Hydroelectrolytic Balance Research Articles

Management of alcohol withdrawal syndrome

The management of alcohol withdrawal syndrome is rather complex because of the frequently associated comorbidities which need to be taken into account, and also because this syndrome is characterized by an unpredictable evolution. International guidelines recommend pharmacological treatment not only as a solution to alleviate the withdrawal syndrome, but also to prevent the further development of medical conditions with a high mortality rate. An accurate administration of the pharmacological treatment is actually not enough. The careful monitoring of vital functions, as well as evaluating both the prognostic and the severity using scales, markers or functional indicators, further contribute to treatment effectiveness. As for the treatment per se, benzodiazepine anxiolytics along with restoring the hydro-electrolytic balance represent the first choice in dealing with alcohol withdrawal syndrome. Other drug classes which have proven their efficacy are anticonvulsants, adrenergic, anesthetic or antipsychotic drugs.

Cardiovascular autonomic dysfunction in patients with idiopathic diabetes insipidus.

Central diabetes insipidus (DI) is a rare disease characterized by the excretion of excessive volumes of dilute urine due to reduced levels of the antidiuretic hormone arginine vasopressin (AVP), caused by an acquired or genetic defect in the neurohypophysis. The aim of this study was to identify any autonomic dysfunction (AD) in patients with DI as a possible cofactor responsible for their reportedly higher mortality. The study involved 12 patients (6 females) with central idiopathic DI and a well-controlled electrolyte balance, and 12 controls matched for age, sex and cardiovascular risk factors, who were assessed using the tilt, lying-to-standing, hand grip, deep breath, Valsalva maneuver and Stroop tests. The tilt test showed a significantly more pronounced decrease in both systolic (- 20.67 ± 18 vs. - 1.92 ± 6.99mmHg, p = 0.0009) and diastolic blood pressure (- 10.5 ± 14.29 vs. - 1.5 ± 5mmHg, p = 0.012) in patients than in controls. Three patients with DI had to suspend the test due to the onset of syncope. The lying-to-standing test also revealed a marked reduction in blood pressure in patients with DI (1.05 ± 0.13 vs. 1.53 ± 0.14, p = 0.0001). Similar results emerged for the Valsalva maneuver (Valsalva ratio, 1.24 ± 0.19 vs. 1.79 ± 0.11, p < 0.0001) and deep breath test (1.08 ± 0.11 vs. 1.33 ± 0.08, p < 0.0001). All the principal autonomic tests performed in the study were concordant in indicating that patients with central DI have an impaired autonomic nervous system function despite a normal hydroelectrolytic balance under desmopressin therapy. This impairment may reflect damage to the autonomic system per se and/or the absence of any vasoactive effect of AVP on vascular smooth muscle. In our opinion, patients with central DI should be educated on how to prevent orthostatic hypotension, and pharmacological treatment should be considered for patients with a more marked impairment.

Hypertonic NaCl versus osmotic stimuli: distinct OVLT neurones can sense the difference to control sympathetic outflow and blood pressure.

