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Urine staining is described as a clinical sign due to the presence of some diseases. The purple colour is rare and can be worrisome. It has only been described in a syndrome called Purple Urine Bag Syndrome (PUBS). This coloration is the result of a urinary tract infection in patients with an indwelling catheter for a long time. An overview of the mechanisms causing this syndrome and of its management and prognosis will be discussed in this short communication.La coloration des urines peut être un signe clinique de la présence de certaines maladies. La couleur violette est rare et peut inquiéter. Elle est uniquement décrite dans un syndrome appelé le syndrome de la poche à urines violette (en anglais, Purple Urine Bag Syndrome ou PUBS). Cette coloration est le témoin d’une infection urinaire chez un patient porteur d’une sonde à demeure. Une revue des mécanismes causant ce syndrome, de sa prise en charge et de son pronostic est détaillée dans cette courte présentation.

Polycystic kidney disease (PKD) is the most prevalent inherited kidney disease. The disease is usually asymptomatic until adulthood. End-stage renal disease occurs generally after the age of 55 years, with a large inter-individual variability. Renal cyst formation begins early in life, and animal models have shown that treatments able to prevent the cyst growth slow down the renal function decline. A treatment by tolvaptan is currently used in adults to decelerate PKD progression. Until now there is no consensus about the appropriate time to screen for PKD in children. However, these scientific progresses raise the interest of determining early (i.e. pediatric) predictive markers of renal function decline.La polykystose rénale autosomique dominante (PRAD) est la maladie rénale génétique la plus fréquente. Le développement insidieusement progressif des kystes rénaux fait que la PRAD est, le plus souvent, asymptomatique jusqu’à l’âge adulte, mais la croissance kystique survient très précocement. L’insuffisance rénale terminale survient, généralement, après l’âge de 55 ans, avec, cependant, une grande variabilité interindividuelle. Les modèles animaux montrent que les traitements ralentissant la croissance du volume rénal freinent parallèlement le déclin de la fonction rénale. Par ailleurs, un traitement récemment utilisé chez l’adulte (le tolvaptan) permet de ralentir la progression de la PRAD. A ce jour, il n’y a pas de consensus sur l’âge de dépistage de la PRAD chez les enfants. Toutefois, les récentes avancées scientifiques suggèrent l’intérêt de déterminer des marqueurs prédictifs précoces, y compris pédiatriques, du déclin de la fonction rénale.

The SARS-CoV-2 virus causes a respiratory distress syndrome, the main symptom of COVID-19 (for "COronaVIrus Disease 2019"). This infectious disease has been causing a major health and socio-economic pandemic since December 2019. The pulmonary alveolus is regarded as the main target of SARS-CoV-2. However, this coronavirus is capable of directly or indirectly affecting other organs, including the kidneys. Here, we summarize the presumed pathophysiology of COVID-19 renal disease. The incidence of acute kidney injury ranges from 0,5 to 22 % of all patients infected with SARS-CoV-2. The need for renal replacement therapy is reported in 5-9 % of patients in intensive care. Histological analysis of renal biopsies mainly shows acute tubular necrosis of varying severity, as well as the congestion of glomerular and peri-tubular capillaries. Endothelitis has been described in few cases. Evidence for a factual inflammation of the glomerulus remains controversial. The medium/long term consequences of COVID-19 nephropathy are unknown and will deserve a tight follow-up.Le virus SARS-CoV-2 provoque un syndrome de détresse respiratoire aiguë, le symptôme principal de l’infection COVID-19 (pour «COronaVIrus Disease 2019»). Cette maladie infectieuse provoque une pandémie de gravité sanitaire et socio-économique majeure depuis décembre 2019. La cible principale du SARS-CoV-2 serait l’alvéole pulmonaire. Néanmoins, ce coronavirus est capable d’affecter directement ou indirectement d’autres organes, y compris les reins. Nous résumons ici la physiopathologie présumée de l’atteinte rénale de la COVID-19. L’incidence de l’insuffisance rénale aiguë varie entre 0,5 à 22 % de tous les patients infectés par le SARS-CoV-2. La nécessité d’une épuration extra-rénale est rapportée chez 5-9 % des patients pris en charge aux soins intensifs. L’analyse histologique de biopsies rénales montre, principalement, une nécrose tubulaire aiguë de sévérité variable, ainsi qu’une congestion des capillaires glomérulaires et péri-tubulaires. Une endothélite a parfois été décrite. L’atteinte inflammatoire du glomérule reste débattue. Les conséquences à moyen/long termes de la néphropathie COVID-19 sont inconnues et mériteront un suivi étroit.

COVID-19 has been the center of global attention and concern for the last months. Patients undergoing dialysis and especially those treated at the hospital are likely to be infected, due to their mandatory presence at the hospital several times a week and due to their intrinsic fragility in regard of chronic kidney disease, often an older age, and the presence of many associated comorbidities. Thereby, patients with chonic kidney disease treated by haemodialysis have higher odds of a more severe COVID-19 infection with a high mortality rate. Prevention is thus a high priority for these patients.Au cours des derniers mois, la COVID-19 a été au centre des préoccupations et de l’attention de chacun. Les patients dialysés, et surtout ceux hémodialysés en centre, représentent une population particulièrement à risque de contamination vu la nécessité de se rendre à l’hôpital plusieurs fois par semaine et compte tenu de leur fragilité intrinsèque liée au statut de malade rénal chronique, un âge souvent plus avancé, et de nombreuses comorbidités. Ils ont donc un risque de développer une infection grave et potentiellement mortelle. Dès lors, la stratégie de prévention est d’une importance capitale pour ces patients.

