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

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.

Massive Obesity and Nephrotic Proteinuria with a Normal Renal Biopsy

“…Simpson [6,7] has proposed that glomerular basement membranes have chemical composition and physical characteristics of thixotropic nature. This implies that local increases in hydrostatic pressure induce localized reductions in the viscosity of the membrane secondary to changes in the lattice arrangement of the basement membrane lipids, making their configuration more random (gel-like).…”

The pancreatic polypeptide-rich lobe of the human pancreas: Definitive identification of its derivation from the ventral pancreatic primordium

“…1A). An annular pancreas results from a defect in rotation of the ventral primordium towards the dorsal pancreatic bud [3]. The fact that all the abnormally-developed tissue showed a distinct pancreatic polypeptide immunofluorescence proves the hypothesis that the ventral primordium is the origin of the pancreatic tissue rich in pancreatic polypeptide.…”

Renal Disease, Polyunsaturated Fatty Acids and Blood Rheology

“…Suppor tive evidence for a functional rather than a morphologi cal basis for renal disease comes from the recent demon stration that transplanted diabetic kidneys lost their stig mata of diabetic nephropathy when grafted into non-dia betic recipients [16]. However, until the effects on renal function of manifestations of disordered haemorheology such as increased blood viscosity [17,18] and poorly deformable red cells [19] are incorporated into concepts of renal function, it is unlikely that the potential of PUFAs to assist in the correction of such abnormalities will be recognised.…”