Despite large fluctuations in salt and water intake, mammals are able to maintain electrolyte concentrations, particularly sodium (Na+) as the major determinant of osmolality of the extracellular fluid (ECF), within narrow physiological limits (∼300 mOsm kg−1). The two distinct sensory systems monitoring Na+ concentration and osmolality in the hypothalamic area of the brain are located outside the blood–brain barrier and are therefore known as circumventricular organs (CVOs). The osmosensitive neurones of CVOs are located in the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Direct projections from these areas to hypothalamic nuclei containing neurosecretory magnocellular neurones promote the release of water-conserving hormones such as arginine vasopressin (McKinley et al. 2001). Interestingly, these neurones also project to smaller parvocellular neurones located within other brain structures, such as the paraventricular nucleus of the hypothalamus (PVN) that modulate sympathetic nerve activity (SNA), an important mechanism in blood pressure (BP) homeostasis. The distinct physiological responses to maintain fluid balance triggered by infusion of hypertonic sodium chloride (NaCl) and equi-osmolar solutions have been debated for decades. McKinley and colleagues (1978) have shown that a peripheral osmoreceptor mechanism was most likely to be responsible for the thirst and antidiuresis induced by intracarotid infusion of hypertonic NaCl or sucrose in sheep. However, they also found support for a periventricular Na+ receptor mechanism because of differential drinking responses to intracerebroventricular (i.c.v.) administration of hypertonic NaCl or sucrose. The SFO seems to be the primary locus of NaCl sensing for the control of salt-intake behaviour at the central level, identified as a sensory mechanism that relies on activation of a Na+ channel (Nax); it is not osmosensing (Hyiama et al. 2004). The SFO is also involved in mediating the central Na+-induced pressor response, since administration of NaCl-rich artificial cerebrospinal fluid (aCSF) into the SFO caused an increase in BP, which was blunted by an angiotensin II type 1 (AT1) receptor antagonist at the same site. However, equi-osmotic infusion of manitol did not change BP, indicating that the pressor response is Na+ specific and not due to osmolality or volume effects (Tiruneh et al. 2013). Not only SFO, but also OVLT neurones are capable of detecting extracellular NaCl concentration and altering the sympathetic nerve discharge in order increase BP (Kinsman et al. 2017b). However, to date, no study has been able to show whether distinct cellular processes of osmosensitive neurones can differentiate between hyperosmolality versus hypertonic NaCl stimulus to selectively control SNA and BP. In this issue of The Journal of Physiology, Kinsman and co-workers (2017a) addressed this important issue by performing an elegant in vivo neurophysiological study. They determined how subsets of OVLT neurones respond differentially to hypertonic NaCl versus osmolality and subsequently regulate the sympathetic nervous system. More precisely, they showed that local injection of hypertonic saline into the OVLT produced an increase in SNA and BP, whereas an equi-osmotic stimulus of mannitol/sorbitol solutions had no effect. Moreover, these authors combined in vitro whole-cell recordings to demonstrate that stimulation with hypertonic saline caused the discharge frequency of OVLT neurones to increase, unlike stimulation with the equi-osmotic mannitol solution. These findings by Kinsman and colleagues (2017a) open several interesting perspectives for further investigation regarding the functional significance of distinct cellular responses of Na+ and osmosensitive OVLT neurones: (i) What are the physiological mechanisms, phenotype and neurotransmitters released by the functionally distinct OVLT neurones? (ii) How do these differences translate to hypertonic NaCl and osmotically driven sympathetic responses and BP control? (iii) Do salt-sensitive rats (e.g. Dahl-Salt) show alterations in OVLT neuronal populations that control hydroelectrolytic balance, sympathetic hyperactivity and hypertension in response to high salt diet? (iv) It would be interesting to determine the contribution of the SFO compared to the OVLT to the sympathetic responses to hypertonic saline and osmolality challenges. Understanding the characteristics of the CVO neurones relating to control of body fluid and cardiovascular homeostasis in response to distinct osmotic stimuli will require a range of techniques from anatomical, molecular, biochemical and pharmaco/opto-genetic tools, and this paper by Kinsman and co-workers (2017a) is a great kick-off in elucidating the complex hierarchy and mechanisms of the osmoregulatory signalling network at the CNS level. None declared. V.R.A. is supported by The National Council for Scientific and Technological Development (CNPq) Research Fellow, and The State of Sao Paulo Research Funding Agency (FAPESP) no. 2016-21991-3.