The gut microbiota refers to the community of microorganisms living in the mammalian digestive tract. Over the past decades, numerous preclinical and clinical studies have suggested that gut microbiota is involved in the physiological homeostasis of the host, particularly in the immune and metabolic systems. Furthermore, the dysfunction of gut microbiota, also called "dysbiosis", has been associated with various diseases, such as the metabolic syndrome or chronic kidney disease. In this review, we summarize the knowledge about the possible role of gut microbiota in the development of arterial hypertension. We detail the pathophysiological mechanisms, namely involving short-chain fatty acids produced by the bacterial fermentation of food carbohydrates. These metabolites are reabsorbed by the intestinal mucosa and interact with a multitude of G-protein coupled receptors at the surface of cells involved in blood pressure regulation, including renal tubular cells. These observations open up innovative diagnostic and therapeutic approaches in arterial hypertension, which is a major public health problem.Le microbiote intestinal désigne la communauté des micro-organismes vivant dans le tube digestif des mammifères. Au cours des dernières années, de nombreuses études précliniques et cliniques ont suggéré que le microbiote intestinal est impliqué dans la régulation physiologique de l’hôte, notamment au niveau des systèmes immunitaires et métaboliques. Bien plus, le dysfonctionnement du microbiote intestinal, également appelé la dysbiose, a été associé à diverses maladies, telles que le syndrome métabolique ou l’insuffisance rénale chronique. Dans la présente revue, nous résumons l’état des connaissances à propos du possible rôle du microbiote intestinal dans le développement de l’hypertension artérielle. Nous en détaillons les mécanismes physiopathologiques impliquant, notamment, les acides gras à chaîne courte produits par la fermentation bactérienne des hydrates de carbone alimentaires. Ces métabolites sont réabsorbés par la muqueuse intestinale et interagissent avec une multitude de récepteurs couplés aux protéines G présents à la surface des cellules impliquées dans la régulation tensionnelle, telles que les cellules tubulaires rénales. Ces observations ouvrent de nouvelles voies diagnostiques et thérapeutiques dans un domaine de santé publique majeur qu’est l’hypertension artérielle.

Hypertension remains one of the most important cardiovascular risk factors. In spite of many efforts for its management, the control of high blood pressure remains insufficient. In the last decade, no new antihypertensive drug was released. The main effort to improve blood pressure control was put on the validation of the hypertensive status, the stimulation of home blood pressure measurement and the therapeutic education of the patients. The releasing in 2018 of new guidelines, which are clear and more simple, would help more efficiently fight against hypertension, the still present silent killer. In Europe, the usual blood pressure target has been kept, i.e.a lowering of blood pressure below 140/90 mmHg in all fit patients whatever their age. Lower target could be proposed according to the patient tolerance. Treatment is decided according to cardiovascular risk evaluation. Quickly a combination of two antihypertensive agents in a single pill is proposed to improve efficacy of the treatment. We also need the help of the family, nurses and pharmacists to increase the chance of a better blood pressure control, which is necessary to get an optimal cardiovascular protection.L’hypertension artérielle reste un des facteurs de risque cardiovasculaire les plus fréquemment rencontrés. Malgré de très nombreux efforts, le contrôle de cette élévation de pression artérielle reste insuffisant. Ces dernières années, à défaut de nouveaux médicaments, une réflexion a été menée pour améliorer l’efficacité de la prise en charge en validant le caractère réel de l’hypertension, en stimulant l’automesure tensionnelle, en améliorant l’éducation thérapeutique et en donnant des consignes simples et claires pour mieux contrôler ce tueur silencieux toujours très présent. En Europe, nous avons conservé les cibles de pression artérielle classiques, c’est-à-dire descendre la pression en-dessous de 140/90 mmHg. On peut cependant tenter de descendre plus bas si le patient le tolère. Le traitement passe par une évaluation du risque cardiovasculaire et associe, assez vite, deux molécules antihypertensives, si possible dans un seul comprimé. Il faut s’entourer aussi de l’aide de la famille, d’infirmières, du pharmacien pour augmenter les chances d’un meilleur contrôle de pression artérielle, gage d’une protection cardiovasculaire optimale.

Chronic kidney disease (CKD) impairs the quality of life and increases the risk for cardiovascular morbimortality. Intensive research is conducted in order to slow down CKD development and progression. During the past decade, a better understanding of the pathophysiological mechanisms of glomerular diseases has highlighted the benefits of rituximab. Progresses have also been made in the understanding of the mechanisms of autosomal polycystic kidney disease, the most frequent inherited kidney disease. These observations led to the discovery and validation of tolvaptan, a blocker of the V2 receptor of the antidiuretic hormone as an innovative treatment. Type 2 diabetic disease is the leading cause worldwide of endstage kidney disease and dialysis. The development of new drugs, such as the gliflozins (inhibiting the sodium glucose reabsorption in the proximal tubule), has contributed to an improvement in the management of the cardiovascular and renal risks especially reducing congestive heart failure rate. Another important progress in nephrology since the beginning of the new century concerns a more precise estimation of the kidney function, which allows to better evaluate the slope of CKD progression and test the influence of different therapeutic approaches aiming at correcting anemia, hyperkalemia, metabolic acidosis and disturbances of calcium and phosphate. The present review summarizes all of these major advances in the field of CKD diagnosis and treatment, and envisions the future of nephrology for the next decade.L’insuffisance rénale chronique (IRC) altère la qualité de vie, expose à une morbi-mortalité cardiovasculaire majorée, et peut conduire à la dialyse chronique et/ ou la transplantation rénale. Tout progrès qui freinerait le développement et la progression de cette IRC est le bienvenu. Au cours de ces dernières années, une meilleure compréhension des mécanismes physiopathologiques de certaines maladies glomérulaires a permis l’utilisation d’un traitement plus ciblé, le rituximab, qui apporte une nouvelle option dans des situations difficiles. Des progrès ont également été faits dans la compréhension des mécanismes expliquant la perte de fonction rénale chez le patient atteint de polykystose rénale autosomique dominante, la maladie rénale génétique la plus fréquente. Les études cliniques ont permis de démontrer la néphro-protection du tolvaptan, un antagoniste des récepteurs V2 de l’hormone antidiurétique. Dans le domaine du diabète de type 2, première cause mondiale de prise en charge en dialyse, l’avènement des gliflozines (inhibiteurs de la réabsorption tubulaire rénale de glucose et de sodium) a été une réelle révolution thérapeutique pour freiner l’évolution de l’insuffisance rénale chronique et limiter le risque cardiovasculaire (surtout la décompensation cardiaque) de ces patients. Enfin, une meilleure estimation de la fonction rénale a permis de mieux situer le patient dans sa vitesse de progression à travers les différents stades de l’IRC. Ce faisant, la gestion des anomalies métaboliques rencontrées au cours de celle-ci, telles qu’anémie, hyperkaliémie, acidose, troubles du métabolisme phosphocalcique, s’est améliorée. Cette revue fait état des avancées majeures dans le domaine du diagnostic de l’IRC et de ses traitements et envisage le futur de la néphrologie dans les 10 prochaines années.

