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See detailLa tomographie par emission de positons au 18F-FDG en pathologie renale non oncologique : indications actuelles et perspectives.
Hanssen, Oriane; Lovinfosse, Pierre; Weekers, Laurent et al

in Nephrologie & therapeutique (2019)

Positron emission tomography combined with computed tomography (PET/CT) is a nuclear imaging technique which provides anatomical and functional information. PET/CT is increasingly used in non-oncological ... [more ▼]

Positron emission tomography combined with computed tomography (PET/CT) is a nuclear imaging technique which provides anatomical and functional information. PET/CT is increasingly used in non-oncological nephrology since conventional radiological approaches after injection of contrast agents are relatively contra-indicated in patients with chronic kidney disease (CKD). PET/CT after i.v. injection of (18)F-fluoro-deoxy-glucose (FDG) is not toxic and is characterized by a high sensitivity. The level of irradiation ( approximately 5mSv) is acceptable. CKD does not significantly influence tissue uptake of (18)F-FDG. The purpose of the present review aims at detailing the non-oncological indications of (18)F-FDG PET/CT in general nephrology and after kidney transplantation. Particularly, (18)F-FDG PET/CT appears useful in the diagnosis of cyst infection in patients with autosomal dominant polycystic kidney disease, as well as in the characterization of retroperitoneal fibrosis. In kidney transplant recipients, (18)F-FDG PET/CT may help in the diagnostic work-up of suspected acute rejection, thereby eventually avoiding unnecessary kidney transplant biopsy. Perspectives in (18)F-FDG PET/CT imaging are discussed, including innovative approaches of image analysis. [less ▲]

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See detailInfusion of third-party mesenchymal stromal cells after kidney transplantation: a phase I-II, open-label, clinical study.
ERPICUM, Pauline ULiege; WEEKERS, Laurent ULiege; DETRY, Olivier ULiege et al

in Kidney International (2019), 95

Mesenchymal stromal cells (MSCs) exhibit anti-inflammatory and immune-regulatory properties, and preclinical studies suggest a potential benefit in solid organ transplantation. We report on the 1-year ... [more ▼]

Mesenchymal stromal cells (MSCs) exhibit anti-inflammatory and immune-regulatory properties, and preclinical studies suggest a potential benefit in solid organ transplantation. We report on the 1-year follow-up of an open-label phase I-II trial of a single infusion of third-party MSC post-kidney transplantation, in addition to standard immunosuppression. Ten kidney transplant recipients from deceased donors received third-party bone marrow MSCs ( approximately 2 x 10(6)/kg) on day 3 +/- 2 post-transplant and were compared to 10 concurrent controls. No adverse effects were noted at MSC injection. One participant with a history of cardiac disease had a non-ST-elevation myocardial infarction approximately 3 hours after MSC infusion. Incidences of opportunistic infections and acute rejection were similar. At day 7 post-transplant, estimated glomerular filtration rate (eGFR) in MSC-treated recipients reached 48.6 ml/min/1.73m(2), compared to 32.5 ml/min/1.73m(2)in controls and 29.3 ml/min/1.73m(2)in our overall cohort of kidney transplant recipients. No difference in eGFR was found at 1 year. MSC-treated recipients showed increased frequencies of regulatory T cells at day 30, with no significant change in B cell frequencies compared to concurrent controls. Four MSC-treated participants developed antibodies against MSC or shared kidney-MSC HLA, with only 1 with MFI >1500. A single infusion of third-party MSC following kidney transplantation appears to be safe, with one cardiac event of unclear relationship to the intervention. MSC therapy is associated with increased regulatory T cell proportion and with improved early allograft function. Long-term effects, including potential immunization against MSC, remain to be studied. [less ▲]

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See detailThe role of FDG PET in detecting rejection after liver transplantation.
Lovinfosse, Pierre; Hustinx, Roland ULiege; Weekers, Laurent et al

in Surgery (2019), 165

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See detailImplications of AMPK in the Formation of Epithelial Tight Junctions
Rowart, Pascal ULiege; Wu, Jingshing; Caplan, Michael J. et al

in International Journal of Molecular Sciences (2018)

Tight junctions (TJ) play an essential role in the epithelial barrier. By definition, TJ are located at the demarcation between the apical and baso-lateral domains of the plasma membrane in epithelial ... [more ▼]