SEVERE INTESTINAL FAILURE IN A CHAGAS’S DISEASE PATIENT AFTER TOTAL COLECTOMY PLUS PARTIAL ILEECTOMY

Introduction: To report the clinical course of a Chagas’s disease patient with severe intestinal failure after resection of the total colon and terminal ileum.Case Report: The patient underwent rectosigmoidectomy (of the sigmoid volvulus, December 2009) and total colectomy plus partial ileectomy (May 2011). Patient evolved with multiple hospitalizations caused by severe diarrhea (up to 23 stools/day), hydroelectrolyte disturbance and acute renal failure, severe protein-energy malnutrition [loss of 34.9% of usual body weight (uBW)], and multiple episodes of sepsis. Were prescribed parenteral nutrition solutions exclusively or concurrently with very small volumes (e.g., 40ml/day) of semi-elemental diet with low fat and high protein. After several weeks predetermined amounts of carbohydrate-rich foods (potatoes, rice, pasta, cassava), vegetables (chayote, carrots), low-fat meat, cream crackers, coconut water and fruit (watermelon, melon, banana) were progressively introduced. After 36 months, the patient was metabolically stable (BW=67.2 kg, weight recovery of 23.6 kg), with hydroelectrolytic balance. Due to the recovery of the functional capacity, the patient was advised to return to his work activities. Conclusions: Chagas’s disease patient submitted to intestinal resection may have severe intestinal failure and protein-energy malnutrition. Specialized nutritional therapy and clinical and laboratory monitoring by a multidisciplinary team, can contribute to better prognostic.

Physical exercise on serum electrolytes and acid base balance in Mangalarga Marchador horses submitted to cavalcade of 4, 8 and 20km

ABSTRACT: Acid-base and electrolyte disorders have been described in horses associated during and after exercise. The aim of the present study was to evaluate the effect of cavalcade competition on the acid-base and hydroelectrolytic balance in Mangalarga Marchador horses. For this purpose, 15 geldings, 6.2 ± 1.2 years old and clinically healthy, were distributed into three groups of five animals each. Horses were trained to take part in cavalcade competitions. Animals were submitted to cavalcade along 4km (G4), 8km (G8), and 20km (G20) at mean speeds of 15km h-1, 12km h-1, and 12km h-1, respectively. From each horse, venous blood samples were collected before exercise (T0) and immediately after (T1) cavalcade. Bicarbonate ion (HCO3-), pH, partial pressure of carbon dioxide (pCO2), partial pressure of oxygen (pO2), base excess (BE), hematocrit (Hct), sodium (Na+), potassium (K+), chloride (Cl-) and lactate were determined. The variables pH, pO2 and pCO2 were corrected in function of rectal temperature of each animal. Blood samples were analyzed for acid-base balance, as well as biochemical and electrolyte parameters using an i-STAT analyzer. Significant (P&lt;0.05) increase in Hct, Na+, pH, HCO3 - and BE were observed after cavalcade in G20 group. Decrease (P&lt;0.05) in K+ and Cl- were also observed in G20 animals after cavalcade (T1). Changes in the acid-base balance and hydroelectrolytic profile of the Mangalarga Marchador after cavalcade of 20km resulted in hypochloremic metabolic alkalosis. The 20km cavalcade induced significant hydroelectrolytic and acid-base imbalances in Mangalarga Marchador horses.

Hypothalamic Vasopressinergic Projections Innervate Central Amygdala GABAergic Neurons: Implications for Anxiety and Stress Coping.

The arginine-vasopressin (AVP)-containing hypothalamic magnocellular neurosecretory neurons (VPMNNs) are known for their role in hydro-electrolytic balance control via their projections to the neurohypophysis. Recently, projections from these same neurons to hippocampus, habenula and other brain regions in which vasopressin infusion modulates contingent social and emotionally-affected behaviors, have been reported. Here, we present evidence that VPMNN collaterals also project to the amygdaloid complex, and establish synaptic connections with neurons in central amygdala (CeA). The density of AVP innervation in amygdala was substantially increased in adult rats that had experienced neonatal maternal separation (MS), consistent with our previous observations that MS enhances VPMNN number in the paraventricular (PVN) and supraoptic (SON) nuclei of the hypothalamus. In the CeA, V1a AVP receptor mRNA was only observed in GABAergic neurons, demonstrated by complete co-localization of V1a transcripts in neurons expressing Gad1 and Gad2 transcripts in CeA using the RNAscope method. V1b and V2 receptor mRNAs were not detected, using the same method. Water-deprivation (WD) for 24 h, which increased the metabolic activity of VPMNNs, also increased anxiety-like behavior measured using the elevated plus maze (EPM) test, and this effect was mimicked by bilateral microinfusion of AVP into the CeA. Anxious behavior induced by either WD or AVP infusion was reversed by CeA infusion of V1a antagonist. VPMNNs are thus a newly discovered source of CeA inhibitory circuit modulation, through which both early-life and adult stress coping signals are conveyed from the hypothalamus to the amygdala.