The incidental finding of renal cysts is a common clinical situation given their high prevalence (~ 50 % after the age of 50) and the continuous improvement of abdomen imaging. Diagnosis is central to appropriately dictate the management of the patient. During the diagnostic work-up, it is important to consider (i) the aspect of the cysts, (ii) their number, (iii) and their location, as well as (iv) the age of the patient and his/her personal and familial medical history, (v) the presence of extra-renal manifestations, (vi) and the renal function (including the urinary sediment). Starting from an atypical clinical case characterized by a rapidly evolving chronic kidney disease associated with bilateral renal cysts, we review the classical diagnostic work-up of kidney cysts. As a conclusion, we propose a diagnostic algorithm including both acquired and hereditary nephropathies.La découverte, souvent fortuite, de kystes rénaux est une situation clinique fréquente vu leur prévalence élevée (~ 50 % dès l’âge de 50 ans) et les progrès de l’imagerie abdominale. Un diagnostic étiologique conditionnera la prise en charge et le pronostic du patient. Lors de la démarche diagnostique, il est important de considérer (i) l’aspect des kystes, (ii) leur nombre et (iii) leur localisation, ainsi que (iv) l’âge du patient et ses antécédents personnels et familiaux, (v) la présence de manifestations extrarénales et (vi) la fonction rénale et le sédiment urinaire. A partir d’un cas clinique inhabituel présentant une insuffisance rénale chronique rapidement progressive associée à des kystes rénaux, nous revoyons la mise au point classique des kystes rénaux. En guise de conclusion, nous proposons un algorithme diagnostique incluant les néphropathies acquises et héréditaires.

New European guidelines for high blood pressure management have just been published in 2018, modifying those published in 2013 and may be seen as a response to those published by the American societies late 2017. The latter proposed a new definition of hypertension (blood pressure equal or higher than 130/80 mmHg), a therapeutic approach based on the evaluation of the cardiovascular risk, and a blood pressure target inferior to130/80 mmHg in all patients, even those older than 80 years still valid. The European guidelines, on the contrary, maintain the definition threshold of hypertension to a blood pressure equal or higher than 140/90 mmHg. This diagnosis remains based on blood pressure determination at the medical office, confirmed if possible by the use of out of the clinic blood pressure measurements such as home blood pressure and/or 24h ambulatory blood pressure measurement. In comparison with 2013, these new guidelines are closer to the American ones for the management, with the need to evaluate the cardiovascular risk before deciding to initiate a drug treatment in addition to lifestyle and diet measures. A medical therapy will be initiated if the risk is very high for blood pressure in the range of high normal blood pressure (130-139/85-89 mmHg). The blood pressure target should be inferior to 130/80 mmHg in people inferior to 65 years. For those older the blood pressure target should be inferior to 140 mmHg but superior to 120 mmHg. The antihypertensive therapy would be, in the majority of the population, a two-drug combination, if possible in a single pill to enhance the medication compliance that should be frequently checked. If the blood pressure lowering remains resistant to three drugs including a diuretic used at high dose, spironolactone would be recommended, at a low dose. In comparison with 2013, the device-based therapies (renal denervation) are no longer recommended.De nouvelles directives européennes pour la prise en charge de l’hypertension artérielle (HTA) ont été publiées en septembre 2018, modifiant quelque peu celles de 2013 et venant en réponse à celles des Américains, présentées en 2017. Ces directives 2017 de la société américaine d’hypertension proposaient une nouvelle définition de l’hypertension artérielle (pression égale ou supérieure à 130/80 mmHg), une approche thérapeutique basée sur un risque cardiovasculaire calculé, et abaissaient les valeurs cibles proposées à inf�rieur a 130/80 mmHg chez quasi tous les patients hypertendus, même âgés de plus de 80 ans encore valides. Les directives européennes, par contre, maintiennent un seuil de définition de l’HTA non changé par rapport à 2013, à savoir une pression artérielle égale ou supérieure à 140/90 mmHg. Le diagnostic de l’HTA repose sur la mesure de pression au cabinet de consultation, mais aidée des mesures en dehors, à savoir l’automesure et/ou la mesure ambulatoire sur 24h. Par rapport à 2013, ces nouvelles directives européennes se rapprochent de celles américaines, pour la prise en charge, en (ré)insistant sur l’évaluation du risque cardiovasculaire pour décider d’un traitement médicamenteux, en plus des règles hygiéno-diététiques. La décision d’introduire un traitement médicamenteux est à prendre pour des pressions dans les valeurs dites normales hautes (130-139/85-89 mmHg) lorsque ce risque cardiovasculaire est fort élevé. Le patient âgé en bonne santé doit aussi bénéficier d’une prise en charge plus stricte. La cible de pression à atteindre recommandée est inf�rieur a 130/80 mmHg pour les patients de moins de 65 ans. Pour les sujets de plus de 65 ans, la cible de pression systolique est inf�rieur a 140 mmHg, mais doit rester sup�rieur a 120 mmHg. La pression diastolique doit être inf�rieur a 80 mmHg (et non plus seulement inf�rieur a 90 comme en 2013). Le traitement antihypertenseur à initier sera, pour la plupart des patients hypertendus, une combinaison de deux molécules différentes, si possible, rassemblées en un seul comprimé, ceci dans le but d’améliorer l’adhésion au traitement, point fort important à vérifier. Si la baisse de la pression résiste à trois médicaments dont un diurétique classique à bonne dose, la spironolactone doit être, si possible ajoutée, à faible dose. Par rapport à 2013, les approches invasives, par dénervation notamment, ne sont plus au goût du jour.