Tight junctions (TJ) play an essential role in the epithelial barrier. By definition, TJ are located at the demarcation between the apical and baso-lateral domains of the plasma membrane in epithelial cells. TJ fulfill two major roles: (i) TJ prevent the mixing of membrane components; and (ii) TJ regulate the selective paracellular permeability. Disruption of TJ is regarded as one of the earliest hallmarks of epithelial injury, leading to the loss of cell polarity and tissue disorganization. Many factors have been identified as modulators of TJ assembly/disassembly. More specifically, in addition to its role as an energy sensor, adenosine monophosphate-activated protein kinase (AMPK) participates in TJ regulation. AMPK is a ubiquitous serine/threonine kinase composed of a catalytic -subunit complexed with regulatory -and -subunits. AMPK activation promotes the early stages of epithelial TJ assembly. AMPK phosphorylates the adherens junction protein afadin and regulates its interaction with the TJ-associated protein zonula occludens (ZO)-1, thereby facilitating ZO-1 distribution to the plasma membrane. In the present review, we detail the signaling pathways up-and down-stream of AMPK activation at the time of Ca2+-induced TJ assembly. [less ▲]

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See detailGenetic deletion of DUSP3 phosphatase attenuates kidney damage and inflammation following ischemia/reperfusion in mouse
Rowart, Pascal ULiege; POMA, Laurence ULiege; Rahmouni, Souad ULiege et al

Poster (2018, May 25)

Background. Renal ischemia-reperfusion (I/R) injury represents an unavoidable event in kidney transplantation. Dual Specificity Phosphatase 3 (DUSP3, also called Vaccinia-H1 Related (VHR)) is highly ... [more ▼]

Background. Renal ischemia-reperfusion (I/R) injury represents an unavoidable event in kidney transplantation. Dual Specificity Phosphatase 3 (DUSP3, also called Vaccinia-H1 Related (VHR)) is highly expressed in endothelial cells, as well as in platelets, monocytes and macrophages. Since DUSP3 is a positive regulator of the innate immune response, its inactivation/deletion may attenuate kidney inflammation and damage caused by I/R. Methods. Ten-weeks-old C57BL/6 wild-type (WT, n=10) versus systemic knock-out (KO, n=10) mice underwent unilateral left renal ischemia for 30 minutes. Right nephrectomy was simultaneously performed. The left kidney was excised and blood sample was collected from inferior vena cava at 48h post reperfusion. Renal function was assessed upon Blood Urea Nitrogen (BUN) levels. Expressions of inflammatory and immune markers were comparatively quantified at both mRNA (real-time qPCR) and protein (immune-blotting and –staining) levels in ischemic vs. non-ischemic kidneys in DUSP3 WT vs. KO mice. Results. BUN reached 259±51 vs 78±11mg/dL in WT and KO, respectively (p<0.01). DUSP3 KO ischemic kidneys showed a reduced number of PCNA- (3-fold, p<0.001), CD11b- (3.5-fold, p<0.001) and F4-80-positive cells (1.7-fold, p<0.001) in comparison to WT. The expression levels of CD11b (2.2-fold, p<0.01), HSP70 (2.7-fold, p<0.01) and PCNA (10-fold, p<0.001) were significantly decreased in DUSP3 KO compared to WT ischemic kidneys. By contrast, a 1.5-fold increase of anti-inflammatory M2 CD206-positive macrophages was observed in DUSP3 KO ischemic kidneys. At transcriptional levels, DUSP3 WT vs. KO ischemic kidneys (normalized to WT sham-operated right kidneys) showed an upregulation of 6.5-fold (p<0.05) vs. 10.5-fold (p<0.01) of M2-type macrophage (Arginase), 4.6-fold (p<0.001) vs. 2.2-fold (p<0.05) of CD11b, 4.5-fold (p<0.001) vs. 0.7-fold (p>0.05) of TNF and 111-fold (p<0.001) vs. 4.5-fold (p>0.05) of KIM-1, respectively. Conclusions. Genetic deletion of DUSP3 attenuates renal I/R-associated damage and inflammation. [less ▲]

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See detailGUT MICROBIOTA AND FAECAL LEVELS OF SHORT CHAIN FATTY ACIDS DIFFER UPON BLOOD PRESSURE LEVELS IN MAN
HUART, Justine ULiege; Leenders, Justine ULiege; Taminiau, Bernard ULiege et al

in Nephrology Dialysis Transplantation (2018, May 18), 33(Issue suppl_1), 368369

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See detailLa souris, le patient, et le faux expert. Décryptage d'une mystification.
Bakker, Julie ULiege; Balthazart, Jacques ULiege; Baron, Frédéric ULiege et al

