Kidney International,
Journal Year:
2020,
Volume and Issue:
97(6), P. 1230 - 1242
Published: Feb. 17, 2020
Chronic
kidney
disease
(CKD)
is
characterized
by
accumulation
of
protein-bound
uremic
toxins
such
as
p-cresyl
sulfate,
glucuronide,
indoxyl
sulfate
and
indole-3-acetic
acid,
which
originate
in
the
gut.
Intestinal
bacteria
metabolize
aromatic
amino
acids
into
p-cresol
indole,
(further
conjugated
colon
mucosa
liver)
acid.
Here
we
measured
fecal,
plasma
urine
metabolite
concentrations;
contribution
gut
bacterial
generation
to
accumulation;
influx
circulating
at
different
stages
CKD.
Feces,
blood
were
collected
from
14
control
individuals
141
patients
with
Solutes
quantified
ultra-high
performance
liquid
chromatography.
To
assess
rate
p-cresol,
indole
fecal
samples
cultured
ex
vivo.
With
CKD
progression,
an
increase
levels
was
observed
plasma,
whereas
these
their
precursors
remained
same
feces
urine.
Anaerobic
culture
showed
no
difference
vivo
acid
generation.
Therefore,
differences
between
cannot
be
explained
rates
gut,
suggesting
retention
due
impaired
function
main
contributor
increased
levels.
Thus,
fractional
clearance
decreased
progression
CKD,
tubular
appeared
more
affected
than
glomerular
filtration
rate,
there
net
lumen
American Journal of Nephrology,
Journal Year:
2014,
Volume and Issue:
39(3), P. 230 - 237
Published: Jan. 1, 2014
Intestinal
microbiome
constitutes
a
symbiotic
ecosystem
that
is
essential
for
health,
and
changes
in
its
composition/function
cause
various
illnesses.
Biochemical
milieu
shapes
the
structure
function
of
microbiome.
Recently,
we
found
marked
differences
abundance
numerous
bacterial
taxa
between
ESRD
healthy
individuals.
Influx
urea
uric
acid
dietary
restriction
fruits
vegetables
to
prevent
hyperkalemia
alter
patients'
intestinal
milieu.
We
hypothesized
relative
abundances
bacteria
possessing
urease,
uricase,
p-cresol-
indole-producing
enzymes
increased,
while
containing
converting
fiber
short-chain
fatty
acids
(SCFA)
reduced
ESRD.Reference
sets
genes
interest
were
compiled
family,
families
showing
differential
12
24
individuals
enrolled
our
original
study
compiled.
Overlap
was
assessed
using
hypergeometric
distribution
tests.Among
19
microbial
dominant
patients,
possessed
5
4
indole
p-cresol-forming
enzymes.
Among
diminished
2
butyrate-forming
Probabilities
these
overlapping
distributions
<0.05.ESRD
patients
exhibited
significant
expansion
p-cresol
forming
enzymes,
contraction
Given
deleterious
effects
indoxyl
sulfate,
urea-derived
ammonia,
beneficial
actions
SCFA,
metabolism
contribute
uremic
toxicity
inflammation.
New England Journal of Medicine,
Journal Year:
2017,
Volume and Issue:
377(18), P. 1765 - 1776
Published: Nov. 1, 2017
The
nutritional
status
of
patients
with
chronic
kidney
disease
is
generally
compromised
and
requires
dietary
adjustments.
This
review
considers
several
aspects
the
management
in
adults.
The Nephron journals/Nephron journals,
Journal Year:
2015,
Volume and Issue:
130(2), P. 92 - 98
Published: Jan. 1, 2015
Chronic
inflammation
is
a
non-traditional
risk
factor
for
cardiovascular
mortality
in
the
chronic
kidney
disease
(CKD)
population.
In
recent
years,
gastrointestinal
tract
has
emerged
as
major
instigator
of
systemic
CKD.
Postmortem
studies
previously
discovered
gut
wall
throughout
digestive
dialysis
patients.
CKD
animals,
colon
associated
with
breakdown
epithelial
tight
junction
barrier
(‘leaky
gut')
and
translocation
bacterial
DNA
endotoxin
into
bloodstream.
Gut
have
also
been
detected
serum
from
patients,
whereby
levels
increase
stage
correlate
severity
The
diet
that
low
plant
fiber
symbiotic
organisms
(in
adherence
potassium,
phosphorus
intake)
can
alter
normal
microbiome,
leading
to
overgrowth
bacteria
produce
uremic
toxins
such
cresyl
indoxyl
molecules.
these
‘leaky
gut'
bloodstream
further
promotes
inflammation,
adverse
outcomes
progression.
Data
are
lacking
on
optimal
yogurt
consumption
would
favor
growth
more
microbiome
while
avoiding
potassium
overload.
Prebiotic
probiotic
formulations
shown
promise
small
clinical
trials,
terms
lowering
improving
quality
life.
evidence
points
strong
relationship
between
intestinal
CKD,
trials
investigating
gut-targeted
therapeutics
needed.
Nephrology Dialysis Transplantation,
Journal Year:
2015,
Volume and Issue:
31(5), P. 737 - 746
Published: April 16, 2015
Chronic
kidney
disease
(CKD)
results
in
systemic
inflammation
and
oxidative
stress
which
play
a
central
role
CKD
progression
its
adverse
consequences.
Although
many
of
the
causes
consequences
have
been
extensively
explored,
little
attention
had
paid
to
intestine
microbial
flora
as
potential
source
these
problems.