The measurement of proteinuria is a very simple tool to screen and manage kidney diseases. Its predictive role is also relevant from a cardiovascular point of view. However, the interpretation of the results is not always easy. Indeed, there are several different methods to detect or measure proteinuria (or albuminuria), varying from the measurement on a 24-hour urine collection to the simplest detection with dipsticks or measurement on a random urine sample. Some methods are measuring total proteins, whereas others are measuring more specifically albuminuria. For all methods, pitfalls exist and will be discussed. A positive result must be confirmed by a quantitative measurement on 24-hour collection or on a first morning sample (this last one can only be interpreted as a ratio to urinary creatinine excretion). Lastly, we will briefly discuss the management of a patient with a new diagnosis of proteinuria (or albuminuria).La recherche d’une protéinurie est un outil simple de dépistage et de suivi de la maladie rénale. Elle a aussi un rôle prédictif important, que ce soit au niveau néphrologique ou cardiovasculaire. Son interprétation n’est cependant pas toujours simple. Il existe, en effet, différentes méthodes pour évaluer la protéinurie (ou l’albuminurie) qui vont d’une mesure sur la récolte de 24h à l’utilisation simple de la bandelette réactive (« tigette ») sur un échantillon urinaire. Certaines méthodes permettent la recherche et/ou la quantification de la protéinurie dite totale, alors que d’autres mesurent plus exclusivement l’albuminurie. Pour toutes les méthodes et pour tous les dosages, des pièges diagnostiques existent et seront discutés. Un résultat positif doit systématiquement être confirmé quantitativement sur un second échantillon soit à partir d’urine de 24h, soit sur un échantillon du matin (la mesure sur échantillon n’étant interprétable que si elle est rapportée à l’excrétion urinaire de créatinine). Enfin, nous tracerons les grandes lignes de la prise en charge d’un patient chez qui une protéinurie (ou une albuminurie) est découverte.

Hypertensive crisis has fortunately become rarer due to a better diagnosis and management of arterial hypertension. However, its development needs urgent management with adapted therapy according to the severity of the blood pressure levels and the associated clinical signs. After confirmation of severe hypertension (blood pressure above or equal to 180/120 mmHg), target organ lesions have to be looked for and according to their pre-sence, an urgent hospitalization has to be immediately organized. Starting active drug therapy often occurs in intensive units with the intravenous route of administration.La crise hypertensive est devenue moins fréquente qu’auparavant, grâce au dépistage de l’hypertension et à sa prise en charge thérapeutique. Cependant, sa survenue expose le patient à un risque vital considérable. Il faut donc ne pas rater le diagnostic et la mise au point pour démarrer rapidement un traitement adapté selon le niveau de pression artérielle et les signes cliniques associés. Après avoir confirmé l’existence d’une hypertension sévère (pression supérieure ou égale à 180/120 mmHg), il faut rechercher la présence d’une défaillance viscérale. Si celle-ci est observée, une hospitalisation urgente s’impose avec un traitement sans attendre, souvent réalisé aux soins intensifs et par voie intraveineuse.

The endothelium plays a vital role as part of the cardiovascular continuum. Risk factors such as hypertension and dyslipidemia unbalance angiotensin II - bradykinin homeostasis, leading to endothelial dysfunction and changes in vascular structure that promote atherosclerosis and thrombosis. When dealing with risk factors, treatment should focus on the prevention and restoration of endothelial function. Not all cardiovascular drugs are able to reverse vascular and structural endothelial dysfunction. Increasing levels of bradykinin is an effect of the use of angiotensin-converting enzyme inhibitors (ACE-Is), and also a fundamental part of their mode of action. The cardiovascular protection observed with ACE-I, and not with sartans, can be explained rationally by the specific effects of bradykinin on the endothelium. In the pharmacological class of ACE-Is, perindopril likely produces the strongest effects on bradykinin, which may explain, at least in part, the documented superiority of this drug in the prevention and treatment of cardiovascular disease.L’endothélium joue un rôle primordial en tant qu’élément du continuum cardiovasculaire. Les facteurs de risque comme l’hypertension et les dyslipidémies déséquilibrent l’homéostasie angiotensine II – bradykinine, ce qui entraîne une dysfonction endothéliale et des modifications de la structure vasculaire favorisant l’athérosclérose et les thromboses. Le but du traitement des facteurs de risque doit être la prévention et la restauration de la fonction endothéliale, mais tous les médicaments à visée cardiovasculaire ne sont pas capables d’inverser la dysfonction endothéliale et les anomalies structurelles vasculaires. L’augmentation des taux de bradykinine est un effet de la prise des inhibiteurs de l’enzyme de conversion (IEC), et représente un élément fondamental de leur mode d’action. La protection cardiovasculaire observée avec les IEC, et non avec les sartans, peut s’expliquer rationnellement par les effets spécifiques de la bradykinine sur l’endothélium. Dans la classe pharmacologique des IEC, c’est probablement le périndopril qui produit les effets les plus puissants sur la bradykinine, ce qui peut expliquer, au moins en partie, la supériorité documentée de ce médicament dans la prévention et le traitement des maladies cardiovasculaires.

