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The optimal diet for chronic kidney disease (CKD) is an issue frequently brought up by patients and/or their relatives during outpatient visits. For patients without malnutrition who are motivated and supported by an experienced multidisciplinary team, the optimal protein intake of 0,6 g/kg of ideal body weight/day is recommended to halt the progression of CKD. A calorie intake of 30 to 35 kcal/kg of ideal body weight/day is necessary to reduce the risk of malnutrition from a low protein diet and to maintain a neutral nitrogen balance. A low-salt diet, namely 5 to 6 g/d, is useful to optimize the treatment of hypertension associated with CKD and to limit fluid overload. At the advanced stage of CKD, it is also necessary to restrict the intake of phosphorus and sometimes potassium. Given the complexity of optimal renal diet, coordination between general practitioners, nephrologists and dietitians is essential to foster optimal care.Patienten mit chronischer Niereninsuffizienz und deren Angehörige fragen häufig nach der optimalen Ernährung. Eine reduzierte Proteinzufuhr von 0,6 g/kg Idealgewicht pro Tag wird bei nicht-unterernährten und motivierten Patienten empfohlen, sofern sie von einem erfahrenen interdisziplinären Team unterstützt werden. Um eine neutrale Stickstoffbilanz aufrechtzuerhalten sowie eine Unterernährung im Rahmen einer proteinarmen Ernährung zu verhindern, wird eine Kalorienzufuhr von 30 bis 35 kcal/Tag empfohlen. Zusätzlich sollte die Salzzufuhr in Anbetracht der häufig komorbiden Hypertonie 5–6 g/Tag nicht überschreiten, was zusätzlich die Natrium-Wasserretention beschränkt. Bei fortgeschrittener Niereninsuffizienz sollte auch empfohlen werden, die Phosphatzufuhr und manchmal auch die Kaliumzufuhr zu limitieren. In Anbetracht der Komplexität der optimalen Ernährung bei Niereninsuffizienz ist eine Koordination zwischen Klinikern, Nephrologen und Ernährungswissenschaftlern unabdingbar.La diète optimale pour la maladie rénale chronique (MRC) est un thème fréquemment discuté par les patients en consultation ambulatoire et/ou par leurs proches. Une diète optimale en protéines, réduite à 0,6 g/kg de poids idéal par jour est proposée pour ralentir la progression de la MRC chez des patients non dénutris, motivés et supportés par une équipe multidisciplinaire et expérimentée. Un apport calorique de 30 à 35 kcal/j est nécessaire pour limiter le risque de dénutrition par une diète pauvre en protéines et pour maintenir une balance azotée neutre. Une diète pauvre en sel, soit 5 à 6 g/jour, est utile pour optimaliser le traitement de l'hypertension artérielle associée à la MRC et pour limiter la surcharge hydrosodée. Lorsque la MRC est avancée, il est nécessaire de limiter également l'apport en phosphore et parfois celui en potassium. Compte tenu de la complexité de la diète rénale optimale, une coordination entre les praticiens, les néphrologues et les diététicien(ne)s est indispensable pour favoriser la prise en charge.

Assessment of volume status is often challenging in daily clinical practice. One of the clinician's tasks is to prevent or to treat organ systems failures that arise from a mismatch between the transport of oxygen and metabolic needs. Renal failure is a frequently encountered in-hospital diagnosis that is known to alter significantly the prognosis. In patients with acute renal failure in particular, the consequences of an inadequate volume management further increase morbidity and mortality.

In dialysis patients, a misevaluation of dry weight may lead to an increased morbidity and mortality. The aim of this cross-sectional multicenter study was to evaluate the association between residual urinary sodium excretion and extracellular volume status in chronically treated hemodialysis patients.Dry weight was determined clinically and by whole-body bioimpedance spectroscopy (Body Composition Monitor, Fresenius Medical Care) prior to a mid-week session in 40 chronic hemodialysis patients with significant residual diuresis (more than 250 mL per day) and receiving treatment in four dialysis centers. Regarding their hydration status assessed by the Body Composition Monitor and in comparison to a healthy reference population, patients were assigned to 1 of the 3 categories: overhydrated, normohydrated and dehydrated. Urine output, urinary sodium excretion and residual renal function were measured for all patients within 30 days before dry weight assessment.The median post-HD session FO was of-0.40 L (IQR: from-1.95 to+0.90) and the median residual urinary sodium excretion was of 64 mmol/L (IQR: 46-79). Among these patients, 16 were normohydated, 16 were dehydrated and 8 were overhydrated. There was a linear relationship between the hydration status after HD session and the urinary sodium excretion (estimate: 5.6±1.5; p0.001). Compared with normohydrated patients, overhydrated patients had a higher residual urinary sodium excretion (estimate: 26±10; p0.01).In this study, urinary sodium excretion is associated with the hydration status evaluated by whole-body bioimpedance spectroscopy.

