Construction of Risk Prediction Model and Risk Score Table for Infant Heart Failure Hospital Death Based on White Blood Cell Count to Total Protein Ratio
Heliyon,
Год журнала:
2025,
Номер
unknown, С. e42365 - e42365
Опубликована: Янв. 1, 2025
Язык: Английский
Acidosis-induced p38-kinase activation triggers an IL-6-mediated crosstalk of renal proximal tubule cells with fibroblasts leading to their inflammatory response
Marie-Christin Schulz,
Nathalie Wolff,
Michael Kopf
и другие.
Cell Communication and Signaling,
Год журнала:
2025,
Номер
23(1)
Опубликована: Апрель 11, 2025
Abstract
Background
Local
interstitial
acidosis
in
chronic
kidney
disease
(CKD)
induces
inflammatory
responses
and
dedifferentiation
of
proximal
tubule
cells
(PTCs),
disrupting
cellular
crosstalk
through
cytokine
COX-2
metabolite
secretion.
This
promotes
a
switch
to
an
fibroblast
phenotype,
further
exacerbating
inflammation
PTC
dedifferentiation.
p38-signaling
downstream
transcription
factors,
including
P-CREB
c-fos,
contribute
these
responses.
study
investigates
the
impact
on
PTCs
fibroblasts,
focusing
role
p38-signaling.
Methods
HK-2
(human
PTCs)
CCD-1092Sk
fibroblasts)
were
exposed
acidic
or
control
media
mono-
coculture
for
30
min,
3
h,
48
h.
Protein
expression
IL-6,
phosphorylated
(P-)
total
CREB,
P-
SRF,
p38
was
analyzed
by
western
blot.
IL-6
secretion
measured
using
ELISA.
The
receptor
activity
assessed
pharmacological
intervention.
Results
In
coculture,
initially
caused
transient
decrease
but
significantly
increased
levels
after
Acidosis
induced
intracellular
within
h
independent
culture
conditions,
with
sustained
protein
increase
only
coculture.
also
enhanced
c-fos
during
first
Regardless
P-SRF
CCDSK
elevated
Acidosis-mediated
effects
P-CREB,
p38-dependent
both
cell
lines.
Finally,
we
pH-dependency
action
found
that
addition
via
not
media.
Thus,
enhances
potentiates
its
receptor-mediated
biological
effects.
Conclusion
identifies
as
key
mediator
tubule-fibroblast
milieu,
promoting
processes.
expression,
secretion,
effects,
kinase
crucial
mediator.
If
validated
vivo,
findings
could
enhance
understanding
CKD
support
early
interventions.
Язык: Английский
Advanced Gouty Nephropathy Complicated With Type 1 Renal Tubular Acidosis: A Case Report
Cureus,
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 8, 2024
This
report
describes
the
case
of
a
53-year-old
woman
with
chronic
kidney
disease
(CKD)
exacerbated
by
gout
flare
who
presented
renal
tubular
acidosis
(RTA),
hypokalemia,
and
hyperuricemia.
Despite
outpatient
management
for
gouty
nephropathy,
patient
experienced
progressive
leading
to
hospitalization.
Upon
admission,
she
was
diagnosed
type
1
RTA,
characterized
metabolic
severe
refractory
initial
potassium
supplementation.
The
patient's
medical
history
included
gout,
failure,
other
comorbidities,
complicating
her
condition.
Treatment
aggressive
replacement
ongoing
CKD.
Over
several
hospital
days,
levels
stabilized,
discharged
on
oral
supplements.
emphasizes
importance
monitoring
electrolyte
imbalances
managing
uric
acid
in
patients
prevent
complications
such
as
RTA.
Comprehensive
strategies,
including
dietary
pharmacological
interventions,
are
critical
progression
nephropathy
improve
outcomes.
Язык: Английский
The mighty proton
Pflügers Archiv - European Journal of Physiology,
Год журнала:
2024,
Номер
476(4), С. 423 - 425
Опубликована: Март 9, 2024
Язык: Английский
Efficacy and safety of oral sodium bicarbonate in kidney-transplant recipients and non-transplant patients with chronic kidney disease: a systematic review and meta-analysis
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Авг. 26, 2024
Introduction
We
investigated
the
efficacy
and
safety
of
oral
sodium
bicarbonate
in
kidney-transplant
recipients
non-transplant
patients
with
chronic
kidney
disease
(CKD),
which
are
currently
unclear.