The use of thiazides as antihypertensive agents has been challenged because associated metabolic adverse events, including new-onset diabetes. However, these metabolic disturbances are less marked with low-dose of hydrochlorothiazide and with thiazide-like diuretics such as chlorthalidone and indapamide. In post hoc analyses of subgroups of patients with hypertension and type 2 diabetes, thiazide(-like) diuretics resulted in a significant reduction in cardiovascular events, all-cause mortality and hospitalization for heart failure compared to placebo. Furthermore, they were shown to be non-inferior to other antihypertensive agents, including blockers of the renin-angiotensin system in diabetic patients without albuminuria. Benefits attributed to thiazide(-like) diuretics (especially at low dose) in terms of cardiovascular protection outweigh the risk of worsening glucose control and inducing other metabolic disorders in patients with type 2 diabetes. Thus low dose thiazide(-like) drugs still play a major role in the treatment of hypertension in patients with type 2 diabetes.L’utilisation des diurétiques de type thiazide a été controversée en raison des divers troubles métaboliques qu’ils sont susceptibles d’induire comme manifestations indésirables, notamment les effets diabétogènes. Ces manifestations sont, cependant, moins marquées pour de faibles doses d’hydrochlorothiazide et pour les thiazidiques apparentés comme la chlorthalidone et l’indapamide. Dans des analyses post hoc de sous-groupes de patients avec un diabète de type 2 et une hypertension artérielle, les diurétiques thiazidiques ont montré une réduction significative des événements cardiovasculaires, de la mortalité toutes causes et des hospitalisations pour insuffisance cardiaque par rapport à un placebo. De plus, ils se sont révélés non inférieurs à d’autres antihypertenseurs, en ce compris les inhibiteurs du système rénine-angiotensine chez les patients sans albuminurie. Les bénéfices attribués aux diurétiques thiazidiques, surtout à faible posologie, en termes de protection cardiovasculaire chez le patient diabétique de type 2 hypertendu dépassent largement les éventuels effets secondaires de détérioration de certains paramètres métaboliques. Ainsi, les diurétiques thiazidiques et apparentés, à faible posologie, gardent une place de choix dans le traitement de l’hypertension artérielle chez les patients avec diabète de type 2.

Differential diagnosis of lower limb oedema is a common exercise in clinical practice. Taking the example of a patient presenting with such clinical picture in the presence of type 2 diabetes and arterial hypertension with coronary heart disease and chronic kidney disease as comorbidities, we discuss here the respective contributions of congestive heart failure, renal impairment (and possibly nephrotic syndrome) and liver disease in the development of lower limb oedema. The focus is made on a careful patient history and a meticulous clinical examination, two crucial steps that should allow prescribing well selected simple complementary procedures and rapidly make the final diagnosis.Le diagnostic différentiel des oedèmes des membres inférieurs est un exercice fréquemment rencontré en pratique clinique. A la lumière de l’histoire d’un patient obèse avec un diabète de type 2 et une hypertension artérielle, compliqués d’une insuffisance coronarienne et d’une néphropathie, présentant des oedèmes des membres inférieurs, les contributions respectives d’une insuffisance cardiaque, d’une altération de la fonction rénale (avec possible syndrome néphrotique) et d’une éventuelle atteinte hépatique sont discutées sur la base d’éléments anamnestiques et cliniques évocateurs. Le diagnostic final sera conforté par les résultats d’examens paracliniques simples, judicieusement sélectionnés.

The syndrome of "post-obstructive diuresis" corresponds to a massive polyuria and natriuresis occurring after the drainage of an obstructive acute kidney injury. Such a complication needs to be readily detected and managed because of the significant risk for haemodynamic disorders. On the basis of a clinical observation, we describe the pathophysiology of post-obstructive diuresis, as well as its diagnostic and therapeutic management.Le syndrome de levée d’obstacle urinaire correspond à une polyurie et une natriurèse massives survenant lors du drainage des voies urinaires dans le cadre d’une insuffisance rénale obstructive. Cette complication doit être rapidement détectée vu les risques de répercussions hémodynamiques sévères. A partir d’une observation clinique, nous décrivons la physiopathologie et la prise en charge diagnostique et thérapeutique du syndrome de levée d’obstacle.

In patients suffering from systemic arterial hypertension, coronary artery disease, or heart failure, beta-blockers and angiotensin-convertase enzyme inhibitors play a major therapeutic and preventive role. Coronary artery disease remains the leading cause of mortality in industrialized countries. Unless adapted preventive strategy, notably pharmacological interventions, cardiovascular events in these patients remain high. One reason for this relative failure is represented by non-adherence to treatment. A treatment consisting in an association in one pill of several different molecules should confer a higher treatment compliance and thus efficacy. This article describes the characteristics of the first available dual association between a cardioselective beta-blocker agent, bisoprolol, and an angiotensin-convertase enzyme inhibitor, perindopril arginine.Chez les patients souffrant d’hypertension artérielle, de maladie coronaire, ou d’insuffisance cardiaque, les bêtabloquants et les inhibiteurs de l’enzyme de conversion de l’angiotensine jouent un rôle thérapeutique et préventif majeur. La maladie coronaire demeure actuellement la première cause de mortalité dans les pays industrialisés. Malgré des mesures préventives adaptées, notamment pharmacologiques, le taux d’événements cardiovasculaires reste élevé chez ces patients. Une des raisons de cet échec relatif réside dans le manque d’observance au traitement. Un traitement antihypertenseur consistant en une association en un seul comprimé de plusieurs molécules distinctes devrait permettre une plus grande adhérence au traitement et donc, efficacité. Cet article décrit les caractéristiques de la première double association fixe entre un bêtabloquant cardio-sélectif, le bisoprolol, et un inhibiteur de l’enzyme de conversion, le perindopril arginine.