The optimal method to assess the adequacy of peritoneal dialysis therapies is controversial. Today, the adequacy must not be considered as a number or a concept assessed only by two parameters (total KT/V urea and total solute clearance) but defined by many more items. In the absence of data, based on theoretical considerations, the reanalysis of the CANUSA study showed that renal kidney function, rather than peritoneal clearance, was associated with improved survival. Residual renal function is considered as a major predictor factor of cardiovascular mortality. Results of this reanalysis were supported by the adequacy data in ADEMEX, EAPOS and ANZDATA studies. Therefore, clinical assessment plays a major role in PD adequacy. The management of fluid balance, the regular monitoring of malnutrition, the control of mineral metabolism and particularly the glucose load, considered as the "corner-stone" of the system, are the main points to be considered in the adequacy of PD patients. The essential goal is to minimize glucose load by glucose-sparing strategies in order to reduce the neoangiogenesis of the peritoneal membrane.

Nutrition and growth are still a major challenge in neonatal intensive care. Many studies have demonstrated that premature infants frequently develop severe cumulative nutritional deficit during the first weeks of life. This malnutrition is the primary etiology of postnatal growth restriction, which is still universally described in very premature infants. Furthermore, both postnatal nutritional deficit and postnatal growth restriction have been associated with adverse long-term outcome in adulthood. Due to their immaturity, premature infants are frequently not fed by the enteral route. Therefore, parenteral nutrition remains an essential therapy in neonatology. Most recent recommendations suggest starting parenteral nutrition as soon as possible after birth with a minimum of 40 kcal/kg/day with around 2-3g/kg/day of amino acids and 1g/kg/day of lipids. Afterwards, intake should increase rapidly during the first week of life, up to 90-120 kcal/kg/day with around 3.5 g/kg/day amino acids and 3g/kg/day of lipids. There is great heterogeneity in parenteral nutrition practices among neonatal units, with frequent discrepancies. This article discusses the principal theoretical aspects of parenteral nutrition in premature infants, the guidelines, and the opportunity to optimize nutritional support routinely, especially in very premature infants.

The syndrome of inappropriate antidiuresis (SIAD; formerly the syndrome of inappropriate secretion of antidiuretic hormone) is the most frequent cause of hyponatremia. A strong association exists between mortality and hyponatremia, which reflects the severity of the underlying disease. In SIAD, hyponatremia is associated with normovolaemia but the assessment of extracellular volume can be difficult. Clinical features are mainly neurological and can lead to death but mechanisms of adaptation can limit cerebral oedema. The notion of mild asymptomatic hyponatremia was questioned by the observation of subclinical neurocognitive impairment, a greater risk of falls and fractures. Aetiologies are classified into six groups: neurologic disorders, infections mainly cerebral, meningeal and pulmonary, drugs in particular antidepressants, tumors, genetic causes, and idiopathic. Symptomatic acute hyponatremia is a therapeutic emergency that is not specific of SIAD. When hyponatremia is asymptomatic, fluid restriction with salt intake is generally sufficient but urea can be an alternative. In chronic SIAD, there is currently no recommendation. Fluid restriction is not always feasible; urea has proved its efficacy, its good tolerance and its long-term harmlessness. Vaptans have demonstrated their good tolerance and their efficacy on the correction of hyponatremia from SIAD in studies subgroups, for moderate hyponatremia and asymptomatic patients. In the only study having compared vaptans and urea, efficacy and tolerance were similar. Because of the cost difference between vaptans and urea and while waiting for follow-up studies, urea appears at present as the first-line treatment of hyponatremia in SIAD.

The discovery of apelin, an endogenous ligand of the orphan APJ receptor, constitutes an important advance in both fundamental research and clinical medicine. Experimental data have shown that apelin has a diuretic effect via its central and renal actions: by inhibiting the phasic activity of vasopressinergic neurons and systemic secretion of vasopressin and its direct effect on the renal microcirculation and probably tubular function. Besides its diuretic action, when injected into the blood stream, apelin decreases blood pressure and increases the contractile force of the myocardium while decreasing pre- and post-load, actions opposing those of vasopressin and angiotensin II. Taken together, these data show that this new circulating vasoactive (neuro)peptide could play a crucial role in maintaining water and electrolyte balance and cardiovascular functions. Finally, a systemic injection of apelin in insulin-resistant mice decreases glycemia and enhances glucose uptake in skeletal muscle and adipose tissue, contributing to homeostatic control of blood glucose. Clinically, the development of non-peptide analogs of the apelin receptor could provide new therapeutic tools potentially useful for the treatment of heart failure, states of water and/or electrolyte retention, and type 2 diabetes mellitus.