Article for general public (2018)

La recherche sur animaux est actuellement encadrée de façon stricte en Wallonie comme dans toute l'Union Européenne (voir l'article de Marc Vandenheede publié dans le Vif). Cette législation et les ... [more ▼]

La recherche sur animaux est actuellement encadrée de façon stricte en Wallonie comme dans toute l'Union Européenne (voir l'article de Marc Vandenheede publié dans le Vif). Cette législation et les contrôles qui y sont associés induisent de nombreuses contraintes pratiques, des charges administratives et des coûts financiers importants que les chercheurs seraient certainement heureux d'éviter s'il existait une alternative à l'expérimentation animale. [less ▲]

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See detailGenetic deletion of DUSP3 phosphatase attenuates kidney damage and inflammation following ischemia/reperfusion in mouse
Rowart, Pascal ULiege; POMA, Laurence ULiege; Rahmouni, Souad ULiege et al

Conference (2018, April 20)

Background. Renal ischemia-reperfusion (I/R) injury represents an unavoidable event in kidney transplantation. Dual Specificity Phosphatase 3 (DUSP3, also called Vaccinia-H1 Related (VHR)) is highly ... [more ▼]

Background. Renal ischemia-reperfusion (I/R) injury represents an unavoidable event in kidney transplantation. Dual Specificity Phosphatase 3 (DUSP3, also called Vaccinia-H1 Related (VHR)) is highly expressed in endothelial cells, as well as in platelets, monocytes and macrophages. Since DUSP3 is a positive regulator of the innate immune response, its inactivation/deletion may attenuate kidney inflammation and damage caused by I/R. Methods. Ten-weeks-old C57BL/6 wild-type (WT, n=10) versus systemic knock-out (KO, n=10) mice underwent unilateral left renal ischemia for 30 minutes. Right nephrectomy was simultaneously performed. The left kidney was excised and blood sample was collected from inferior vena cava at 48h post reperfusion. Renal function was assessed upon Blood Urea Nitrogen (BUN) levels. Expressions of inflammatory and immune markers were comparatively quantified at both mRNA (real-time qPCR) and protein (immune-blotting and –staining) levels in ischemic vs. non-ischemic kidneys in DUSP3 WT vs. KO mice. Results. BUN reached 259±51 vs 78±11mg/dL in WT and KO, respectively (p<0.01). DUSP3 KO ischemic kidneys showed a reduced number of PCNA- (3-fold, p<0.001), CD11b- (3.5-fold, p<0.001) and F4-80-positive cells (1.7-fold, p<0.001) in comparison to WT. The expression levels of CD11b (2.2-fold, p<0.01), HSP70 (2.7-fold, p<0.01) and PCNA (10-fold, p<0.001) were significantly decreased in DUSP3 KO compared to WT ischemic kidneys. By contrast, a 1.5-fold increase of anti-inflammatory M2 CD206-positive macrophages was observed in DUSP3 KO ischemic kidneys. At transcriptional levels, DUSP3 WT vs. KO ischemic kidneys (normalized to WT sham-operated right kidneys) showed an upregulation of 6.5-fold (p<0.05) vs. 10.5-fold (p<0.01) of M2-type macrophage (Arginase), 4.6-fold (p<0.001) vs. 2.2-fold (p<0.05) of CD11b, 4.5-fold (p<0.001) vs. 0.7-fold (p>0.05) of TNF and 111-fold (p<0.001) vs. 4.5-fold (p>0.05) of KIM-1, respectively. Conclusions. Genetic deletion of DUSP3 attenuates renal I/R-associated damage and inflammation. [less ▲]

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See detailGenetic deletion of DUSP3 phosphatase attenuates kidney damage and inflammation following ischemia/reperfusion in mouse
Rowart, Pascal ULiege; POMA, Laurence ULiege; Rahmouni, Souad ULiege et al

Conference (2018, March 16)

Background. Renal ischemia-reperfusion (I/R) injury represents an unavoidable event in kidney transplantation. Dual Specificity Phosphatase 3 (DUSP3, also called Vaccinia-H1 Related (VHR)) is highly ... [more ▼]