This clinical case draws attention to the importance of stopping some medications in case of gastrointestinal disturbances that could induce dehydration. The latter can provoke an acute renal failure, which may lead to a toxic accumulation of these pharmacological agents and/or increase their nephrotoxicity. This may induce a vicious circle that is potentially dangerous and even fatal. Three pharmacological classes that are widely used in clinical practice are considered as examples, metformin, inhibitors of the renin-angiotensin system and nonsteroidal anti-inflammatory drugs. For each of them, the pathophysiology of the complication will be briefly discussed. Some patient risk profiles where caution is mandatory will be also emphasized.Cette vignette clinique attire l’attention sur l’importance d’interrompre certains médicaments en cas de troubles digestifs susceptibles d’entraîner une déshydratation. En effet, cette dernière peut provoquer une insuffisance rénale aiguë qui va contribuer à une accumulation toxique de ces médicaments et/ou augmenter leur néphrotoxicité. Il peut s’ensuivre un véritable cercle vicieux, potentiellement dangereux, voire mortel. Trois classes de médicaments, très fréquemment prescrites, sont prises à titre d’exemple, la metformine, les inhibiteurs du système rénine-angiotensine et les anti-inflammatoires non stéroïdiens. Pour chacune d’entre elles, la physiopathologie de la complication sera brièvement discutée. Il sera également mis l’accent sur certains profils de risque de patients chez lesquels la plus grande prudence s’impose.

Besides the well accepted need to treat hyperuricemia associated with gout, some large observational studies and small prospective therapeutic trials have suggested that treating asymptomatic hyperuricemia, especially by xanthine oxidase inhibition, the enzyme producing uric acid, could be beneficial for cardiovascular and renal risk prevention. This article discusses the literature about this promising approach, which, however, requests prospective validation.

Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited disease characterised by the progressive development of multiple and bilateral cysts in kidneys and other organs. Most patients with ADPKD will develop, sooner or later, end-stage renal disease (ESRD). The morbidity and mortality associated with ESRD prompt physicians to identify early ADPKD patients considered as "rapid progressors", who have the greatest risk to rapidly develop ESRD. The rate of progression can be assessed by clinical--especially with the "predicting renal outcome in polycystic kidney disease score" (PROPKD-Score)-, biological (a decline of the glomerular filtration rate (GFR) of 4.4-5.9 ml/min/year and/or the doubling of serum creatinine within a 36-month period), or radiological criteria (total kidney volume (TKV) adjusted for the size600 cc/m and/or TKV annual growth rate5 %). Nowadays, there is no curative treatment for ADPKD. However, vasopressin-2 receptor antagonists, such as tolvaptan, appear to slow down the growth of renal cysts and the slope of GFR decline. The current management of ADPKD patients is mostly based on correcting the risk factors for progression, i.e. encouraging (over)-hydration, normalizing blood pressure, stimulating smoking cessation.

The diabetic kidney disease is the most frequent cause of end stage renal disease in Western countries. Its detection is obtained by simultaneously measuring urinary albumin excretion and estimating glomerular filtration rate through serum creatinine dosage. Many type 1 and type 2 diabetic patients can present decreased glomerular filtration rate before the occurrence of increased urinary albumin. While waiting for promising new pharmacological approaches currently evaluated in clinical trials, the best approach to stop the epidemic of diabetic nephropathy remains an early and individual multifactorial approach controlling the glucose level (without inducing hypoglycaemia), blood pressure (using a renin-angiotensin blocker), dyslipidaemia and over-weight.

Hypertension has a high world-wide prevalence, affecting more than 25 % of the population; it remains the silent killer number one in cardiovascular pathology. Although lowering high blood pressure is protective, perfect control of hypertension is far from being optimal in spite of many international guidelines regularly updated according to published scientific studies. A personalized approach of hypertension management is an attractive way to improve this situation. Tools are developing (pharmacogenetics, pharmacometabolomics), but their use in daily clinical practice seems premature. At the present time, it is the physician experience which offers the best opportunity to propose the best treatment to the best patient. The management of hypertension remains a difficult task in some cases. Patient education is also crucial to improve drug compliance.

Systemic lupus erythematosus (SLE) is an inflammatory disease with multiple and disabling consequences, including the psychological status. The prevalence of major depressive episodes among patients suffering from SLE is significantly higher than in healthy people, or people suffering from other inflammatory diseases. While it is obvious that its chronic disease status with a frequently pejorative ending, as well as the number of treatments it requires, are contributing factors, it is likely that due to its pathogenic mechanisms, SLE causes direct injury to the brain, leading to a depressive symptomatology. Numerous hypotheses are under consideration. We shall review them all, recall a few epidemiologic features, add histology and medical imaging contributions and discuss the importance of setting up a fitting therapy for such patients.

Hypophosphatemia is defined by a serum phosphate level lower than 0.8 mmol/l. If hypophosphatemia is chronically maintained, it is associated with muscular, osteous, neurological or cardio-respiratory disorders. We describe a patient with isolated hypophosphatemia, detail the mechanisms of phosphate homeostasis, and envisage the differential diagnosis of hypophosphatemia. Furthermore, we propose a sequential decisional algorithm based on basic biological tests and few complementary investigations. Treatment options are reviewed.

Chronic kidney disease (CKD) is a frequent affection, most often detected by evaluation of the glomerular filtration rate (GFR). Measuring GFR by a reference method is not possible for every single patient, even if these methods are probably underused. However, serum creatinine has several limitations of which clinicians should be aware. Knowing these limitations, creatinine and creatinine-based equations (including other parameters like age, gender and ethnicity) still represent the most used and easiest way to detect and assess CKD.

Triplixam is a fixed dose combination of three well known antihypertensive agents, with complementary activities, to control blood pressure in patients with arterial hypertension: perindopril, an angiotensin converting enzyme inhibitor, indapamide, a diuretic whith thiazide-like effects but also specific properties, and amlodipine, a long-acting calcium antagonist of the dihydropyridine family. The potential synergic action allows better control of blood pressure with once daily administration, while limiting the incidence of adverse events. Various presentations with different dosages are available to facilitate individualized therapy. Warnings and precautions for use of every molecule should of course be respected. Such a fixed dose combination should contribute to limit clinical inertia and to improve therapeutic compliance.