Cardiovascular disease remains the leading cause of death in ESRD patients related to long-standing hypertension. Early studies had recognized the favourable effect of PD in controlling hypertension but it was soon realized that such benefit was not sustained. A U shaped trend of hypertension in patients on PD has been recently demonstrated as a result of a steadily increased blood pressure partly attributed to fluid retention resulting from lower sodium removal with time. Effort in selecting the best strategy of ultrafiltration for a single patient along with a careful and frequent monitoring of combined 24 hours sodium elimination coupled with dietician counseling can improve significantly fluid an sodium balance which in turn will result in much better blood pressure control. The contribution of progress in biocompatibility of PD fluid that better preserve renal function and the implementation of the first glucose polymer Icodextrin were key interventions in that aim. Further studies should be conducted to assess the power of innovative PD solutions--Low Sodium PDF and/or Bimodal Ultrafiltration--in enhancing fluid and sodium removal during CAPD/APD programmes.

The determination of the magnesium status is difficult, since a cheep, sensitive and usable test remains to be found. Serum magnesium only signals severe deficiencies, which are in athletes. Blood cell magnesium may detect a subclinical deficiency, the significance of which is however very controversial. The "magnesium loading test" is the standard method, but it is too complex for the practice. A mixed diet with sufficient energy covers the needs of athletes of all levels. When the plasma magnesium levels are in normal range, supplements offer no significant benefits in terms of performance. The usefulness of magnesium in the treatment of exercise related muscle cramps is most probably widely exaggerated. Various other electrolyte dysbalances as well as venous insufficiency are certainly more important factors.

Hypernatremia exerts its main effect on the brain through the osmotic gradient it creates on either side of the blood brain barrier, which is impermeable to sodium. This generates a transfer of water from the intracellular to the vascular sector leading to temporary cell shrinkage. Osmoregulation permits cerebral cells to accumulate osmoactive molecules in order to restore their initial volume. It has been demonstrated in animals with brain injury that intracellular dehydration occurs essentially in the nonlesioned hemisphere. In most experimental studies, the reduction in cerebral volume obtained by hypertonic saline (HS) perfusion is accompanied by an intracranial pressure decrease, even under hemorrhagic shock conditions. Initially, clinical studies successfully used HS, as an alternative to mannitol, in the treatment of acute and refractory intracranial hypertension. Then continuous infusion of HS, with the objective of inducing hypernatremia, had produced encouraging effects on intracranial pressure control. However, these results were limited to non-randomized studies, without control groups and mainly in pediatric patients. Nevertheless, the use of HS on intracranial hypertension, refractory to conventional treatments, could be reasonable under strict monitoring of natremia as well as its adverse effects.

In the kidney, the fine control of NaCl absorption takes place in the distal nephron and is controlled by aldosterone and vasopressin. This review summarizes the effects of vasopressin on Na+ transport mediated by the amiloride-sensitive epithelial sodium channel (ENaC) and the cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel in immortalized or primary cultured cortical collecting duct cells, expressing either the wild-type ENaC subunits, or mutations, or deletions of the PY domain of the beta- or gamma-ENaC subunits responsible for Liddle's syndrome, an inherited form of hypertension due to excessive salt absorption.

To study the effects of microgravity on the mechanisms involved in the regulation of body hydrous status, total body water (TBW), plasma volume (PV), and its main regulating hormones (plasma renin, aldosterone, atrial natriuretic peptide (ANP), anti-diuretic hormone (ADH)) were determined, by isotopic dilution, Dill and Costill's formula, and radio-immunologic dosages, in 9 male subjects submitted to a 90-d head-down bed rest (HDBR). ADH was determined in 24 h urinary collection as well as osmolality, sodium, and potassium. Body mass decreased (-2.8 +/- 0.8 kg) as well as TBW(-7.2% +/- 0.9%, i.e., -2.6 +/- 0.7 kg) and PV (-4.7% +/- 1.8%). Renin and aldosterone were enhanced (+109.0% +/- 15.4% and +87.2% +/- 38.9%, respectively). Simultaneously, we observed a decrease in ANP (-33.2% +/- 20.4%). Other variables, including ADH, were not affected by HDBR. Body mass and TBW decrease (and consequently lean body mass) are associated with muscle atrophy. Renin, aldostrerone, and ANP modifications are well explained by the decrease in PV, which was not enough to induce ADH changes. It suggests that in man, the main regulatory factor for ADH secretion is osmolality, when PV is modestly and progressively decreased without arterial pressure modification, which was the case in the present protocol.

