Diagnostics,
Journal Year:
2022,
Volume and Issue:
12(1), P. 180 - 180
Published: Jan. 12, 2022
Contrast-induced
nephropathy
(CIN)
is
an
impairment
of
renal
function
that
occurs
after
the
administration
iodinated
contrast
medium
(CM).
Kidney
dysfunction
in
CIN
considered
transient
and
reversible
most
cases.
However,
it
third
common
cause
hospital-acquired
acute
kidney
injury
associated
with
increased
morbidity
mortality,
especially
high-risk
patients.
Diagnostic
interventional
procedures
require
intravascular
CM
are
being
used
increasing
frequency,
among
elderly,
who
can
be
particularly
susceptible
to
due
multiple
comorbidities.
Therefore,
identifying
exact
mechanisms
its
risk
factors
crucial
not
only
provide
optimal
preventive
management
for
at-risk
patients,
but
also
increase
feasibility
diagnostic
procedure
use
CM.
induces
by
impairing
hemodynamics
generation
reactive
oxygen
species,
addition
direct
cytotoxicity.
Periprocedural
hydration
widely
accepted
strategy
date.
Here,
we
review
latest
research
results
on
pathophysiology
CIN.
AJP Regulatory Integrative and Comparative Physiology,
Journal Year:
2020,
Volume and Issue:
319(6), P. R690 - R702
Published: Oct. 14, 2020
Glomerular
filtration
rate
(GFR)
is
acutely
increased
following
a
high-protein
meal
or
systemic
infusion
of
amino
acids.
The
mechanisms
underlying
this
renal
functional
response
remain
to
be
fully
elucidated.
Nevertheless,
they
appear
culminate
in
preglomerular
vasodilation.
Inhibition
the
tubuloglomerular
feedback
signal
appears
critical.
However,
nitric
oxide,
vasodilator
prostaglandins,
and
glucagon
also
important.
increase
GFR
during
acid
reveals
“renal
reserve,”
which
can
utilized
when
physiological
demand
for
single
nephron
increases.
This
has
led
concept
that
subclinical
disease,
before
basal
begins
reduce,
reserve
recruited
manner
preserves
function.
extension
once
decline
detected,
disease
already
well
progressed.
likely
applies
both
contexts
chronic
kidney
acute
injury.
Critically,
its
corollary
deficits
have
potential
provide
early
detection
dysfunction
reduced.
There
growing
evidence
acids
used
identify
patients
at
risk
developing
either
injury
as
treatment
target
large
multicenter
clinical
trials
are
required
test
these
propositions.
A
renewed
effort
understand
physiology
warranted.
Frontiers in Cell and Developmental Biology,
Journal Year:
2020,
Volume and Issue:
8
Published: Feb. 27, 2020
Inflammasomes,
multiprotein
complex
induced
by
harmful
factors
in
the
body,
play
a
crucial
role
innate
immunity.
Activation
of
inflammasomes
lead
to
activation
casepase-1
and
then
secretion
inflammatory
cytokines,
including
IL-1β
IL-18,
subsequently
leading
type
cell
death
called
pyroptosis.
There
are
two
types
signaling
pathways
involved
process
inflammasome
activation:
canonical
non-canonical
pathway.
The
pathway
is
mainly
dependent
on
casepase-1;
signal
pathway,
which
was
recently
discovered,
caspase-11,
but
also
meditated
caspase-4,
caspase-5
caspase-8.
Kidney
inflammation
basically
associated
with
factor
exudation
infiltration.
Several
studies
have
showed
that
closely
related
kidney
diseases,
especially
NLRP3
inflammasome,
regulating
fibrosis.
In
this
review,
we
focus
relationship
between
different
kinds
disease
via
both
pathways.
Journal of Cardiovascular Pharmacology,
Journal Year:
2022,
Volume and Issue:
79(6), P. 904 - 913
Published: March 31, 2022
Contrast-induced
acute
kidney
injury
(CI-AKI)
causes
clinically
acquired
nephropathy
in
patients
who
undergo
coronary
interventions.
Hypoxic
to
proximal
tubular
epithelial
cells
is
a
pathological
mechanism
of
CI-AKI.
Previous
studies
have
shown
that
hypoxia
activates
HIF-1α/HE4/NF-κB
enhance
renal
fibrosis,
and
the
SGLT-2
inhibitor
luseogliflozin
inhibits
hypoxia-inducible
factor
(HIF)-1α
expression
reduce
progression
diabetic
nephropathy.