Background. Renal ischemia-reperfusion (I/R) injury represents an unavoidable event in kidney transplantation. Dual Specificity Phosphatase 3 (DUSP3, also called Vaccinia-H1 Related (VHR)) is highly expressed in endothelial cells, as well as in platelets, monocytes and macrophages. Since DUSP3 is a positive regulator of the innate immune response, its inactivation/deletion may attenuate kidney inflammation and damage caused by I/R. Methods. Ten-weeks-old C57BL/6 wild-type (WT, n=10) versus systemic knock-out (KO, n=10) mice underwent unilateral left renal ischemia for 30 minutes. Right nephrectomy was simultaneously performed. The left kidney was excised and blood sample was collected from inferior vena cava at 48h post reperfusion. Renal function was assessed upon Blood Urea Nitrogen (BUN) levels. Expressions of inflammatory and immune markers were comparatively quantified at both mRNA (real-time qPCR) and protein (immune-blotting and –staining) levels in ischemic vs. non-ischemic kidneys in DUSP3 WT vs. KO mice. Results. BUN reached 259±51 vs 78±11mg/dL in WT and KO, respectively (p<0.01). DUSP3 KO ischemic kidneys showed a reduced number of PCNA- (3-fold, p<0.001), CD11b- (3.5-fold, p<0.001) and F4-80-positive cells (1.7-fold, p<0.001) in comparison to WT. The expression levels of CD11b (2.2-fold, p<0.01), HSP70 (2.7-fold, p<0.01) and PCNA (10-fold, p<0.001) were significantly decreased in DUSP3 KO compared to WT ischemic kidneys. By contrast, a 1.5-fold increase of anti-inflammatory M2 CD206-positive macrophages was observed in DUSP3 KO ischemic kidneys. At transcriptional levels, DUSP3 WT vs. KO ischemic kidneys (normalized to WT sham-operated right kidneys) showed an upregulation of 6.5-fold (p<0.05) vs. 10.5-fold (p<0.01) of M2-type macrophage (Arginase), 4.6-fold (p<0.001) vs. 2.2-fold (p<0.05) of CD11b, 4.5-fold (p<0.001) vs. 0.7-fold (p>0.05) of TNF and 111-fold (p<0.001) vs. 4.5-fold (p>0.05) of KIM-1, respectively. Conclusions. Genetic deletion of DUSP3 attenuates renal I/R-associated damage and inflammation. [less ▲]

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See detailIntérêt du dépistage et du traitement de l'acidose métabolique chez l'insuffisant rénal chronique
Georges, benoit; Huart, Justine ULiege; KRZESINSKI, Jean-Marie ULiege et al

in Revue Médicale Suisse (2018), 14(1455-1458),

L’acidose métabolique est une anomalie biologique fréquente et précoce de l’insuffisance rénale chronique (IRC). Les complications liées à cet état sont multiples et touchent notamment l’os, le muscle et ... [more ▼]

L’acidose métabolique est une anomalie biologique fréquente et précoce de l’insuffisance rénale chronique (IRC). Les complications liées à cet état sont multiples et touchent notamment l’os, le muscle et le métabolisme protidique, sans parler du risque accru d’hyperkaliémie. Une causalité entre acidose métabolique et accélération du déclin rénal a été démontrée. La mesure du taux de bicarbonate sérique doit, dès lors, faire partie du suivi biologique systématique du patient en IRC dont le taux de filtration glomérulaire s’abaisse en dessous de 50 ml/min/1,73 m². Le dépistage et le traitement de l’acidose métabolique sont en effet simples et peu coûteux. La correction de l’acidose métabolique, notamment par le bicarbonate de sodium, permet de ralentir la progression de l’insuffisance rénale. [less ▲]

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See detailWhat we need to know about lipid-associated injury in case of renal ischemia/reperfusion.
ERPICUM, Pauline ULiege; Rowart, Pascal ULiege; Defraigne, Jean-Olivier ULiege et al

in American Journal of Physiology. Renal Physiology (2018)

Renal segmental metabolism is reflected by the complex distribution of the main energy pathways along the nephron, with fatty acid oxidation preferentially used in the cortex area. Ischemia/reperfusion ... [more ▼]