Our
recent
studies
revealed
significant
disruption
colonic,
ileal,
jejunal
gastric
epithelial
tight
junction
different
models
rats.
Moreover,
barrier
structure
function
found
uremic
animals
was
replicated
cultured
human
colonocytes
exposed
plasma
vitro
We
further
changes
composition
colonic
bacterial
humans
with
advanced
CKD.
Together,
uremia-induced
impairment
intestinal
gut
microbiome
contribute
toxicity
by
accommodating
translocation
endotoxin,
fragments
other
noxious
luminal
products
circulation.
In
addition,
bacteria
are
main
several
well-known
pro-inflammatory
toxins
such
indoxyl
sulfate,
p-cresol
trimethylamine-N-oxide
as-yet
unidentified
retained
compounds
end-stage
renal
patients.
This
review
is
intended
provide
an
overview
effects
on
their
pathogenesis
toxicity.
interventions
aimed
at
mitigating
abnormalities
briefly
discussed.
Gut Microbes,
Journal Year:
2013,
Volume and Issue:
5(2), P. 202 - 207
Published: Dec. 20, 2013
The
maintenance
of
blood
pressure
homeostasis
is
a
complex
process
which
carefully
regulated
by
variety
inputs.
We
recently
identified
two
sensory
receptors
(Olfactory
receptor
78
and
G
protein
couple
41)
as
novel
regulators
pressure.
Both
Olfr78
Gpr41
are
for
short
chain
fatty
acids
(SCFAs),
we
showed
that
propionate
(a
SCFA)
modifies
in
manner
differentially
modulated
the
absence
either
or
Gpr41.
In
addition,
renin
release
an
Olfr78-dependent
manner.
Our
study
also
demonstrated
antibiotic
treatment
modulates
null
mice,
indicating
SCFAs
produced
gut
microbiota
likely
influence
regulation.
this
addendum,
summarize
findings
our
recent
provide
perspective
on
implications
interactions
between
control.
Journal of Translational Medicine,
Journal Year:
2019,
Volume and Issue:
17(1)
Published: Jan. 3, 2019
Dysbiosis
represents
changes
in
composition
and
structure
of
the
gut
microbiome
community
(microbiome),
which
may
dictate
physiological
phenotype
(health
or
disease).
Recent
technological
advances
efforts
metagenomic
metabolomic
analyses
have
led
to
a
dramatical
growth
our
understanding
microbiome,
but
still,
mechanisms
underlying
microbiome-host
interactions
healthy
diseased
state
remain
elusive
their
elucidation
is
infancy.
Disruption
normal
microbiota
lead
intestinal
dysbiosis,
barrier
dysfunction,
bacterial
translocation.
Excessive
uremic
toxins
are
produced
as
result
alteration,
including
indoxyl
sulphate,
p-cresyl
trimethylamine-N-oxide,
all
implicated
variant
processes
kidney
diseases
development.
This
review
focuses
on
pathogenic
association
between
(the
gut-kidney
axis),
covering
CKD,
IgA
nephropathy,
nephrolithiasis,
hypertension,
acute
injury,
hemodialysis
peritoneal
dialysis
clinic.
Targeted
interventions
probiotic,
prebiotic
symbiotic
measures
discussed
for
potential
re-establishing
symbiosis,
more
effective
strategies
treatment
patients
suggested.
The
novel
insights
into
dysbiosis
helpful
develop
therapeutic
preventing
attenuating
complications.
Inflammatory Intestinal Diseases,
Journal Year:
2016,
Volume and Issue:
1(3), P. 135 - 145
Published: Jan. 1, 2016
<b><i>Background:</i></b>
Increased
intestinal
permeability
due
to
barrier
dysfunction
is
supposed
cause
microbial
translocation
which
may
induce
low-grade
inflammation
in
various
diseases.
However,
this
series
of
events
has
not
been
comprehensively
evaluated
yet.
<b><i>Summary:</i></b>
Intestinal
epithelial
and
increased
have
described
patients
with
inflammatory
bowel
disease
(IBD),
irritable
syndrome
(IBS),
alcoholic
liver
disease,
nonalcoholic
steatohepatitis
(NASH),
cirrhosis,
acute
pancreatitis,
primary
biliary
cholangitis
(PBC),
type
1
2
diabetes,
chronic
kidney
heart
failure
(CHF),
depression,
other
Most
clinical
reports
used
either
assays
challenge
tests
or
measurement
circulating
bacterial
markers
like
endotoxin
for
assessment
‘the
leaky
gut'.
The
assessed
by
the
often
related
changes
tight
junction
proteins
epithelium
levels.
In
IBD,
NASH,
PBC,
obstructive
jaundice,
severe
CHF,
endotoxemia
proinflammatory
cytokinemia
found
addition
permeability.
serum
IBS
antiflagellin
antibodies
antilipid
A
were
detected,
respectively,
together
cytokinemia.
site
infection,
localized
intestine
IBD
IBS,
includes
extraintestinal
organs
relation
gut
dysbiosis
gradually
clarified.
<b><i>Key
Messages:</i></b>
Although
no
direct
cause-and-effect
relationship
confirmed,
all
experimental
data
suggest
importance
hyperpermeability
a
new
target
prevention
therapy.
Considering
close
gut'
major
diseases,
we
can
conclude
that
meticulous
dietetic
probiotic
approaches
recover
healthy
microbiota
potential
make
breakthrough
management
these
diseases
tomorrow.