Journal of Translational Medicine,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Feb. 18, 2024
The
global
incidence
of
Chronic
Kidney
Disease
(CKD)
is
steadily
escalating,
with
discernible
linkage
to
the
intricate
terrain
intestinal
microecology.
microbiota
orchestrates
a
dynamic
equilibrium
in
organism,
metabolizing
dietary-derived
compounds,
process
which
profoundly
impacts
human
health.
Among
these
short-chain
fatty
acids
(SCFAs),
result
from
microbial
metabolic
processes,
play
versatile
role
influencing
host
energy
homeostasis,
immune
function,
and
intermicrobial
signaling,
etc.
SCFAs
emerge
as
pivotal
risk
factors
CKD's
development
prognosis.
This
paper
review
elucidates
impact
gut
metabolites,
specifically
SCFAs,
on
CKD,
highlighting
their
modulating
inflammatory
responses,
oxidative
stress,
cellular
autophagy,
milieu,
signaling
cascades.
An
in-depth
comprehension
interplay
between
kidney
disease
pathogenesis
may
pave
way
for
utilization
biomarkers
CKD
progression
prognosis
or
novel
adjunctive
therapeutic
strategies.
AJP Renal Physiology,
Journal Year:
2019,
Volume and Issue:
316(6), P. F1211 - F1217
Published: March 13, 2019
The
gut
microbiome
is
composed
of
a
diverse
population
bacteria
that
have
beneficial
and
adverse
effects
on
human
health.
has
recently
gained
attention
increasingly
noted
to
play
significant
role
in
health
number
disease
states.
Increasing
urea
concentration
during
chronic
kidney
(CKD)
leads
alterations
the
intestinal
flora
can
increase
production
gut-derived
toxins
alter
epithelial
barrier.
These
changes
lead
an
acceleration
process
injury.
A
strategies
been
proposed
interrupt
this
pathway
injury
CKD.
purpose
review
summarize
CKD,
tools
used
study
microbial
population,
attempts
its
composition
for
therapeutic
purposes.
Kidney International,
Journal Year:
2017,
Volume and Issue:
92(3), P. 634 - 645
Published: April 8, 2017
Gut
microbiota
is
involved
in
the
metabolism
of
uremic
solutes.
However,
precise
influence
to
retention
solutes
CKD
obscure.
To
clarify
this,
we
compared
adenine-induced
renal
failure
and
control
mice
under
germ-free
or
specific
pathogen-free
(SPF)
conditions,
examining
metabolite
profiles
plasma,
feces,
urine
using
a
capillary
electrophoresis
time-of-flight
mass
spectrometry-based
approach.
Mice
with
conditions
demonstrated
significant
changes
plasma
metabolites.
Among
183
detected
solutes,
levels
11
including
major
toxins,
were
significantly
lower
than
SPF
failure.
These
considered
microbiota-derived
included
indoxyl
sulfate,
p-cresyl
phenyl
cholate,
hippurate,
dimethylglycine,
γ-guanidinobutyrate,
glutarate,
2-hydroxypentanoate,
trimethylamine
N-oxide,
phenaceturate.
Metabolome
profiling
showed
that
these
classified
into
three
groups
depending
on
their
origins:
completely
derived
from
(indoxyl
sulfate),
both
host
(dimethylglycine),
dietary
components
(trimethylamine
N-oxide).
Additionally,
resulted
disappearance
colonic
short-chain
fatty
acids,
decreased
utilization
intestinal
amino
more
severe
damage
Microbiota-derived
acids
efficient
acid
may
have
renoprotective
effect,
loss
factors
exacerbate
Thus,
contributes
substantially
production
harmful
but
conversely,
growth
without
has
effects
progression.
Clinical Science,
Journal Year:
2018,
Volume and Issue:
132(5), P. 509 - 522
Published: March 9, 2018
In
chronic
kidney
disease
(CKD),
influx
of
urea
and
other
retained
toxins
exerts
a
change
in
the
gut
microbiome.