Renal segmental metabolism is reflected by the complex distribution of the main energy pathways along the nephron, with fatty acid oxidation preferentially used in the cortex area. Ischemia/reperfusion injury (IRI) is due to the restriction of renal blood flow, rapidly leading to a metabolic switch towards anaerobic conditions. Subsequent unbalance between energy demand and oxygen/nutrient delivery compromises kidney cell functions, resulting to a complex inflammatory cascade including the production of reactive oxygen species (ROS). Renal IRI especially involves lipid accumulation. Lipid peroxidation is one of the major events of ROS-associated tissue injury. Here, we briefly review the current knowledge of renal cell lipid metabolism in normal and ischemic conditions. Next, we focus on renal lipid-associated injury, with emphasis on its mechanisms and consequences during the course of IRI. Finally, we discuss preclinical observations aiming at preventing and/or attenuating lipid-associated IRI. [less ▲]

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See detailCopeptin in the Diagnosis of Diabetes Insipidus.
Mekahli, Djalila; Jouret, François ULiege

in New England Journal of Medicine (2018), 379(18), 1784-5

The diagnostic and prognostic yields of copeptin, a surrogate biomarker of arginine vasopressin secretion, are currently investigated in various disorders linked to arginine vasopressin regulation ... [more ▼]

The diagnostic and prognostic yields of copeptin, a surrogate biomarker of arginine vasopressin secretion, are currently investigated in various disorders linked to arginine vasopressin regulation, including heart failure, sepsis, or the metabolic syndrome. More specifically, patients with autosomal dominant polycystic kidney disease (ADPKD), which has a prevalence of 1 in 400 to 1000 live births, show significantly higher plasma copeptin levels than controls. Plasma copeptin levels independently correlate with ADPKD progression. Copeptin secretion after hypertonic saline stimulation in patients with ADPKD is unknown. In the study involving 144 patients with hypotonic polyuria, Fenske et al. elegantly show that measuring plasma copeptin after infusion of 3% saline over a period of 3 hours has greater diagnostic accuracy than 17-hour water deprivation. This test will probably replace the water-deprivation test in the diagnostic workup of polyuria, with a copeptin cutoff level of more than 4.9 pmol per liter. It is not clearly mentioned that this cutoff value is a delta — that is, a change in the plasma copeptin level at a plasma sodium level of 147 mmol per liter or more versus baseline. It would have been relevant to provide pretest copeptin levels according to subgroup. Indeed, specific conditions, such as ADPKD, are essentially characterized by an increased plasma copeptin level, a fact that may pragmatically skew the diagnostic yield of copeptin measurement after hypertonic saline stimulation in the challenging context of hypotonic polyuria. [less ▲]

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See detailVps34/PI3KC3 deletion in kidney proximal tubules impairs apical trafficking and blocks autophagic flux, causing a Fanconi-like syndrome and renal insufficiency.
Grieco, Giuseppina; Janssens, Virginie; Gaide Chevronnay, Heloise P. et al

in Scientific Reports (2018), 8(1), 14133

Kidney proximal tubular cells (PTCs) are highly specialized for ultrafiltrate reabsorption and serve as paradigm of apical epithelial differentiation. Vps34/PI3-kinase type III (PI3KC3) regulates ... [more ▼]

Kidney proximal tubular cells (PTCs) are highly specialized for ultrafiltrate reabsorption and serve as paradigm of apical epithelial differentiation. Vps34/PI3-kinase type III (PI3KC3) regulates endosomal dynamics, macroautophagy and lysosomal function. However, its in vivo role in PTCs has not been evaluated. Conditional deletion of Vps34/PI3KC3 in PTCs by Pax8-Cre resulted in early (P7) PTC dysfunction, manifested by Fanconi-like syndrome, followed by kidney failure (P14) and death. By confocal microscopy, Vps34(/) PTCs showed preserved apico-basal specification (brush border, NHERF-1 versus Na(+)/K(+)-ATPase, ankyrin-G) but basal redistribution of late-endosomes/lysosomes (LAMP-1) and mis-localization to lysosomes of apical recycling endocytic receptors (megalin, cubilin) and apical non-recycling solute carriers (NaPi-IIa, SGLT-2). Defective endocytosis was confirmed by Texas-red-ovalbumin tracing and reduced albumin content. Disruption of Rab-11 and perinuclear galectin-3 compartments suggested mechanistic clues for defective receptor recycling and apical biosynthetic trafficking. p62-dependent autophagy was triggered yet abortive (p62 co-localization with LC3 but not LAMP-1) and PTCs became vacuolated. Impaired lysosomal positioning and blocked autophagy are known causes of cell stress. Thus, early trafficking defects show that Vps34 is a key in vivo component of molecular machineries governing apical vesicular trafficking, thus absorptive function in PTCs. Functional defects underline the essential role of Vps34 for PTC homeostasis and kidney survival. [less ▲]

