Re: Preeclampsia, Hypothyroidism, and Hyperviscosity
As it is a long time since I heard Dr.John Hobbs report on his
findings re blood viscosity in pre-eclampsia, in my previous submission
all I did was to draw attention to the published information concerning
increased blood viscosity in that condition.
If Dr.Levine's observations are correct, does this mean that the
early investigators had reported erroneous information ? In their 2003
paper (Maynard et al) it was claimed that it was endothelial dysfunction
which was responsible for the proteinuria. But there is published
evidence which shows that the glomerular basement membrane is a
thixotropic gel, which exhibits pressure-dependent permeability. Thus the
higher the filtration pressure, the larger the proteins in the filtrate.
When blood viscosity is increased, from whatever cause, this will be
reflected in a proteinuria, as after filtration with an elevated
filtration pressure, the blood in the efferent arteriole is hyperviscous
and impairs blood flow in the peritubular plexus.
I am left with the thought that the authors are unaware of the fact
that if the internal environment is changed, then the shape populations of
red cells change and become poorly deformable. Note that poorly
deformable red cells have been recorded in pre-eclampsia.
Dr.Levine may also find of some interest the reports which relate
blood pressure to blood viscosity. While these date back to 1930, the
more recent work of Letcher et al is significant. The quoted references
seem to indicate that the various authors have failed to recognise the
physiological consequences of changes in the physical properties of blood.
Rapid Response:
Re: Preeclampsia, Hypothyroidism, and Hyperviscosity
As it is a long time since I heard Dr.John Hobbs report on his
findings re blood viscosity in pre-eclampsia, in my previous submission
all I did was to draw attention to the published information concerning
increased blood viscosity in that condition.
If Dr.Levine's observations are correct, does this mean that the
early investigators had reported erroneous information ? In their 2003
paper (Maynard et al) it was claimed that it was endothelial dysfunction
which was responsible for the proteinuria. But there is published
evidence which shows that the glomerular basement membrane is a
thixotropic gel, which exhibits pressure-dependent permeability. Thus the
higher the filtration pressure, the larger the proteins in the filtrate.
When blood viscosity is increased, from whatever cause, this will be
reflected in a proteinuria, as after filtration with an elevated
filtration pressure, the blood in the efferent arteriole is hyperviscous
and impairs blood flow in the peritubular plexus.
I am left with the thought that the authors are unaware of the fact
that if the internal environment is changed, then the shape populations of
red cells change and become poorly deformable. Note that poorly
deformable red cells have been recorded in pre-eclampsia.
Dr.Levine may also find of some interest the reports which relate
blood pressure to blood viscosity. While these date back to 1930, the
more recent work of Letcher et al is significant. The quoted references
seem to indicate that the various authors have failed to recognise the
physiological consequences of changes in the physical properties of blood.
Competing interests:
None declared
Competing interests: No competing interests