ironjustice

I suppose since erythrocytosis is NOW been found to be a .. marker ..
of diabetes .. it may **explain** the high rate of kidney damage found
in those with .. diabetes.

Erythrocytosis causes kidney damage.

<<snip>>
degenerative processes in kidney characterized by increased vascular
permeability, chronic progressive inflammation, hemosiderin
deposition, and general vasodilatation.
<<snip>>

Am J Physiol Regul Integr Comp Physiol
Excessive erythrocytosis in adult mice overexpressing erythropoietin
leads to hepatic, renal, neuronal, and muscular degeneration
Katja Heinicke,1,2 Oliver Baum,3 Omolara O. Ogunshola,1 Johannes Vogel,
1 Thomas Stallmach,4 David P. Wolfer,5 Stephan Keller,1 Klaus Weber,6
Peter D. Wagner,2 Max Gassmann,1 and Valentin Djonov3
1Institute of Veterinary Physiology, Vetsuisse Faculty and Zurich
Center for Integrative Human Physiology (ZIHP), 4Department of
Pathology, and 5Institute of Anatomy, University of Zurich, Zurich;
3Institute of Anatomy, University of Berne, Berne; 6RCC Ltd, Itingen,
Switzerland; and 2Division of Physiology, Department of Medicine,
University of California San Diego, La Jolla, California

Submitted 6 March 2006 ; accepted in final form 8 May 2006


To investigate the consequences of inborn excessive erythrocytosis, we
made use of our transgenic mouse line (tg6) that constitutively
overexpresses erythropoietin (Epo) in a hypoxia-independent manner,
thereby reaching hematocrit levels of up to 0.89. We detected
expression of human Epo in the brain and, to a lesser extent, in the
lung but not in the heart, kidney, or liver of tg6 mice. Although no
acute cardiovascular complications are observed, tg6 animals have a
reduced lifespan. Decreased swim performance was observed in 5-mo-old
tg6 mice. At about 7 mo, several tg6 animals developed spastic
contractions of the hindlimbs followed by paralysis. Morphological
****ysis by light and electron microscopy showed degenerative
processes in liver and kidney characterized by increased vascular
permeability, chronic progressive inflammation, hemosiderin
deposition, and general vasodilatation. Moreover, most of the animals
showed severe nerve fiber degeneration of the sciatic nerve, decreased
number of neuromuscular junctions, and degeneration of skeletal muscle
fibers. Most probably, the developing demyelinating neuropathy
resulted in muscular degeneration demonstrated in the extensor
digitorum longus muscle. Taken together, chronically increased Epo
levels inducing excessive erythrocytosis leads to multiple organ
degeneration and reduced life expectancy. This model allows
investigation of the impact of excessive erythrocytosis in individuals
suffering from polycythemia vera, chronic mountain sickness, or in
subjects tempted to abuse Epo by means of gene doping.

chronic mountain sickness; erythropoietin doping; neurodegeneration;
neuromuscular junctions; polycythemia; vascular permeability

--------------------------------------------------------------------------------

Address for reprint requests and other correspondence: V. Djonov,
Institute of Anatomy, Univ. of Berne, Baltzerstrasse 2, CH-3009 Berne
9/Switzerland (e-mail: djonov@ana.unibe.ch)

Am J Physiol Regul Integr Comp Physiol 291: R947-R956, 2006. First
published May 11, 2006; doi:10.1152/ajpregu.00152.2006
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<<snip>>
Antioxidants and iron chelators have also been shown to retard
functional and
morphologic changes observed in progressive kidney disease
<<snip>>

Kidney Int Suppl. 2004 Oct(91):S50-5. Links


Oxidants and iron in chronic kidney disease.


Shah SV.


Division of Nephrology, Department of Medicine, University of Arkansas
for
Medical Sciences, Little Rock, Arkansas.


Oxidants and iron in chronic kidney disease. Oxidants derived either
from
leukocytes in proliferative glomerular nephritis or from resident
glomerular
cells in nonproliferative glomerulonephritis have been shown to have
several
biologic effects relevant to chronic kidney disease. These include:
the ability
of oxidants to damage glomerular ba*****t membrane (GBM) and to
directly induce
proteinuria; effects that would lead to a fall in the glomerular
filtration
rate; and effects that would account for the morphologic changes
observed in
chronic kidney disease. In experimental models the role of oxidants
has been
demonstrated in both proliferative glomerulonephritis (e.g., anti-GBM
antibody
disease) as well as experimental models of minimal change disease and
membranous nephropathy. Oxidants have also been shown to be an
important
mediator of the various pathways that have been implicated in
diabetic
nephropathy. Antioxidants and iron chelators have also been shown to
retard
functional and morphologic changes observed in progressive kidney
disease.
Taken together, these experimental studies suggest an important role
of
oxidants in chronic kidney disease.


PMID: 15461704 [PubMed - in process]


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