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See detailControversies in the management of the haemodialysis-related arteriovenous fistula following kidney transplantation.
Vanderweckene, Pauline ULiege; Weekers, Laurent ULiege; Lancellotti, Patrizio ULiege et al

in Clinical Kidney Journal (2018), 11(3), 406-412

Arteriovenous fistula (AVF) is regarded as the best vascular access for chronic haemodialysis (HD). Still, AVF inherently causes significant haemodynamic changes. Although the necessity for vascular ... [more ▼]

Arteriovenous fistula (AVF) is regarded as the best vascular access for chronic haemodialysis (HD). Still, AVF inherently causes significant haemodynamic changes. Although the necessity for vascular access despite its putative cardiovascular complications favours AVF creation in patients under chronic HD, one may question whether sustaining a functional AVF after successful kidney transplantation extends the haemodynamic threat. Small prospective series suggest that AVF ligation causes rapid and sustained reduction in left ventricular hypertrophy. Still, the benefits of such a cardiac remodelling in long-terms of cardiovascular morbi-mortality still need to be proven. Furthermore, the elevation of diastolic blood pressure and arterial stiffness caused by AVF ligation may blunt the expected cardio-protection. Finally, the closure of a functioning AVF may accelerate the decline of kidney graft function. As a whole, the current management of a functioning AVF in kidney transplant recipients remains controversial and does not rely on strong evidence-based data. The individual risk of graft dysfunction and a return to chronic HD also needs to be balanced. Careful pre-operative functional assessments, including cardio-pulmonary testing and estimated glomerular filtration rate slope estimation, may help better selection of who might benefit the most from AVF closure. Large-scale prospective, ideally multi-centric, trials are essentially needed. [less ▲]

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See detailCXCL12 and MYC control energy metabolism to support adaptive responses after kidney injury.
Yakulov, Toma A.; Todkar, Abhijeet P.; Slanchev, Krasimir et al

in Nature Communications (2018), 9(1), 3660

Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos ... [more ▼]

Kidney injury is a common complication of severe disease. Here, we report that injuries of the zebrafish embryonal kidney are rapidly repaired by a migratory response in 2-, but not in 1-day-old embryos. Gene expression profiles between these two developmental stages identify cxcl12a and myca as candidates involved in the repair process. Zebrafish embryos with cxcl12a, cxcr4b, or myca deficiency display repair abnormalities, confirming their role in response to injury. In mice with a kidney-specific knockout, Cxcl12 and Myc gene deletions suppress mitochondrial metabolism and glycolysis, and delay the recovery after ischemia/reperfusion injury. Probing these observations in zebrafish reveal that inhibition of glycolysis slows fast migrating cells and delays the repair after injury, but does not affect the slow cell movements during kidney development. Our findings demonstrate that Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair, and potentially also during tumor invasion and metastasis. [less ▲]

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See detailOxidative stress in chronic kidney disease
Daenen, K.; Andries, A.; Mekahli, D. et al

in Pediatric Nephrology (2018)

Oxidative stress (OS), defined as disturbances in the pro-/antioxidant balance, is harmful to cells due to the excessive generation of highly reactive oxygen (ROS) and nitrogen (RNS) species. When the ... [more ▼]

Oxidative stress (OS), defined as disturbances in the pro-/antioxidant balance, is harmful to cells due to the excessive generation of highly reactive oxygen (ROS) and nitrogen (RNS) species. When the balance is not disturbed, OS has a role in physiological adaptations and signal transduction. However, an excessive amount of ROS and RNS results in the oxidation of biological molecules such as lipids, proteins, and DNA. Oxidative stress has been reported in kidney disease, due to both antioxidant depletions as well as increased ROS production. The kidney is a highly metabolic organ, rich in oxidation reactions in mitochondria, which makes it vulnerable to damage caused by OS, and several studies have shown that OS can accelerate kidney disease progression. Also, in patients at advanced stages of chronic kidney disease (CKD), increased OS is associated with complications such as hypertension, atherosclerosis, inflammation, and anemia. In this review, we aim to describe OS and its influence on CKD progression and its complications. We also discuss the potential role of various antioxidants and pharmacological agents, which may represent potential therapeutic targets to reduce OS in both pediatric and adult CKD patients. © 2018, IPNA. [less ▲]