There
is
decreased
number
beneficial
bacteria
that
produce
short-chain
fatty
acids,
an
essential
nutrient
for
colonic
epithelium,
concurrent
with
increase
uremic
such
as
indoxyl
sulphate,
p-cresyl
trimethylamine-N-oxide
(TMAO).
Due
to
intestinal
wall
inflammation
degradation
intercellular
tight
junctions,
gut-derived
translocate
into
bloodstream
exert
systemic
effects.
this
review,
we
discuss
evidence
supporting
role
promoting
multiorgan
dysfunction
via
inflammatory,
oxidative
stress,
apoptosis
pathways.
End-organ
effects
include
vascular
calcification,
fibrosis,
anemia,
impaired
immune
system,
adipocyte
insulin
resistance,
low
turnover
bone
disease.
Higher
blood
levels
are
associated
increased
cardiovascular
events
mortality
CKD
population.
Clinical
trials
have
examined
interventions
trap
toxic
products
or
reverse
microbial
dysbiosis
oral
activated
charcoal
AST-120,
prebiotics
probiotics
not
shown
impact
on
survival
outcomes
but
were
limited
by
sample
size
short
trials.
summary,
microbiome
major
contributor
adverse
progression
CKD.
Frontiers in Microbiology,
Journal Year:
2020,
Volume and Issue:
11
Published: June 25, 2020
The
gastrointestinal
(GI)
microbiome
of
cats
and
dogs
is
increasingly
recognized
as
a
metabolically
active
organ
inextricably
linked
to
pet
health.
Food
serves
substrate
for
the
GI
plays
significant
role
in
defining
composition
metabolism
microbiome.
microbiome,
turn,
facilitates
host's
nutrient
digestion
production
postbiotics,
which
are
bacterially
derived
compounds
that
can
influence
Consequently,
owners
have
shaping
through
food
they
choose
provide.
Yet,
clear
understanding
impact
these
choices
on
thus
overall
health
pet,
lacking.
Pet
foods
formulated
contain
typical
nutritional
building
blocks
carbohydrates,
proteins,
fats,
but
include
microbiome-targeted
ingredients,
such
prebiotics
probiotics.
Each
categories,
well
their
relative
proportions
food,
affect
and/or
function
Accumulating
evidence
suggests
dietary
components
may
not
only
disease,
also
allergies,
oral
health,
weight
management,
diabetes,
kidney
disease
changes
Until
recently,
focus
research
was
characterize
alterations
states,
while
less
effort
has
been
devoted
how
nutrition
by
modifying
function.
This
review
summarizes
examines
impacting
host
variety
states.
Understanding
modulate
reveal
new
avenues
enhancing
resilience
dogs.
Oxidative Medicine and Cellular Longevity,
Journal Year:
2019,
Volume and Issue:
2019, P. 1 - 16
Published: Oct. 3, 2019
Diabetic
nephropathy
is
the
leading
cause
of
chronic
kidney
disease
(CKD)
in
western
countries.
Notably,
it
has
a
rapidly
rising
prevalence
China.
The
patients,
commonly
complicated
with
cardiovascular
diseases
and
neurologic
disorders,
are
at
high
risk
to
progress
into
end-stage
renal
(ESRD)
death.
However,
pathogenic
mechanisms
diabetic
have
not
been
determined.
Cellular
senescence,
which
recently
gained
broad
attention,
thought
be
an
important
player
onset
development
nephropathy.
In
this
issue,
we
generally
review
cellular
senescence
nephropathy,
involve
telomere
attrition,
DNA
damage,
epigenetic
alterations,
mitochondrial
dysfunction,
loss
Klotho,
Wnt/β-catenin
signaling
activation,
persistent
inflammation,
accumulation
uremic
toxins.
Moreover,
highlight
potential
therapeutic
targets
provide
clues
for
clinical
strategies.