We observed oat-cell lung carcinoma in a man who presented with diabetes insipidus. The chest radiograph showed a suspect nodule within a context of major nicotine addiction. Histopathological examination of the transbronchial biopsy confirmed the diagnosis of oat-cell carcinoma. Brain CT revealed metastasis to the pituitary gland and the pituitary stalk. Vasopressin was undetectable. This case illustrates an uncommon clinical presentation of small-cell lung carcinoma. Oat-cell carcinoma can modify osmoregulation in two different ways. Only sporadic cases of neurogenic diabetes insipidus due to the primary involvement of small-cell lung carcinoma have been reported. More often, this type of lung tumor is associated with inappropriate antidiuretic hormone secretion.

Cyclo-oxygenase catalyses the conversion of arachidonic acid and O2 into prostaglandins. Its two isoenzymes, COX-1 and COX-2, have different functions. COX-1 is expressed in constituent form in most tissues where it controls the production of arachidonic acid metabolites which maintain the physiological tissue integrity. By contrast, COX-2 is only induced in response to inflammatory stimuli, resulting in the production of inflammation mediating prostaglandins. Conventional non-steroidal anti-inflammatories inhibit both enzymes in a non-specific manner. The recent development of specific COX-2 inhibitors, which retain the same anti-inflammatory efficacy but do not have the gastric side effects of conventional treatment related to COX-1 inhibition, gives them a greater safety margin. However, coronary events are observed in patients treated with COX-2 inhibitors. This risk, seemingly confirmed at least at higher dosages, has been attributed to a disequilibrium in the balance of thromboxane A2/prostacyclin (TxA2/PGI2) which they induce. Paradoxically, COX-2 inhibitors also have several favorable effects on atheromatous plaque progression and its inflammatory component, not only in vitro but also therapeutically, including situations where platelet activation and arterial thrombosis are predominant, such as in acute coronary syndrome. The salt retention induced by COX-2 inhibitors could also be the origin of an increase in blood pressure, and in susceptible subjects it could provoke cardiac decompensation. These multiple cardiovascular risks tinge the safety profile of COX-2 inhibitors, especially in elderly subjects and those with multiple pathology, for whom extra surveillance is required.

Non-steroidal antiinflammatory drugs (NSAIDs) are known to have adverse effects on kidney function. Situations with stimulated renin-angiotensin system (RAS) like volume depletion or preexisting chronic renal failure predispose to acute renal failure (ARF) via inhibition of prostaglandin synthesis by NSAIDs. To date NSAIDs are frequently used as antipyretic drugs even in situations predisposing to ARF.Within 20 months seven children presenting with diarrhea and/or vomiting and fever were treated with therapeutic doses (11.5-32 mg/kg per day) of ibuprofen for 1-3 days before developing ARF. Maximum plasma creatinine levels were 180-650 pmol/l. One patient required emergency dialysis for hyperkalemia, uremia, and hyperphosphatemia. After cessation of NSAID treatment and rehydration all patients recovered completely with a normalized creatinine level after 3-9 days. Once the acute phase is controlled long-term outcome is excellent.NSAIDs are potentially dangerous in situations with, even moderate, volume depletion.

HYPERKALIEMIA AND RENAL FAILURE: Nonsteroidal anti-inflammatory drugs (NSAIs) may induce hyperkaliemia and renal failure. With regard to these complications, the notion of a risk factor is fundamental. Selective cyclooxygenase-2 inhibitors (Cox-2) do not provide any notable advantages with regard to the incidence of hyperkaliemia and renal failure. OEDEMA AND BLOOD PRESSURE: The NSAIs provoke salt-water retention which is responsible for oedema in 2 to 5% of patients (here again the notion of a risk factor is important). The salt-water retention is implied in the increase in blood pressure and the decompensation of heart failure. It has been shown that the incidence of oedema and the increase in blood pressure was significantly reduced with celecoxib compared with rofecoxib. This might have a crucial impact on the mean and long term follow-up of cardiovascular risk in these patients.The results of the VIGOR study that demonstrated an increase in risk of myocardial infarction with rofecoxib, can probably be explained by an anti-thrombotic effect of naproxene, the high dose of rofecoxib used, the type of patients included or the fact that aspirin had been contraindicated. A recent study suggested that the cardiovascular risk was greater with rofecoxib than with celecoxib and with NSAIs when the dose of rofecoxib used was greater than 25mg/day. In this case control study, the cardiovascular risk was identical with celecoxib and NSAIs, whatever the dose used, but increased with a relative risk rate of 1.7 with the doses of rofecoxib greater than 50mg/day. In cases treated with aspirin Some NSAIs can reduce the anti-aggregant effects of aspirin whereas this effect is not observed with Cox-2 selective inhibitors. Hence, the latter should be the pharmacological agents of choice in patients treated with aspirin.

