The Italian Journal of Pediatrics/Italian journal of pediatrics,
Journal Year:
2024,
Volume and Issue:
50(1)
Published: Feb. 5, 2024
Abstract
Background
Acute
kidney
injury
(AKI)
in
patients
with
multisystem
inflammatory
syndrome
(MIS),
COVID-19
related
infection
has
been
increasingly
recognized
a
paucity
of
data
on
AKI
incidence,
mortality,
and
the
requirement
renal
replacement
therapy
children
MIS
(MIS-C).
Methods
This
is
retrospective
study
evaluating
prevalence,
severity,
management
outcomes
cohort
Egyptian
MIS-children
(MIS-C)
post-COVID
infection.
Patients
were
included
if
they
met
criteria
for
MIS-C
based
CDC
guidelines.
All
evaluated
diagnosis
staging
according
to
Kidney
Disease
Improving
Global
Outcomes
(KDIGO)
criteria.
Results
Between
March
2021
June
2023,
total
655
confirmed
cases
admitted
then
followed
up
our
hospital,
whom
138
(21%)
diagnosed
MIS-C.
Fifty-one
developed
associated
infection,
42
analysis.
Thirty-one
had
formerly
healthy
kidney,
51%
(16
patients)
classified
as
KDIGO
stage
3,
5
needed
hemodialysis
13
mechanical
ventilation.
Higher
WBCs
count,
serum
ferritin
admission
more
severe
(KDIGO
3)
(
p
=
0.04),
while
multivariate
analysis
showed
high
be
independent
predictor
0.02).
Two
(2/31)
died
during
hospital
admission,
no
residual
impairment
was
reported
at
time
discharge
previously
normal
functions.
Conclusion
More
than
one-third
develop
AKI.
Avoidance
nephrotoxic
drugs,
early
recognition,
prompt
AKI,
including
well-timed
commencement
dialysis
cases,
favorable
outcomes.
JCI Insight,
Journal Year:
2022,
Volume and Issue:
7(11)
Published: April 26, 2022
COVID-19
infection
causes
collapse
of
glomerular
capillaries
and
loss
podocytes,
culminating
in
a
severe
kidney
disease
called
COVID-19–associated
nephropathy
(COVAN).
The
underlying
mechanism
COVAN
is
unknown.
We
hypothesized
that
cytokines
induced
by
trigger
expression
pathogenic
APOL1
via
JAK/STAT
signaling,
resulting
podocyte
phenotype.
Here,
based
on
9
biopsy-proven
cases,
we
demonstrated
for
the
first
time,
to
best
our
knowledge,
protein
was
abundantly
expressed
podocytes
endothelial
cells
(GECs)
kidneys
but
not
controls.
Moreover,
majority
patients
with
carried
2
risk
alleles.
show
recombinant
SARS-CoV-2
acted
synergistically
drive
through
pathway
primary
human
GECs,
micro-organoids
derived
from
carrier
alleles,
blocked
JAK1/2
inhibitor,
baricitinib.
demonstrate
cytokine-induced
JAK/STAT/APOL1
signaling
reduced
viability
organoid
rescued
Together,
results
support
conclusion
COVID-19–induced
are
sufficient
COVAN-associated
podocytopathy
JAK
inhibitors
could
block
this
process.
These
findings
suggest
may
have
therapeutic
benefits
managing
cytokine-induced,
APOL1-mediated
podocytopathy.
Annual Review of Medicine,
Journal Year:
2022,
Volume and Issue:
74(1), P. 1 - 13
Published: Sept. 15, 2022
COVID-19
can
cause
acute
kidney
injury
and
may
or
exacerbate
chronic
diseases,
including
glomerular
diseases.
SARS-CoV-2
infection
of
cells
has
been
reported,
but
it
remains
unclear
if
viral
causes
disease.
The
most
important
in
patients
with
include
impaired
renal
perfusion
immune
dysregulation.
Chronic
disease,
especially
failure
replacement
therapy
transplant,
is
associated
markedly
increased
mortality.
Persons
severe
disease
have
excluded
from
clinical
trials
therapies,
so
therapeutic
approaches
must
be
extrapolated
studies
without
Some
medications
used
to
treat
should
avoided
at
reduced
dosages
transplant
recipients.
Additional
research
needed
determine
the
optimal
strategies
prevent
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(12), P. 6389 - 6389
Published: June 9, 2024
Long
COVID
(LC),
also
referred
to
as
Post
COVID-19
Condition,
Post-Acute
Sequelae
of
SARS-CoV-2
Infection
(PASC),
and
other
terms,
represents
a
complex
multisystem
disease
persisting
after
the
acute
phase
COVID-19.
Characterized
by
myriad
symptoms
across
different
organ
systems,
LC
presents
significant
diagnostic
management
challenges.
Central
disorder
is
role
low-grade
inflammation,
non-classical
inflammatory
response
that
contributes
chronicity
diversity
observed.
This
review
explores
pathophysiological
underpinnings
LC,
emphasizing
importance
inflammation
core
component.
By
delineating
pathogenetic
relationships
clinical
manifestations
this
article
highlights
necessity
for
an
integrated
approach
employs
both
personalized
medicine
standardized
protocols
aimed
at
mitigating
long-term
consequences.
The
insights
gained
not
only
enhance
our
understanding
but
inform
development
therapeutic
strategies
could
be
applicable
chronic
conditions
with
similar
features.
