Extracellular ATP acts on P2Y2 purinergic receptors to facilitate HIV-1 infection

Contact with HIV-1 envelope protein elicits release of ATP through pannexin-1 channels on target cells; by activating purinergic receptors and Pyk2 kinase in target cells, this extracellular ATP boosts HIV-1 infectivity

Prise en charge du purpura rhumatoïde de l'adulte avec atteinte rénale (intérêt des échanges plasmatiques ?)

ANGERS-BU Médecine-Pharmacie (490072105) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Hyperkaliémie en médecine générale

L hyperkaliémie est un trouble ionique relativement fréquent en médecine générale. Le rein étant l organe principal de régulation de l homéostasie potassique, adapte les sorties aux entrées. L hyperkaliémie menaçante (à partir de 6,5 mmol/L) peut mettre en jeu le pronostic vital et nécessite une conduite diagnostique et thérapeutique rigoureuse et urgente. Toute suspicion d hyperkaliémie menaçante impose la réalisation d un ECG car le risque principal est cardiaque.Une hyperkaliémie peut survenir selon trois mécanismes: un transfert exagéré du compartiment intracellulaire vers le compartiment extracellulaire, une diminution de la capacité d excrétion rénale, un excès d apport. La cause la plus fréquente d hyperkaliémie reste d origine iatrogène. Les différentes études montrent que la population cible de l hyperkaliémie iatrogène est la personne âgée ayant déjà un facteur favorisant à l hyperkaliémie (insuffisance rénale, diabète). Les résultats d une étude rétrospective récente sur l association inhibiteurs de l enzyme de converstion et spironolactone dans les Pays de la Loire montrent que l association a été utilisé selon les recommandations chez seulement 15% des patients.Il est important de doser la réserve alcaline dans le cadre du bilan des dyskaliémies car il existe un lien très fort entre l état acido-basique et la kaliémie; l acidose augmente la kaliémie et l alcalose diminue la kaliémie. Une hyperkaliémie peut être corrigée en médecine de ville en cas d acidose associée (réserve alcaline basse) par une alcalinisation per os (eau de Vichy ou gélules de bicarbonates de sodium).ANGERS-BU Médecine-Pharmacie (490072105) / SudocSudocFranceF

Intérêt du cross-match en transplantation rénale chez les patients non immunisés (à propos d'une cohorte angevine de 51 patients)

RENNES1-BU Santé (352382103) / SudocLYON1-BU Santé (693882101) / SudocSudocFranceF

Etude du taux de lymphocytes d'une cohorte de patients transplantés rénaux bénéficiant d'une immunosuppression par tacrolimus monothérapie à partir du 6ème mois

ANGERS-BU Médecine-Pharmacie (490072105) / SudocSudocFranceF

A case of severe osteomalacia secondary to phosphate diabetes in a renal transplant recipient

International audienceTransient hypophosphatemia is frequently observed during the first months after renal transplantation and is usually asymptomatic. Phosphate diabetes is defined as inadequate tubular phosphorus reabsorption leading to persistent renal phosphorus wasting, which is an important but overlooked cause of osteodystrophy in the post-renal transplantation population. We report the case of a 58-year-old male who presented with severe multiple osteoarticular pains within 3 months after successful first kidney transplantation. Bone disease was attributed initially to mild hyperparathyroidism secondary to vitamin D deficiency. Despite the correction of the hyperparathyroidism, the withdrawal of corticosteroids, and the reduction of immunosuppressive treatment to tacrolimus-based monotherapy, the osteoarticular pains persisted. Skeletal investigations at month 9 post-transplantation demonstrated a significant bone mineral density loss associated with osteomalacia and osteoporosis on the bone biopsy. Laboratory data showed persistent hypophosphatemia, and phosphate diabetes was then diagnosed explaining the post-transplant bone disease. A tacrolimus-induced renal tubular disorder was suspected to contribute to the excessive renal phosphorus wasting. The replacement of tacrolimus by sirolimus, in addition to oral phosphorus and vitamin D supplementations, led to the disappearance of pains, the normalization of urinary and plasma phosphate level, and a significant improvement of bone mineralization.</p

Anti-Pentraxin Antibodies in Autoimmune Diseases: Bystanders or Pathophysiological Actors?

International audiencePentraxins are soluble innate immunity receptors involved in sensing danger molecules. They are classified as short (CRP, SAP) and long pentraxin subfamilies, including the prototypic long pentraxin PTX3. Pentraxins act mainly as bridging molecules favoring the clearance of microbes and dead cells. They are also involved in many other biological processes, such as regulation of complement activation, inflammation and tissue homeostasis. Autoantibodies directed against pentraxins have been reported in various autoimmune diseases, especially in systemic lupus erythematosus and ANCA-associated vasculitis. In this review, we review the main biological characteristics and functions of pentraxins and summarize data concerning autoantibodies directed against pentraxins in the context of autoimmune diseases and discuss their potential pathological role

Serum Magnesium after Kidney Transplantation: A Systematic Review

Magnesium (Mg) status has recently drawn close attention in chronic kidney disease and in kidney transplant recipients. This review aims to evaluate the body of evidence linking hypomagnesemia to clinical consequences in these specific populations. After a brief summary of the main mechanisms involved in Mg regulation and of Mg status in end-stage renal disease, the review focuses on the relationship between hypomagnesemia and cardiovascular risk in kidney transplant recipients. A body of evidence in recent studies points to a negative impact of hypomagnesemia on post-transplant diabetes mellitus (PTDM) and cardiovascular risk, which currently represent the main threat for morbidity and mortality in kidney transplantation. Deleterious biological mechanisms induced by hypomagnesemia are also discussed. While data analysis enables us to conclude that hypomagnesemia is linked to the development of PTDM, studies prospectively evaluating the impact of hypomagnesemia correction after kidney transplantation are still lacking and needed

Complement alternative pathway in ANCA-associated vasculitis: Two decades from bench to bedside

International audienceAnti-neutrophil cytoplasmic autoantibodies (ANCA)-associated vasculitides (AAVs) are small vessel vasculitides involving predominantly ear-nose-throat, kidneys, lungs and nerves. AAVs are life-threatening diseases, especially in their most severe forms such as necrotizing crescentic glomerulonephritis (GN) and/or intra-alveolar hemorrhage. Unlike immune complex GN or anti-glomerular basement membrane GN, AAVs are classified as pauci-immune GN. However, based on recent insights from animal models, the view of AAVs as a complement-unrelated disease has been challenged. Indeed, complement activation, and especially complement alternative pathway (cAP) activation, has been shown to be determinant in AAV pathogenesis through C5a generation, a potent chemoattractant for neutrophils with priming capacities. Here, we review in vitro and in vivo data supporting the role of cAP in murine models and in human AAVs. These findings, together with the need to eradicate glucocorticoid toxicity, led to the development of an anti-C5aR molecule, CCX168, also known as avacopan. Its development and future opportunities are also discussed