Physical exercise in the heat causes severe disturbances in homeostasis. The need for evaporative thermolysis is increased due to the combination of endogenous and exogenous heat production. Despite a marked increase in cardiac output, muscles and skin must compete for sufficient blood flow. In addition progressive dehydration can impair the ability of the cardiocirculatory to adjust adequately. The most serious risk associated with exercise in a hot environment is heat stroke. Although deleterious effects of dehydration occur only if large amounts of water and electrolytes are lost without being replaced, even moderate fluid depletion can reduce both physical and cognitive performance. Another mechanism by which heat exposure directly affects performance involves core temperature elevation which can induce profound changes in muscular activity and energy consumption, thereby accelerating exhaustion. Prevention of deleterious effects on health and performance requires an effective rehydration strategy to maintain body fluid balance. This strategy must optimize all three potentially limiting factors for fluid replacement, i.e., fluid intake, gastric emptying, and intestinal absorption. Practical guidelines are given to answer the questions of when, what and how much to drink.

Osteoarthritis (OA) is the most common joint disease and OA of the knee, in particular, is the major cause of chronic disability among people > 65 years. Because nonsteroidal anti-inflammatory drugs (NSAIDs) improve symptoms in many patients with OA, it is widely considered that OA pain is due to synovial inflammation. However, OA pain may arise also from subchondral bone, the joint capsule ligaments, tendons, entheses and periarticular muscle spasm. In many patients, the relief of OA pain and overall satisfaction with therapy may be as great with paracetamol (acetaminophen [APAP]) as with an NSAID. Cyclo-oxygenase (COX)-1-sparing NSAIDs (coxibs) are no more effective in the treatment of OA pain than non-selective NSAIDs and, although they may significantly decrease the risk of serious adverse effects related to gastrointestinal ulcers (GI) and ulcer complications, their gastroprotective effect may be reduced by concomitant administration of low-dose aspirin. Also, they may increase the risk of myocardial infarction in predisposed individuals. Because coxibs do not inhibit platelet aggregation, if prophylaxis against thromboembolic disease is required in patients being treated with a selective COX-2 inhibitor, low-dose aspirin should be used in conjunction with the coxib. Furthermore, nonselective NSAIDs and coxibs may have adverse effects on the kidney, fracture healing and salt and water homeostasis. This paper discusses the relative positioning of APAP, NSAIDs and coxibs in the management of OA, on the basis of considerations of tolerability, efficacy and costs.

Assessment of haemodynamic effects of 250 ml hypertonic saline 7.5% (HS) perfusion in critically ill patients with severe sepsis or septic shock.Observational study.Twelve mechanically ventilated patients with severe sepsis or septic shock requiring a pulmonary artery catheter and volume loading.Two hundred and fifty millilitres HS were given over 15 min. Were measured: heart rate (HR), mean arterial pressure (MAP) and pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), cardiac index (CI), indexed systemic vascular resistance (ISVR), indexed pulmonary vascular resistance (IPVR), plasma sodium, chloride, protein and haemoglobin concentrations and arterial blood lactate. Studied parameters were assessed at baseline (T(0)) and 5 (T(0)) and 105 min (T(120)) after the end of HS infusion.MAP, HR and RAP were not altered. HS increased PAPM (25 +/- 5-30 +/- 6 mmHg), PCWP (13 +/- 3-18 +/- 4 mmHg) and CI (3.5 +/- 1.2-4.6 +/- 1.1 l/min per m(2)) at T(20) (P0.05). ISVR and IPVR were decreased at T(20). Protein and haemoglobin were decreased at T(20). Sodium and chloride were increased at T(20) (from 136 +/- 4 to 147 +/- 4 and from 110 +/- 6 to 123 +/- 6 mmol/l, respectively, P0.01) and T(120).In patients with severe sepsis or septic shock, 250 ml HS transiently (120 min) increases CI and PCWP and induces an increase in sodium and chloride concentrations.