Hydroelectrolytic balance of Brazilian jiu-jitsu athletes during a simulated competition

To analyze the hydroelectrolytic balance of Brazilian jiu-jitsu athletes during a simulated competition. Eight athletes were analyzed in simulated competition (four matches of 10 min). Blood lactate and rating of perceived exertion (6–20 scale) were used to infer the intensity of the matches. Blood samples were taken to determine the serum levels of osmolality, total protein and some electrolytes (chlorides, sodium, potassium, calcium, magnesium, phosphorus and iron). The lactate concentration changed during the simulated competition (F 7.49 = 35.5; P < 0.001; η 2 = 0.85), with an increase post-match compared to the pre-match in matches 1, 2 and 4, but not for match 3. For rating of perceived exertion, no changes were found during the competition (F 3.21 = 9.4; P = 0.440; η 2 = 0.12). The matches did not change the osmolality, chlorides, sodium, potassium, magnesium and iron values. For total protein, a difference was observed between the time-points (F 2.8; 19.6 = 4.6; P = 0.015; η 2 = 0.40), with lower concentrations in pre-match 2 than pre-match 1, post-matches 2 and 3. The calcium concentration was also affected by the simulated competition (F 7.49 = 4.0; P = 0.002; η 2 = 0.37), with values lower in pre-match 2 than post-matches 1 and 2. The phosphorus serum was changed by matches (F 3.1; 21.7 = 18.6; P < 0.001; η 2 = 0.73), with post-match 1 values higher than the pre-matches 1, 2, 3 and 4 and post-match 3. The pre-match 4 values were lower than post-matches 2 and 4. Although there were some changes during simulated competition, important alterations in the hydroelectrolytic balance did not occur.

Exocrine Pancreatic Insufficiency: A Literature Review

Exocrine pancreatic insufficiency (EPI) is a clinical entity that manifests as a mal absorption syndrome. Its relationship with multiple worldwide-highly prevalent pancreatic and extra pancreatic affections constitutes a major health problem due to high morbidity and mortality rates. The underlying disease requires an exhaustive assessment to identify possible nutritional deficiencies so as to prevent future complications. An impaired hydro electrolytic balance and low levels of serum nutritional markers indicate or predict EPI in high risk subjects. Unfortunately, pancreatic exocrine function test available so far do not diagnose early stages of the disease but they are quite effective in advanced EPI. Imaging studies are essential in the overall management of EPI as they may provide information regarding the etiology and structural pancreatic modifications. ERCP, despite post-procedure complications, is considered the gold standard due to its diagnostic and therapeutic properties. Treatment is based on pancreatic enzyme replacement therapy (PERT) along with nutritional supplements intake and good control of the underlying disease.

The type-1 cannabinoid receptor modulates the hydroelectrolytic balance independently of the energy homeostasis during salt load

Hydroelectrolytic imbalances, such as saline load (SL), trigger behavioral and neuroendocrine responses, such as thirst, hypophagia, vasopressin (AVP) and oxytocin (OT) release and hypothalamus–pituitary–adrenal (HPA) axis activation. To investigate the participation of the type-1 cannabinoid receptor (CB1R) in these homeostatic mechanisms, male adult Wistar rats were subjected to SL (0.3M NaCl) for four days. SL induced not only increases in the water intake and plasma levels of AVP, OT and corticosterone, as previously described, but also increases in CB1R expression in the lamina terminalis, which integrates sensory afferents, as well as in the hypothalamus, the main integrative and effector area controlling hydroelectrolytic homeostasis. A more detailed analysis revealed that CB1R-positive terminals are in close apposition with not only axons but also dendrites and secretory granules of magnocellular neurons, particularly vasopressinergic cells. In satiated and euhydrated animals, the intracerebroventricular administration of the CB1R selective agonist ACEA (0.1μg/5μL) promoted hyperphagia, but this treatment did not reverse the hyperosmolality-induced hypophagia in the SL group. Furthermore, ACEA pretreatment potentiated water intake in the SL animals during rehydration as well as enhanced the corticosterone release and prevented the increase in AVP and OT secretion induced by SL. The same parameters were not changed by ACEA in the animals whose daily food intake was matched to that of the SL group (Pair-Fed). These data indicate that CB1Rs modulate the hydroelectrolytic balance independently of the food intake during sustained hyperosmolality and hypovolemia.

