Echinocytes in the blood of hyperproteinaemic mice with proteinuria. Is the effect of such cells on blood viscosity the cause of the proteinuria?

Early studies in this series failed to obtain evidence for the cause of hyperproteinaemic proteinuria although it was speculated that blood viscosity, increased because of high plasma protein levels, might play a significant role. As we had no means of measuring blood viscosity it was decided to investigate the effects of reducing blood viscosity in a small number of mice made anaemic before subjecting them to albumin overload. All but one of the mice given injections i.p. of 250 mg HSA on 2 successive days developed proteinuria within 24 h of the first injection. This result seemed to show that altered blood viscosity was not a factor in the mechanism of the hyperproteinaemic proteinuria. However, it has been shown that changes in the red cell environment can lead to red cell deformation resulting in an increase in blood viscosity. To check on this possibility another small group of mice were injected with HSA as previously. On the morning after their second injection the mice were bled by percutaneous heart puncture and the blood was examined by scanning electron microscopy. This showed that a vast preponderance of red cells, probably more than 95%, were echinocytes. Although no measurements of blood viscosity were made, it can be speculated that hyperproteinaemic proteinuria is caused by the intraglomerular effects of blood with increased viscosity (because of the red cell transformation) being made more viscous by glomerular filtration. Enhanced protein filtration would occur because of the increase in glomerular pressure needed to restore flow of viscous blood at the efferent arteriole.(ABSTRACT TRUNCATED AT 250 WORDS)