Human arterial hypertension is a complex trait, partly determined by genetic factors. From the analysis of familial studies, it has been estimated that approximately 30% of the blood pressure variance within a population was of genetic origin. Three main types of human studies have been undertaken to try to identify susceptibility genes to hypertension. The first one corresponds to the systematic analysis of the so-called candidate genes, i.e. genes encoding proteins, enzymes, receptors, which are known to belong to pathways controlling blood pressure. Up to now, the most interesting results have been obtained on genes encoding the renin angiotensin system, the a adducin, the G protein subunit beta 3, and adrenergic receptors. The genome wide scan approach corresponds to a systematic analysis of evenly spaced markers throughout the genome in sibling pairs or in more complex families. This second strategy has shown that there was not a single locus that was regularly found by several studies, but rather several possible loci which most often have not been replicated from one study to another one. Among those, the long arm of the human chromosome 17 (17q12-q21) is in synteny with a blood pressure locus found in spontaneously hypertensive rats. The third approach, up to now the most successful, corresponds to the identification of major genes involved in rare Mendelian forms of hypertension. For example, genes responsible for Liddle syndrome, glucocorticoid remediable aldosteronism, apparent mineralocorticoid excess have been characterized and have demonstrated the importance of sodium and water homeostasis in blood pressure control.

Diarrhea occurs in 2 to 70% of tube-fed patients, depending on their disease (with an increased risk in critically ill patients) and on the definition of diarrhea used.Diarrhea increases morbidity, particularly since the nutritional goals are harder to reach.Relevant causes today are related to the nutrition (irregular and too high output, jejunal site, low sodium and fiber contents), to the patient (malnutrition, stress, underlying diseases), and predominantly to concomitant treatments (antibiotics, with an increased risk of Clostridium difficile infection, laxative-containing drugs).Treatment of the cause is only valid when it has been identified. Symptomatic treatment principally combines compensation for water and electrolyte loss and drugs that slow down the transit. Prevention associates the regulation of the administration rate and the fight against Clostridium difficile. Restoration of the colonic microflora appears the key to success and some prebiotics and probiotics have demonstrated preventive effects. Further research in this direction is warranted.

There are five types of oedema: vasogenic, cytotoxic, interstitial, hyperemic and osmotic. The differences lie on the type and localization of the oedema, the state of the blood-brain barrier (BBB) and the pathological context. Under physiological conditions, the osmolarity of extra cellular fluids (ECFs) is equal on both sides of the BBB. However, the pathophysiological variations of circulating osmolarity (including acute hyponatremia and hypernatremia) do not affect, at the same time, the osmolarity of cerebral ECFs. This situation generates an osmotic gradient on either side of the BBB. The latter, if intact, behaves like a semi-permeable membrane allowing water transport according to the osmotic laws. Depending on its direction, water movement could induce cerebral liquid inflation (i.e. osmotic oedema) or cerebral dehydration. In case of osmotic insult, cerebral cell modify their active osmotic molecular contents in order to limit volume variation. There are two types of osmoactive molecules, organic (i.e. ideogenic osmoles: amino acids, polyols and trimethylamines) and non organic (i.e. electrolytes). In the event of plasma hypotonicity, cerebral cells expel active osmotic molecules to reduce the osmotic gradient and water movement thereby reducing edema. The opposite reaction is observed in the case of hypertonic insult. This cerebral osmoregulation becomes more effective, the slower the osmotic disorder. It explains, for example, why patients with chronic and severe hyponatremia could be asymptomatic. Severe osmotic oedema is observed mainly in water intoxication, acute hyponatremia or too rapid reduction of hyperosmolarity. However, osmotic oedema is not limited to extreme clinical circumstances. Hyponatremia, even modest, could modify cerebral blood volume and impair osmoregulation. Generally these minor modifications do not affect normal brain tissue. In the presence of cerebral lesion, osmoregulation operates only in areas of preserved BBB. The pathological zones are therefore exposed to osmotic oedema (even in cases of moderate hyponatremia) with deterioration of both clinical status and intracranial pressure. This authentic phenomenon could be insidious and difficult to differentiate from osmotic central oedema. Hyponatremia constitutes an authentic secondary cerebral insult of systemic origin, an entity clearly identified by experimental studies to justify the choice between crystalloids and colloids in neuroanaesthesia and neurointensive care. These studies have revealed an increase in water content in normal brain tissues after administration of hypotonic solutions. The increase in plasma osmolarity as a treatment modality using mannitol or hypertonic saline is based on the same concepts. The most remote indication is the occurrence of a reactive mydriasis in the context of trauma for example. More recently, therapeutic hypernatremia has been proposed to control intracranial hypertension.