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See detailLinking gut microbiota to cardiovascular disease and hypertension: Lessons from chronic kidney disease.
Meijers, B.; Jouret, François ULiege; Evenepoel, P.

in Pharmacological Research (2018), 133

Bidirectional interactions exist between the kidneys and the gut. These interactions are commonly referred to as the gut-kidney axis. Chronic kidney disease (CKD) leads to disturbances of the gut ... [more ▼]

Bidirectional interactions exist between the kidneys and the gut. These interactions are commonly referred to as the gut-kidney axis. Chronic kidney disease (CKD) leads to disturbances of the gut ecosystem. Key features include the increase of protein fermentation at the expense of carbohydrate fermentation and a disrupted epithelial barrier. A disturbed gut ecosystem may contribute to the high burden of cardiovascular disease in patients with CKD. The present review discusses the impact of CKD on the gut microenvironment and provides an update as to how gut dysbiosis and a leaky gut may be linked to accelerated cardiovascular disease and hypertension. [less ▲]

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See detailOxidative stress in autosomal dominant polycystic kidney disease: player and/or early predictor for disease progression?
Andries, Asmin; Daenen, Kristien; Jouret, François ULiege et al

in Pediatric nephrology (Berlin, Germany) (2018)

Autosomal dominant polycystic kidney disease (ADPKD), caused by mutations in PKD1 or PKD2 genes, is the most common hereditary renal disease. Renal manifestations of ADPKD are gradual cyst development and ... [more ▼]

Autosomal dominant polycystic kidney disease (ADPKD), caused by mutations in PKD1 or PKD2 genes, is the most common hereditary renal disease. Renal manifestations of ADPKD are gradual cyst development and kidney enlargement ultimately leading to end-stage renal disease. ADPKD also causes extrarenal manifestations, including endothelial dysfunction and hypertension. Both of these complications are linked with reduced nitric oxide levels related to excessive oxidative stress (OS). OS, defined as disturbances in the prooxidant/antioxidant balance, is harmful to cells due to the excessive generation of highly reactive oxygen and nitrogen free radicals. Next to endothelial dysfunction and hypertension, there is cumulative evidence that OS occurs in the early stages of ADPKD. In the current review, we aim to summarize the cardiovascular complications and the relevance of OS in ADPKD and, more specifically, in the early stages of the disease. First, we will briefly introduce the link between ADPKD and the early cardiovascular complications including hypertension. Secondly, we will describe the potential role of OS in the early stages of ADPKD and its possible importance beyond the chronic kidney disease (CKD) effect. Finally, we will discuss some pharmacological agents capable of reducing reactive oxygen species and OS, which might represent potential treatment targets for ADPKD. [less ▲]

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See detailGenetic susceptibility to delayed graft function following kidney transplantation: a systematic review of the literature.
Huart, Justine; Krzesinski, Jean-Marie ULiege; Jouret, François ULiege

in Clinical Kidney Journal (2018), 11(4), 586-596

Delayed graft function (DGF) is defined as the need for dialysis within 7 days following kidney transplantation (KTx). DGF is associated with increased costs, higher risk for acute rejection and decreased ... [more ▼]

Delayed graft function (DGF) is defined as the need for dialysis within 7 days following kidney transplantation (KTx). DGF is associated with increased costs, higher risk for acute rejection and decreased long-term graft function. Renal ischaemia/reperfusion (I/R) injury plays a major role in DGF occurrence. Single nucleotide polymorphisms (SNPs) in certain genes may aggravate kidney susceptibility to I/R injury, thereby worsening post-transplant outcomes. The present article proposes an extensive review of the literature about the putative impact of donor or recipient SNPs on DGF occurrence in kidney transplant recipients (KTRs). Among 30 relevant PubMed reports, 16 articles identified an association between 18 SNPs and DGF. These polymorphisms concern 14 different well-known genes and one not-yet-identified gene located on chromosome 18. They have been categorized into five groups according to the role of the corresponding proteins in I/R cascade: (i) oxidative stress, (ii) telomere shortening, (iii) chemokines, (iv) T-cell homeostasis and (v) metabolism of anti-inflammatory molecules. The remaining 14 studies failed to demonstrate any association between the studied SNPs and the occurrence of DGF. A better understanding of the genetic susceptibility to renal I/R injury may help prevent DGF and improve clinical outcomes in KTRs. [less ▲]

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