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      A Hypothesis Proposing Increased Blood Viscosity as a Cause of Proteinuria and Increased Vascular Permeability

      Nephron

      S. Karger AG

      Blood viscosity, Proteinuria, Vascular permeability, Biological thixotropy, Basement membranes, Blood rheology

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          Abstract

          Currently accepted concepts of renal and vascular physiology are inadequate to explain the reversible increases in vascular permeability which occur during episodes of increased blood viscosity. On the basis that all basement membranes exhibit biological thixotropy, it has been suggested that basement membranes are pressure dependent. The physiological significance of increased blood viscosity lies in the associated increase in peripheral vascular resistance which develops because of altered blood rheology. In order to overcome the peripheral resistance, intravascular pressure rises, and if adequate pressures develop, plasma proteins may deform and pass through the vascular basement membrane. This is considered to be the mechanism of proteinuria. In the treatment of high blood viscosity disorders it is suggested that the immunosuppressant drug, Thiamphenicol, may be useful because of its ability to induce a reversible dose-related depression of erythropoiesis, and thereby reduce blood viscosity.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1982
          1982
          03 December 2008
          : 31
          : 1
          : 89-93
          Affiliations
          Pathology Department, University of Otago Medical School, Dunedin, New Zealand
          Article
          182623 Nephron 1982;31:89–93
          10.1159/000182623
          7110479
          © 1982 S. Karger AG, Basel

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          Page count
          Pages: 5
          Categories
          Hypothesis

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