Emphysematous pyelonephritis is defined as the presence of gas-producing bacteria in the kidney and in peri-nephretic areas. Even if it is rare, the mortality rate of this affection is between 50% and 90%. The E. coli is responsible in 60% of the cases. We report a case of a 50 years old male patient, with under diagnosed diabetics, how is admitted with pains in the left flank, fever, troubled urine, hematuria and worsening of general state. The diagnostic of emphysematous pyelonephritis was confirmed by CT Scan. In spite of adapted antibiotherapy to the renal function, insulinotherapy and correction of hydro-electrolytic troubles, the patient died with septic shock associated to digestive bleeding. Based on this case and a review of the literature, the authors describe the different features of this disease. Only an urgent nephrectomy after a short reanimation can improve the prognostic.

Mannitol 20% (M) and NaCl 7.5% (H) are hypertonic solutions used in-patient in hypovolaemic shock and in case of increased ICP. To our knowledge no study in humans compared them in an equiosmolar load. The objectives of this study were to compare the pharmacokinetics of both solutions in an equiosmolar load with an isotonic solution (NaCl 0.9% (C)) in terms of osmolarity, electrolytes and haemodynamic parameters over time.Prospective, randomized, controlled study.Thirty ASA I and II patients undergoing non haemorrhagic surgery under general anesthesia.Three groups were studied (groups M, H and C), each receiving an equiosmolar load (4.95 mOsm kg(-1)) of solutions of mannitol 20%, saline 7.5% and saline 0.9% over ten minutes. Vital parameters (non invasive blood pressure, heart rate, oesophageal temperature) were monitored and blood samples (hemoglobin, hematocrit, K(+), Na(+), Cl(-), urea, creatinine, glucose, mannitolemia, osmolarity) were assessed preoperatively and intraoperatively at times 0, 3, 5, 10, 15, 30, 45, 60, 90, 120, 150 min of perfusion.In both hypertonic groups, osmolarity was maximal at the end of infusion (group M: 329 +/- 7 mOsm l(-1); group H: 321 +/- 11 mOsm l(-1)); at the same time, Na(+) value was lowest in group M: 129 +/- 3 mmol l(-1) and highest in group H: 151 +/- 5 mmol l(-1), P0.001) with normalisation at 60 min. These results were also statistically significant when compared to the isotonic group (group C: osmolarity: 296 +/- 3 mOsm l(-1), P0.001; Na(+): 140 +/- 2 mmol l(-1), P0.001). Plasma volume expansion was statistically significantly larger in-group C between 10 and 15 min compared to both hypertonic groups (haematocrit: group C: 35 +/- 4%, group M: 39 +/- 5%; group H: 41 +/- 3%, P0.004). Haemodynamic parameters were similar in the 3 groups with however a trend towards lowers HR in the mannitol group, particularly at T10. Temperature was lower in the control group because of the volume infused. Cl(-) was higher in the H group.A single infusion of 4.95 mOsm kg(-1) of mannitol 20% or NaCl 7.5% induces a similar osmolar variation over time with a maximal effect after 10 min.

Severely burned patients are at high risk for developing respiratory failure at any time during their treatment. The lung of a thermally injured patient may sustain many injuries such as smoke inhalation, physical forces, inflammation and infection. The knowledge of the mechanisms of burn injury, physical exam findings, laboratory studies, relevant radiologic examinations, and fiberoptic bronchoscopy allow an early and accurate diagnosis of pulmonary damage. The treatment consists of oxygenation, mechanical ventilation, surgical treatment of burn wounds and trauma, and possible therapy for poisoning. The respiratory injuries are one of the main factors responsible for high mortality in burned patients. Better understanding of the pathophysiology and inflammatory response will lead to future therapeutic advances.

The treatment of diarrhoea relies on the maintenance or restoration of hydration with maintenance of an adequate nutritional intake. Racecadotril has been shown to reduce the stools output during acute diarrhoea. The present work was aimed at measuring the number of emergency department visits for acute diarrhoea either the children received racecadotril or not.Racecadotril and rehydration were compared with rehydration alone in children aged three months to three years who had acute diarrhoea and were evaluated in the emergency department (ED). The primary end point was the number of medical exams during the week after starting treatment. Secondary end points were the number of stools during the first 48 hours, the duration of the diarrhoea and the weight on day 7.One hundred and sixty-six children were alternatively randomized to the treated and the control groups. There was no difference for age, degree of dehydration and length of illness before the first visit between the groups. Whatever type of rehydration (oral or i.v.), the treated group had a significant lower number of stools (p0.001) and a faster recovery (p10(-9)). The children receiving racecadotril needed less additional ED visits for the same episode (p0.05). There was no difference for the weight-gain on day 7.This study demonstrates the efficacy of racecadotril as adjuvant therapy to oral and i.v. rehydration in the treatment of acute diarrhoea and a fewer emergency department second visit before recovery.