However,
therapeutic
effects
mechanisms
inhibitors
on
CI-AKI
are
unclear.
We
explored
role
pathway
how
dapagliflozin
effectively
treats
by
inhibiting
this
pathway.
In
vitro,
were
divided
into
control,
hypoxia,
+
dapagliflozin,
pSilencer-HIF-1α
groups.
Cellular
apoptosis,
related
protein
evaluated
immunofluorescence,
western
blotting,
flow
cytometry,
respectively.
Dapagliflozin
significantly
decreased
oxygen
consumption,
HIF-1α,
human
epididymis
4
(HE4),
NF-κB
expression,
apoptotic
compared
with
control
(P
<
0.01).
vivo,
rats
(C),
diabetes
(D),
contrast
media,
media
Rats
latter
2
groups
treated
for
days.
was
induced
intravenously
injecting
indomethacin,
N-nitro-l-arginine
methyl
ester,
iohexol.
The
elucidated
assessing
function,
H&E
staining,
immunohistochemistry.
Serum
creatinine,
urea
nitrogen,
TUNEL-positive
cells,
HE4,
histopathological
scores
increased
C,
D,
Thus,
may
ameliorate
through
suppression
signaling
vitro
vivo.
ACS Applied Materials & Interfaces,
Journal Year:
2023,
Volume and Issue:
15(14), P. 17664 - 17674
Published: April 3, 2023
Acute
kidney
injuries
(AKI)
have
serious
short-term
or
long-term
complications
with
high
morbidity
and
mortality
rate,
thus
posing
great
health
threats.
Developing
high-performance
NIR-II
probes
for
noninvasive
in
situ
detection
of
AKI
via
fluorescent
optoacoustic
dual-mode
imaging
is
significance.
Yet
chromophores
often
feature
long
conjugation
hydrophobicity,
which
prevent
them
from
being
renal
clearable,
limiting
their
applications
the
diseases.
To
fully
exploit
advantageous
features
heptamethine
cyanine
dye,
while
overcoming
its
relatively
poor
photostability,
to
strive
design
a
probe
imaging,
herein,
we
developed
PEG3-HC-PB,
water
soluble,
biomarker
activatable
has
good
photostability.
As
probe,
fluorescence
(900-1200
nm)
quenched
due
existence
electron-pulling
phenylboronic
group
(responsive
element),
it
exhibits
weak
absorption
peak
at
830
nm.
Meanwhile,
presence
overexpressed
H2O2
region
case
AKI,
converted
phenylhydroxy
group,
enhances
emission
(600-900
eventually
produces
conspicuous
signals
imaging.
This
enables
contrast-agent-induced
ischemia/reperfusion-induced
mice
using
real-time
3D-MSOT
response
H2O2.
Hence,
this
can
be
used
as
practicable
tool
detecting
AKI;
additionally,
strategy
could
provide
insight
into
other
large-conjugation
multifarious
biological
applications.
JCI Insight,
Journal Year:
2021,
Volume and Issue:
unknown
Published: July 6, 2021
The
mitochondrial
enzyme
aldehyde
dehydrogenase
2
(ALDH2)
catalyzes
the
detoxification
of
acetaldehyde
and
endogenous
lipid
aldehydes.
Approximately
40%
East
Asians,
accounting
for
8%
human
population,
carry
E504K
mutation
in
ALDH2
that
leads
to
accumulation
toxic
reactive
aldehydes
increases
risk
cardiovascular
disease,
cancer,
Alzheimer
among
others.
However,
role
acute
kidney
injury
(AKI)
remains
poorly
defined
is
therefore
subject
present
study
using
various
cellular
organismal
sources.
In
murine
models,
which
AKI
was
induced
by
either
contrast
agent
iohexol
or
renal
ischemia/reperfusion,
KO,
activation/overexpression
were
associated
with
increased
decreased
injury,
respectively.
tubular
epithelial
cells
(RTECs),
upregulated
Beclin-1
expression,
promoted
autophagy
activation,
eliminated
ROS.
vivo
vitro,
both
3-MA
siRNAs
inhibited
abolished
ALDH2-mediated
renoprotection.
mice
iohexol-induced
AKI,
knockdown
RTECs
AAV-shRNA
impaired
activation
aggravated
injury.
proximal
HK-2
exposed
iohexol,
potentiated
attenuated
apoptosis.
overexpression
pretreatment
regulated
mitigating
apoptosis
summary,
our
data
collectively
substantiate
a
critical
via
involving
pathway.