A hypothesis proposing increased blood viscosity as a cause of proteinuria and increased vascular permeability.
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.
D001809:Blood Viscosity; D002199:Capillary Permeability; D005919:Glomerular Filtration Rate; D006801:Humans; D011507:Proteinuria / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D013839:Thiamphenicol / Q000627:therapeutic use
D013839:Thiamphenicol