The relationship between arteriovenous access flow (Qa) and cardiovascular changes is complex. Several studies have shown cardiac remodeling and symptoms of heart failure for high-flow arteriovenous ...fistulas (AVF). To evaluate the early cardiovascular impact of AVF. Forty-seven patients with an AVF, hospitalized for the evaluation of high-flow AVF or a pre-kidney transplant assessment were included. We collected clinical and biological data. We also collected data of the assessment by transthoracic echocardiography, functional evaluation by 6-min-walk test and peak oxygen consumption, and measurement of coronary flow reserve by dynamic myocardial perfusion imaging. The measurement of Qa was performed by color Doppler ultrasound and then indexed to the body surface area (Qai) and to the cardiac output (CO) (Qa/CO). Patients were poorly symptomatic (18 and 1 patients NYHA stage 2 and 3, respectively). There was no correlation between Qa, Qai, or Qa/CO and functional status, assessed by peak oxygen consumption (
P
= 0.891;
P
= 0.803;
P
= 0.939, respectively). Symptomatic patients did not have higher Qa, Qai or Qa/CO than asymptomatic (2260 vs 2197 mL/min,
P
= 0.402; 1257 vs 1256 mL/min/m
2
,
P
= 0.835; and 34% vs 37%,
P
= 0.701, respectively). There was no correlation between Qa, Qai or Qa/CO and left ventricular end-diastolic volume or left ventricular ejection fraction. There was no correlation between coronary flow reserve and these 3 parameters of vascular access flow. However, the global longitudinal strain (GLS) was correlated with Qa and Qa/CO (
R
= 0.331,
P
= 0.023 and
R
= 0.380,
P
= 0.008, respectively). Increase of Qa or Qa/CO was associated with an alteration of the GLS. A cut-off value of 2250 mL/min for Qa allowed 83% sensitivity and 63% specificity for detecting an alteration of the GLS > − 18%. A cut-off value of 33% for Qa/CO allowed 92% sensitivity and 65% specificity. Impact of AVF on cardiac parameters is weak. However, GLS is the first parameter to be impacted by the flow of the fistula. Systematic transthoracic echocardiography evaluation with measurement of GLS should be proposed for all patients with Qa > 2250 mL/min or Qa/CO > 33%, to detect those at higher risk of cardiac impact of the AVF.
Epithelial repair following acute kidney injury (AKI) requires epithelial-mesenchyme-epithelial cycling associated with transient re-expression of genes normally expressed during kidney development ...as well as activation of growth factors and cytokine-induced signaling. In normal kidney, the Hnf-1beta transcription factor drives nephrogenesis, tubulogenesis and epithelial homeostasis through the regulation of epithelial planar cell polarity and expression of developmental or tubular segment-specific genes. In a mouse model of ischemic AKI induced by a 2-hours hemorrhagic shock, we show that expression of this factor is tightly regulated in the early phase of renal repair with a biphasic expression profile (early down-regulation followed by transient over-expression). These changes are associated to tubular epithelial differentiation as assessed by KSP-cadherin and megalin-cubilin endocytic complex expression analysis. In addition, early decrease in Hnf1b expression is associated with the transient over-expression of one of its main target genes, the suppressor of cytokine signaling Socs3, which has been shown essential for renal repair. In vitro, hypoxia induced early up-regulation of Hnf-1beta from 1 to 24 hours, independently of the hypoxia-inducible factor Hif-1alpha. When prolonged, hypoxia induced Hnf-1beta down-regulation while normoxia led to Hnf-1beta normalization. Last, Hnf-1beta down-regulation using RNA interference in HK-2 cells led to phenotype switch from an epithelial to a mesenchyme state. Taken together, we showed that Hnf-1beta may drive recovery from ischemic AKI by regulating both the expression of genes important for homeostasis control during organ repair and the state of epithelial cell differentiation.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
L’association pancréatite aiguë – microangiopathie thrombotique (MAT) n’est pas univoque. Les deux observations rapportées ici et les données de la littérature illustrent qu’une pancréatite aiguë, ...quelle qu’en soit la cause, peut se compliquer d’une MAT, ou qu’inversement, une MAT peut être responsable dans 4 % des cas d’une pancréatite aiguë symptomatique. Dans les deux situations, la présence d’un auto-anticorps dirigé contre ADAMTS-13 peut être détecté, sa recherche doit être systématique.
Acute pancreatitis and thrombotic microangiopathy is an established association: but which is the cause, which is the consequence? Thanks to two case reports and a literature review, we put to light an unequivocal link. Indeed, thrombotic microangiopathy may be responsible for ischemic pancreatitis. On the other hand, acute pancreatitis, whatever its cause, may trigger thrombotic microangiopathy. In either case, an anti-ADAMTS-13 antibody can be detected: its research is mandatory.
Acute pancreatitis and thrombotic microangiopathy is an established association: but which is the cause, which is the consequence? Thanks to two case reports and a literature review, we put to light ...an unequivocal link. Indeed, thrombotic microangiopathy may be responsible for ischemic pancreatitis. On the other hand, acute pancreatitis, whatever its cause, may trigger thrombotic microangiopathy. In either case, an anti-ADAMTS-13 antibody can be detected: its research is mandatory.
Epithelial repair following acute kidney injury (AKI) requires epithelial-mesenchyme-epithelial cycling associated with transient re-expression of genes normally expressed during kidney development ...as well as activation of growth factors and cytokine-induced signaling. In normal kidney, the Hnf-1 beta transcription factor drives nephrogenesis, tubulogenesis and epithelial homeostasis through the regulation of epithelial planar cell polarity and expression of developmental or tubular segment-specific genes. In a mouse model of ischemic AKI induced by a 2-hours hemorrhagic shock, we show that expression of this factor is tightly regulated in the early phase of renal repair with a biphasic expression profile (early down-regulation followed by transient over-expression). These changes are associated to tubular epithelial differentiation as assessed by KSP-cadherin and megalin-cubilin endocytic complex expression analysis. In addition, early decrease in Hnf1b expression is associated with the transient over-expression of one of its main target genes, the suppressor of cytokine signaling Socs3, which has been shown essential for renal repair. In vitro, hypoxia induced early up-regulation of Hnf-1 beta from 1 to 24 hours, independently of the hypoxia-inducible factor Hif-1 alpha . When prolonged, hypoxia induced Hnf-1 beta down-regulation while normoxia led to Hnf-1 beta normalization. Last, Hnf-1 beta down-regulation using RNA interference in HK-2 cells led to phenotype switch from an epithelial to a mesenchyme state. Taken together, we showed that Hnf-1 beta may drive recovery from ischemic AKI by regulating both the expression of genes important for homeostasis control during organ repair and the state of epithelial cell differentiation.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
![Hnf-1[beta] Transcription F...](http://api.summon.serialssolutions.com/2.0.0/image/issn/XR4PS5YY4K/1932-6203/small "Hnf-1[beta] Transcription Factor Is an Early Hif-1[alpha]-Independent Marker of Epithelial Hypoxia and Controls Renal Repair")
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