American Journal of Kidney Diseases,
Journal Year:
2024,
Volume and Issue:
84(1), P. 102 - 110
Published: Feb. 9, 2024
Two
variant
alleles
of
the
gene
apolipoprotein
L1
(APOL1),
known
as
risk
variants
(RVs),
are
a
major
contributor
to
kidney
disease
burden
in
those
African
descent.
The
APOL1
protein
contributes
innate
immunity
and
may
protect
against
Trypanosoma,
HIV,
Salmonella,
leishmaniasis.
However,
effects
carrying
1
or
more
RVs
contribute
variety
processes
starting
early
utero
can
be
exacerbated
by
other
factors
(or
"second
hits").
Indeed,
these
genetic
variations
interact
with
environmental
exposures,
infections,
systemic
modify
health
outcomes
across
life
span.
This
review
focuses
on
APOL1-associated
diseases
through
life-course
perspective
discusses
how
exposure
second
hits
impact
long-term
outcomes.
APOL1-related
typically
presents
adolescents
young
adults,
individuals
harboring
likely
progress
failure
than
who
lack
APOL-1
RVs.
Ongoing
research
is
aimed
at
elucidating
association
RV
adverse
donor
recipient
transplant
Unfortunately,
there
currently
no
established
treatment
for
nephropathy.
Long-term
needed
evaluate
protective
associated
different
stages
life.
Biomolecules,
Journal Year:
2022,
Volume and Issue:
12(2), P. 298 - 298
Published: Feb. 12, 2022
The
onset
of
coronavirus
disease
(COVID-19)
as
a
pandemic
infection,
has
led
to
increasing
insights
on
its
pathophysiology
and
clinical
features
being
revealed,
such
noticeable
kidney
involvement.
In
this
study,
we
describe
the
histopathological,
immunofluorescence,
ultrastructural
biopsy-proven
injury
observed
in
series
SARS-CoV-2
positive
cases
our
institution
from
April
2020
November
2021.
We
retrieved
retrospectively
reviewed
nine
(two
pediatric
seven
adults)
that
experienced
nephrotic
syndrome
(six
cases),
acute
clinically
silent
microhematuria
leukocyturia.
Kidney
biopsies
were
investigated
by
means
light
microscopy,
direct
electron
microscopy.
primary
diagnoses
minimal
change
(four
tubular
necrosis
collapsing
glomerulopathy
C3
(one
case).
None
showed
viral
or
viral-like
particles
analysis.
Novel
specific
histologic
biopsy
related
infection
have
been
gradually
disclosed
reported,
harboring
relevant
therapeutic
implications.
Recognizing
properly
diagnosing
renal
involvement
patients
experiencing
COVID-19
could
be
challenging
(due
lack
proof
e.g.,
particles)
requires
proper
integration
pathological
data.
Kidney International,
Journal Year:
2024,
Volume and Issue:
105(5), P. 980 - 996
Published: Feb. 27, 2024
Collapsing
focal
segmental
glomerulosclerosis
(FSGS),
also
known
as
collapsing
glomerulopathy
(CG),
is
the
most
aggressive
variant
of
FSGS
and
characterized
by
a
rapid
progression
to
kidney
failure.
Understanding
CG
pathogenesis
represents
key
step
for
development
targeted
therapies.
Previous
work
implicated
telomerase
protein
component
TERT
in
pathogenesis,
transgenic
expression
adult
mice
resulted
resembling
that
seen
human
primary
HIV-associated
nephropathy
(HIVAN).
Here,
we
used
telomerase-induced
mouse
model
(i-TERTci
mice)
identify
mechanisms
inhibit
pathogenesis.
Inactivation
WIP1
phosphatase,
p53
target
acting
negative
feedback
loop,
blocked
disease
initiation
i-TERTci
mice.
Repression
upon
deficiency
was
associated
with
senescence
enhancement
required
transforming
growth
factor-β
functions.
The
efficacy
pharmacologic
treatment
reduce
severity
both
HIVAN
(Tg26
then
assessed.
Pharmacologic
inhibition
enzymatic
activity
either
or
Tg26
promoted
partial
remission
proteinuria
ameliorated
histopathologic
features.
Histological
well
high-throughput
sequencing
methods
further
showed
selective
does
not
promote
fibrosis
inflammation.
Thus,
our
findings
suggest
targeting
may
be
an
effective
therapeutic
strategy
patients
CG.
Renal Failure,
Journal Year:
2024,
Volume and Issue:
46(1)
Published: April 1, 2024
Severe
acute
respiratory
syndrome
coronavirus-2
(SARS-COV-2)
infection
is
well
established
as
a
systemic
disease
including
kidney
damage.
The
entry
point
into
the
renal
cell
remains
angiotensin-converting
enzyme
2
(ACE-2)
receptor
and
spectrum
of
lesions
broad,
with
clear
predominance
structural
functional
tubular
lesions.
most
common
form
glomerular
injury
collapsing
glomerulopathy
(CG),
which
strongly
associated
apolipoprotein
L1(APOL-1)
risk
variants.
These
lesions,
are
secondary
to
direct
or
indirect
effects
SARS-CoV-2,
can
progress
chronicity
specific
long
COVID-19
in
absence
any
other
cause.
Residual
inflammation
SARS-CoV-2
infection,
addition
(AKI)
transitional
state
without
severe
histological
may
be
responsible
for
greater
function
decline
mild-to-moderate
COVID-19.
This
review
discusses
evidence
markers
patients
triggers
low-grade
that
explain
post-COVID-19
period.