Neuroendocrine Regulation of Hydromineral Homeostasis.

Since the crucial evolutionary change from an aqueous to a terrestrial environment, all living organisms address the primordial task of equilibrating the ingestion/production of water and electrolytes (primarily sodium) with their excretion. In mammals, the final route for the excretion of these elements is mainly through the kidneys, which can eliminate concentrated or diluted urine according to the requirements. Despite their primary role in homeostasis, the kidneys are not able to recover water and solutes lost through other systems. Therefore, the selective stimulation or inhibition of motivational and locomotor behavior becomes essential to initiate the search and acquisition of water and/or sodium from the environment. Indeed, imbalances affecting the osmolality and volume of body fluids are dramatic challenges to the maintenance of hydromineral homeostasis. In addition to behavioral changes, which are integrated in the central nervous system, most of the systemic responses recruited to restore hydroelectrolytic balance are accomplished by coordinated actions of the cardiovascular, autonomic and endocrine systems, which determine the appropriate renal responses. The activation of sequential and redundant mechanisms (involving local and systemic factors) produces accurate and self-limited effector responses. From a physiological point of view, understanding the mechanisms underlying water and sodium balance is intriguing and of great interest for the biomedical sciences. Therefore, the present review will address the biophysical, evolutionary and historical perspectives concerning the integrative neuroendocrine control of hydromineral balance, focusing on the major neural and endocrine systems implicated in the control of water and sodium balance.

Effects of arginine vasopressin (AVP) deficiency on basal mean arterial blood pressure in the rat

The role of AVP controlling the mean arterial blood pressure (MBP) in basal conditions remains unclear. We described that neurointermediate pituitary lobectomy (NIL) in rats, induced an early but transient diabetes insipidus and low MBP (8 weeks after lobectomy). To elucidate the chronological effects of NIL, we evaluated the AVP serum levels, water intake and urine output (diabetes insipidus, DI), and MBP immediately (0 to 6 hours post NIL) and 3, 15, 45 and 90 days post NIL. The renin, angiotensin II and aldosterone system (RAAS) was assessed at 3 and 45 days post NIL. Values were compared with the respective SHAM operated groups. Results: NIL caused significant and permanent AVP serum level decrease (10.6 ± 0.8 vs 2.4 ± 0.16 pg/ml (SD), SHAM vs NIL), transient DI (15‐30 days of duration) and permanent decrease of the MBP in 70% of the NIL animals (106.8 ± 3.15 vs 73.8 ± 3.2 mmHg). Hypotension was apparent 20‐30 minutes after NIL. No significant differences in the RAAS were evident.ConclusionsWe propose that in non‐stressed animals, basal serum levels of AVP are required to maintain the hydro‐electrolytic balance and MBP. Further studies are needed to explain why some animals did not develop hypotension, and to determine how cardiovascular, renal and hormone adaptive mechanisms in the NIL group support their survival.Supported by UAA‐PIFF and CONACYT, México and the Jarislowsky and L. Carr‐Harris Foundations

Signaling pathways involved in renal oxidative injury: role of the vasoactive peptides and the renal dopaminergic system.

The physiological hydroelectrolytic balance and the redox steady state in the kidney are accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Angiotensin II, atrial natriuretic peptide and intrarenal dopamine play a pivotal role in this interactive network. The balance between endogenous antioxidant agents like the renal dopaminergic system and atrial natriuretic peptide, by one side, and the prooxidant effect of the renin angiotensin system, by the other side, contributes to ensuring the normal function of the kidney. Different pathological scenarios, as nephrotic syndrome and hypertension, where renal sodium excretion is altered, are associated with an impaired interaction between two natriuretic systems as the renal dopaminergic system and atrial natriuretic peptide that may be involved in the pathogenesis of renal diseases. The aim of this review is to update and comment the most recent evidences about the intracellular pathways involved in the relationship between endogenous antioxidant agents like the renal dopaminergic system and atrial natriuretic peptide and the prooxidant effect of the renin angiotensin system in the pathogenesis of renal inflammation.