High blood pressure is very frequent in the elderly; it represents a real threat for the patient's health and a source of huge costs for the economic system. Systolic hypertension is the most frequent form observed in the old, due to large arteries stiffness. Antihypertensive therapy has proven effective to decrease significantly the cardiovascular morbi-mortality and total mortality in this population. A non pharmacological approach is also very useful, but should not be too restrictive. Blood pressure target in patients older than 65 (and, particularly, in octogenarians) is 150/80 mmHg. Blood pressure should be checked in the upright position before changing the drug dosage. The first line therapy in the old should generally be a calcium channel antagonist or a low dose diuretic.

From age 30 onwards, kidney function physiologically decreases although this deterioration cannot yet be called chronic kidney disease. The latter appears in those exposed to cardiovascular risk factors associated with inflammation and oxidative stress. A diffuse atherosclerosis then develops Patients with a decreased glomerular filtration rate, especially below the threshold of 45 ml/min, are characterised by a poor physical heath and by cognitive disorders, leading to frailty. In these conditions, a management strategy to reduce the increased risk of acute kidney injury should be outlined and the need for renal replacement therapy be considered. One must try to maintain the best possible quality of life, promoting in some situations a conservative approach.

The 2013 guidelines for arterial hypertension have just been released by the European Societies of Cardiology and Hypertension. As already discussed in earlier versions, the decision to treat must be based on the assessment of the cardiovascular risk. The value of out-of-the office blood pressure measurements to confirm the diagnosis of hypertension is underlined and the authors stress the need for a close follow up of non pharmacological therapeutic measures. A novelty, however, consists in the simplification of the blood pressure target under treatment, which must be140/90 mmHg in the vast majority of patients, except for octogenerians whose systolic blood pressure target should be150 mmHg. For resistant hypertension, renal denervation and carotid baroreceptor stimulation are proposed as new invasive modes of therapy; their clinical values, however, remain to be confirmed.

Orthostatic hypotension (OH) is a rather common phenomenon in clinical practice. It may occur in 5-10 % of normal individuals, but its prevalence increases with age and various pathologies, so that it may rise above 35 % in certain subgroups of patients. OH is associated with various comorbidities, in particular cardio-cerebro-vascular accidents and falls (especially in the elderly), and may even increase mortality. It is, however, difficult to determine whether OH is simply a marker of frailty or whether it is really a risk factor. OH treatment involves physical manoeuvres or medications, which aim at inducing a peripheral vasoconstriction (midodrine, etilefrine) or an increase of circulating blood volume (9-alpha-fluohydrocortisone). However, their use should be cautious, because of a risk of arterial hypertension in supine position.

Orthostatic hypotension (OH) is defined by a drop in arterial blood pressure (BP) of at least 20 mmHg for systolic BP and 10 mmHg for diastolic BP after standing. Symptoms are generally quite typical, but may also be rather vague. Diagnosis may be easily made by the physician in his/ her office, and confirmed, if necessary, by more sophisticated measurements. Pathophysiology is generally rather complex, but mostly involves a defect in the autonomic nervous system, in its sympathetic component. Failure of peripheral vasoconstriction seems to play a more important role than the defect in reflex tachycardia. Causes of OH are multiples. OH may occur in healthy subjects, when exposed to exceptional circumstances, but is more generally associated with various diseases, either neurological disorders or pathologies characterized by hypovolemia. Medications can also aggravate the risk of OH, among which some antihypertensive or psychotropic agents. Elderly people, especially frailty subjects, are exposed to a high risk of OH, whose origin is often multifactorial, and this complication may have serious medical consequences.

Routinely measuring blood pressure is still performed according to the auscultatory method using recognition of Korotkoff sounds. This usual technique is, however, often mishandled and is thus a source of error in the estimation of the true blood pressure level. Accuracy of such measure is, however, of paramount importance to be useful in daily medical practice. This methodology paper more specifically written for medical students recalls the essential principles of blood pressure measurement at the medical office, but also at home.

The blockade of the renin-angiotensin system (RAS) improves the prognosis of patients with complications related to diabetes, hypertension or, in general, atherosclerosis. Several observational studies have suggested the use of a dual blockade of the RAS to benefit from a better cardiorenal protection. However, recent randomized controlled studies failed to demonstrate that a dual blockade exert a better protection than single blockade, but showed a higher risk for renal complications and hyperkalemia. To decrease the residual risk, other opportunities may be recommended such as reinforcement of low salt diet, use of supraphysiological dose of a monotherapy inhibiting the RAS (perhaps prescribed at the evening) or addition of an aldosterone antagonist. However, all these approaches, as dual therapy, may also increase the risk of hypotension and renal insufficiency and thus require to be used under strict medical supervision.

The interest of chronotherapy in the field of arterial hypertension is progressively rising, especially in treated hypertensive patients characterized by a small decrease of their blood pressure during the night, and therefore often presenting a high cardiovascular risk. There are more and more data showing that administration of one antihypertensive drug in the evening (and even aspirin) can improve the blood pressure control during the night and the day/night blood pressure pattern, and so can diminish the level of risk. The role of chronotherapy also emphasizes the interest of 24 h ambulatory blood pressure monitoring in the management of high risk hypertensive patients.