Human body weight is about 70% water; 55% of the water are in cells and 45% in extracellular compartments, mainly body fluids. Each compartment has its own osmoregulatory system. The mechanisms of intracellular osmoregulation likely appeared with the cell itself, i.e. in primitive prokaryotes, some 3.8 billions years ago. Osmotic stress responses observed in present-day bacteria, yeast, plant and animals cells in culture are very similar. Variations in the cell volume entail an extension or retraction of plasma membrane that activates mechanically-gated ion channels or mechanoreceptors. Some of them have been cloned from E. coli, the nematode C. elegans, the drosophila. Osmotic stress determines an intracellular cascade of transactivations, the last transcription factor binding to a Tonicity response element (TonE) of osmoprotective genes. These genes encode enzymes synthesizing compatible osmolytes that reequilibrate the osmotic pressure. Volume and osmolality of the biological fluids (le milieu intérieur) are regulated by neuroendocrine reflexes involving an afferent neural limb from baro- and osmo-receptors to hypothalamus and an efferent endocrine limb from neurosecretory cells to target cells, the hydroosmotic cells localized in osmoregulatory organs. Afferent signals trigger the biosynthesis and the processing of neurohypophyseal preprohormones in magnocellular neurons of the supraoptic and paraventricular nuclei of hypothalamus. Vasopressin in mammais and vasotocin in other vertebrates, endowed with antidiuretic and antinatriuretic properties, act on hydroosmotic cells localized in the nephron collecting duct. A specific vasopressin receptor, the V2 type receptor, located in the basolateral membrane of the principal cells, is coupled with an heterotridimeric protein Gs that activates adenylate cyclase. The cAMP product, in turn, stimulates the protein kinase A (PKA). The latter mobilizes 5 effectors located in the apical membrane: 1) the water channel aquaporin 2; 2) the urea transporter UT1; 3) the amiloride-sensitive sodium channel ENaC; 4) the inward-rectifying potassium channel ROM-K1; 5) the chloride channel CFTR. Modulation of each effector is ensured by an A kinase anchoring protein (AKAP). The effectors are transported from cytosol to apical membrane through transport vesicles equipped with membrane fusion proteins (such as VAMP2) that recognize specific apical membrane proteins (such as syntaxins). Water flows into principal cells from collecting duct lumen through AQP2 and flows out to interstitium through AQP3 and AQP4 and finally reachs blood circulation through AQP1 capillaries. Vasopressin orchestrates the live effectors so as to keep water and solutes reabsorptions in balance with volaemia and osmolality set points.

Vasopressin, like all the other neuro-hormonal systems, is activated in patients with cardiac insufficiency. Vasopressin attaches itself to two distinct specific receptors. It is through the intermediary of the renal V2 receptor, controlling the reabsorption of water by the collecting duct, that vasopressin finely regulates the blood osmolarity. The ubiquitous V1a receptor is essentially responsible for the vasoconstrictor effect of the hormone. Some specific antagonists for these two receptors have now been evaluated in various pathologies such as SIADH, cirrhosis or cardiac insufficiency. In this situation the mixed antagonists, anti-V1a-V2, seem more appropriate than the specific V1a or V2 receptor antagonists. The results of the first human studies are encouraging. The mixed antagonists reduce the pulmonary capillary pressure and increase diuresis and clearance of free water. But further studies are necessary to confirm these results and to demonstrate a reduction in morbidity and mortality before adding this class of medication to the therapeutic arsenal for our patients with cardiac insufficiency.

Adult growth hormone deficiency is characterized by changes in body composition: increase in total fat, decrease in lean mass and osteopenia, with a fall in Bone Mineral Content (BMC) and in Bone Mineral density (BMD) leading to a rise in risk of fracture. We have analyzed the changes in body composition in 21 adults treated from 9 to 78 months, by dual X-RAY absorptiometry (DEXA). We've demonstrated a gain in bone mass and density, particularly of axial skeleton; a latence of minimum 12 months has been necessary to objective these changes. The balance of fat and lean mass has been poorly modified by treatment except for the lean mass of the trunk, which is significantly increased. We think that the usual doses of rGH, based on IGF-1 level, are perhaps underestimated.