here.
      Methodologic aspects including causes of factitious hyperphosphatemia and hypophosphatemia are summarized. The differential diagnosis of hyperphosphatemia is reviewed under its three broad causes: decreased glomerular filtration rate, increased exogenous or endogenous phosphate load, and increased renal tubular phosphate reabsorption. The differential diagnosis of hypophosphatemia is reviewed under its three broad causes: inadequate gastrointestinal input, excess phosphate losses, and transcellular shifts. The consequences of hyperphosphatemia and hypophosphatemia are outlined with a focus on pathophysiologic and clinicochemical sequelae. A laboratory perspective is emphasized in outlining management strategies.
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