Methods
PubMed,
Cochrane
Library,
Embase,
Web
Science
were
searched
for
randomized
controlled
trials
investigating
versus
placebo
or
standard
treatment
CKD.
Results
Sixteen
studies
(two
studies,
280
patients)
CKD
(14
1,380
included.
With
patients,
slowed
kidney-function
declines
(standardized
mean
difference
[SMD]:
0.49,
95%
confidence
interval
[CI]:
0.14–0.85,
p
=
0.006)
within
≥12
months
(SMD:
0.75
[95%
CI:
0.12–1.38],
0.02),
baseline-serum
<22
mmol/L
0.41
0.19–0.64],
0.0004)
increased
serum-bicarbonate
levels
(mean
[MD]:
2.35
1.40–3.30],
<
0.00001).
In
recipients,
did
not
preserve
graft
function
-0.07
-0.30–0.16],
0.56)
but
blood
pH
(MD:
0.02
0.00–0.04],
0.02).
No
significant
adverse
events
occurred
(risk
ratio
[RR]:
0.89,
0.47–1.67],
0.72;
RR
1.30
0.84–2.00],
0.24,
respectively).
However,
correlated
diastolic
pressure
worsened
hypertension
edema
2.21
0.67–3.75],
0.005;
RR:
1.44
1.11–1.88],
0.007;
1.28
1.00–1.63],
0.05,
Discussion
Oral
may
slow
decline
taking
supplementation
a
baseline
serum
level
mmol/L,
without
preserving
recipients.
Sodium
increase
pressure,
elevate
higher
incidence
worsening
edema.
Systematic
Review
Registration:
https://www.crd.york.ac.uk/prospero/
,
identifier
CRD42023413929.
Язык: Английский
Was ist gesichert in der Therapie der metabolischen Azidose bei chronischer Nierenkrankheit?
Deleted Journal,
Год журнала:
2024,
Номер
65(12), С. 1209 - 1215
Опубликована: Ноя. 8, 2024
Zusammenfassung
Eine
präzise
Regulation
des
Säure-Basen-Haushalts
ist
für
viele
Organe
und
physiologische
Prozesse
essenziell.
Säureretention
metabolische
Azidose
(MA)
sind
häufige
Komplikationen
bei
chronischer
Nierenkrankheit
(„chronic
kidney
disease“
[CKD])
treten
auch
nach
Nierentransplantation
auf.
Neben
diätetischen
Maßnahmen
kommen
medikamentöse
Therapien
zur
Azidosekorrektur
zum
Einsatz,
mit
Natrium(hydrogen)karbonat
als
am
häufigsten
eingesetzter
Substanz.
Mehrere
Studien
konnten
einen
positiven
Effekt
einer
auf
die
CKD-Progression
aufzeigen.
Die
Studienresultate
jedoch
nicht
einheitlich
es
von
eher
kleineren
Behandlungseffekten
auszugehen.
Nach
konnte
bisher
keine
positive
Wirkung
Transplantatfunktion
nachgewiesen
werden.
MA
eingeschränkten
Knochenqualität
assoziiert,
wobei
Alkaliinterventionsstudien
bislang
Marker
Knochenstoffwechsels,
Knochendichte
gezeigt
haben.
erhöhten
kardiovaskulären
Ereignisrate
Interventionsstudien
harten
Endpunkten
fehlen
bis
dato.
Interventionsstudie
wesentlichen
Limitationen
Alkalitherapie
Mortalität
zeigen.
scheint
sich
positiv
den
Protein-
Muskelkatabolismus
auszuwirken,
eine
Verbesserung
der
körperlichen
Leistungsfähigkeit
in
geriatrischen
Population
werden
konnte.
Bezüglich
endokrinologischen
Effekte
existieren
nur
sehr
wenige
Studien.
Hier
zeigten
ein
günstiger
Glukosestoffwechsel
möglicher
Nutzen
Bezug
Schilddrüsenfunktion
prädialytischen
Patienten
CKD.
Aufgrund
insgesamt
geringen
moderaten
Evidenz
sowie
angesichts
teilweise
widersprüchlichen
Studienlage
wird
aktualisierten
Leitlinien
Kidney
Disease:
Improving
Global
Outcomes
(KDIGO)
Empfehlung
Erwachsene
abgeschwächt
Alkalibehandlung
vorgeschlagen,
um
Serumbikarbonat
<
18
mmol/l
(bislang
22
mmol/l)
damit
verbundenen
zu
vermeiden.