Essential hypertension, defined as a blood pressure equal to or above 140/90 mmHg, is a common (25% of the population), but complex disease the phenotype of which results from interactions between numerous genes and environmental factors. The role attributable to genetic factors amounts to some 25% among hypertensive families, but can reach 65% when monozygotic twins are compared. In the present state of our knowledge, there is no hope to obtain a genetic test of value for the diagnosis and prognosis of hypertension. An individualized environmental approach, applied early in life, is the only worhtwhile attitude. Nonetheless, in the presence of a subject with still normal blood pressure values, but with a family history of hypertension, the physician should firmly recommend an appropriate hygieno-dietetic lifestyle with a view to lower blood pressure, or retard the development of arterial hypertension

Both diabetes mellitus and arterial hypertension are commonly observed in a single patient. However, the relationship between these two entities is rather complex and there is a great heterogeneity regarding the underlying pathophysiological mechanisms and the clinical presentations. These particularities may have important consequences from a therapeutic point of view, as far as blood pressure targets or even pharmacological strategies are concerned. The present article will discuss the various causes of hypertension in the different types of diabetes, the different forms of hypertension in the diabetic patient, the modalities of treating hypertension in presence of various specific complications (metabolic syndrome, coronary heart disease or renal impairment), and the specificities when hypertension is associated with diabetic cardiovascular autonomic neuropathy.

Arterial hypertension is commonly observed in patients with type 2 diabetes and aggravates cardiovascular and renal outcomes. Lowering blood pressure is thus a key objective in this population. However, systolic and diastolic blood pressure levels to be reached remain controversial and targets should probably be adjusted according to patient's individual characteristics ("personalized medicine"). This clinical case summarizes the main arguments for selecting blood pressure targets, as far as benefits/risks ratio is concerned, in type 2 diabetic patients with a metabolic syndrome but without complications, with a nephropathy, or with coronary artery disease.

The consultation for dizziness is a common problem in clinical practice. Because of the apparent lack of specificity of the complaints, there is a rather high risk to prescribe a variety of sophisticated exams, which will not be very helpful in absence of a well oriented anamnesis and a pertinent clinical examination. The present paper aims at describing a global medical approach, essentially based upon a detailed anamnesis (semiological, chronological and therapeutical arguments), to which may be added a few simple clinical and technical complementary data. This strategy should allow obtaining quite easily pertinent arguments for a differential diagnosis between reactive hypoglycaemia, (orthostatic) hypotension, and hyperventilation crisis (spasmophilia).

Oedema is a frequent disorder and the easily detectable consequence of an increase of fluid located in the interstitial tissue. It could be localized or generalized and related either to a primary disturbance of hemodynamics at the capillary level, due to a modification of the Starling's law components with secondary water and saline retention, or to a primary retention of salt and water linked to a kidney abnormality. Generalized forms are pitting oedema, most often painless, white, bilateral and symmetric, distributed at the lower part of the body (localisation according to the gravitation law). They are different in their characteristics from localized oedema or lymphoedema which are tough. We propose a diagnostic approach based on medical history, clinical examination which allows a confident medical diagnosis and so an adapted therapy.

We report the case of an acute renal failure due to an acute interstitial nephropathy (ATIN) induced by non steroidal anti-inflammatory drugs (NSAID). Even though this pathology is a rare cause of acute renal failure, it still requires special attention in view of the fact that it induces a high risk of acute morbidity but it also can evolve into chronic renal failure. Its differential diagnosis with other causes of acute renal failure becomes essential because of the different therapeutic care. In this article, we are going to briefly sum up the reasoning to adopt in order to diagnose an acute renal failure.

Therapeutic inertia, i.e. the absence of introduction of an antihypertensive treatment or on adjustment of its intensity by the medical doctor if the blood pressure is elevated or the goal not reached, is frequent and does play a role in the insufficient control of blood presure in the hypertensive population. The responsibility of the medical doctor is high in this respect. A strict medical approach is required, step by step, to correct this lack of reaction.

Overwhelming evidence indicates that the treatment of arterial hypertension is beneficial, but, in practice, less than 50% of treated hypertensive patients have well-controlled blood pressure. The success of treatment relies upon adherence (for both non pharmacologic and drug treatment) by the patient. This problem of observance is multifactorial. Several factors play a role: the patient, his/her illness, his/her treatment and the therapeutic environment where the relationship between the medical doctor and the patient is crucial. To improve observance, but also treatment persistence we need to think about it. Observance must be discussed with the patient at each visit. An excellent relationship between doctor and patient, education about hypertension, its risks, and the ways to avoid complications, the choice of a well tolerated and simple treatment progressively introduced, the intervention in this management of the family and the pharmacist, the development of home self blood pressure measurement by the patient are all important ways to improve adherence. This could reduce the cardiovascular complications related to high blood pressure and thus decrease the general costs for the society.

A successful transplantation implies that immunosuppressive drugs will have to be taken during the whole patient's life. Poor drug compliance is a multifactorial problem, that is particularly dangerous in organ transplantation as it can lead to loss of graft function and return to dialysis treatment. The medical doctor must stimulate the patient's adherence to the strict therapeutic drug protocol. The patient must also be reminded at each medical consultation of the importance of such rigorous drug intake. This bad (or non) compliance is particularly well demonstrated a long time after transplantation. The medical staff, all the health participants, but also the family members must continuously fight against non compliance, which is inherent to any chronic disease.

Patients suffering from end-stage renal disease (ESRD) have a very reduced quality of life accompanied by a severe emotional distress (high worries-anxiety-depression). However, in Belgium, no regular psychological intervention is proposed to dialyzed patients. Our objective is to show that psychological intervention can significantly decrease the emotional distress of patients with ESRD. Eleven sessions of structured interventions are proposed to ESRD patients. Eligibility criteria are to be major, to not present confusion or/and dementia, to have been on dialysis treatment for at least 3months, to have obtained 14 or more on HAD-scale. Interventions carry on the management of anxious and depressive symptoms and of the disease itself. This constitutes three independent modules. Questionnaires are filled in by the patients at various stages to evaluate the anxiety and the depression (HADS), the worries (Penn State) and the quality of life (KDQoL-SF). Results for the 47 ESRD patients show a significant reduction of the scores of anxiety, depression and worries and a significant growth of quality of life. In parallel, a decrease in the serum calcium-phosphorus product analyzed before dialysis has been noted.