The involvement of aldosterone on vascular insulin resistance: implications in obesity and type 2 diabetes.

Aldosterone, a mineralocorticoid hormone produced at the adrenal glands, controls corporal hydroelectrolytic balance and, consequently, has a key role in blood pressure adjustments. Aldosterone also has direct effects in many organs, including the vasculature, leading to many cellular events that influence proliferation, migration, inflammation, redox balance and apoptosis.Aldosterone effects depend on its binding to mineralocorticoid receptors (MR). Aldosterone binding to MR triggers two pathways, the genomic pathway and the non-genomic pathway. In the vasculature e.g., activation of the non-genomic pathway by aldosterone induces rapid effects that involve activation of kinases, phosphatases, transcriptional factors and NAD(P)H oxidases.Aldosterone also plays a crucial role on systemic and vascular insulin resistance, i.e. the inability of a tissue to respond to insulin. Insulin has a critical role on cell function and vascular insulin resistance is considered an early contributor to vascular damage. Accordingly, aldosterone impairs insulin receptor (IR) signaling by altering the phosphatidylinositol 3-kinase (PI3K)/nitric oxide (NO) pathway and by inducing oxidative stress and crosstalk between the IR and the insulin-like growth factor-1 receptor (IGF-1R).This mini-review focuses on the relationship between aldosterone and vascular insulin resistance. Evidence indicating MR antagonists as therapeutic tools to minimize vascular injury associated with obesity and diabetes type 2 is also discussed.

New components of the renin-angiotensin system: alamandine and the MAS-related G protein-coupled receptor D.

The renin-angiotensin system is an important component of the central and humoral mechanisms of blood pressure and hydro-electrolytic balance control. Angiotensin II is a key player of this system. Twenty-five years ago the first manuscripts describing the formation and actions of another peptide of the RAS, angiotensin-(1-7), were published. Since then several publications have shown that angiotensin-(1-7) is as pleiotropic as angiotensin II, influencing the functions of many organs and systems. The identification of the ACE homologue ACE2 and, a few years later, Mas, as a receptor for angiotensin-(1-7) contributed a great deal to establish this peptide as a key player of the RAS. Most of the actions of angiotensin-(1-7) are opposite to those described for angiotensin II. This has led to the concept of two arms of the RAS: one comprising ACE/AngII/AT1R and the other ACE2/Ang-(1-7)/Mas. More recently, we have described the identification of a novel component of the RAS, alamandine, which binds to the Mas-related G protein coupled receptor D. This peptide is formed by decarboxylation of the Asp residue of angiotensin-(1-7), leading to the formation of Ala as the N-terminal amino acid. Alternatively, it can be formed by hydrolysis of Ang A, by ACE2. Its effects include vasorelaxation, central effects similar to those produced by angiotensin-(1-7), blunting of isoproterenol-induced heart fibrosis, and anti-hypertensive action in SHR. The putative enzyme responsible for alamandine formation from angiotensin-(1-7) is under investigation. The identification of this novel component of the RAS opens new venues for understanding its physiological role and opens new putative therapeutic possibilities for treating cardiovascular diseases.

Protocolo diagnóstico de la insuficiencia renal en el paciente oncológico

Acute renal failure (ARF) consists in a deterioration of the renal function produced suddenly (hoursdays-weeks). It consists in a decrease of glomerular filtration rate (GFR). The decrease in GFR leads to failure of nitrogenous waste products excretion with the consequent elevation of urea and creatinine and impossibility to maintain hydroelectrolytic balance. According to the etiology of ARF, its is considered prerenal, parenchymatous or obstructive origin. Management of ARF, independently of whether the patient is a cancer patient or not, includes treating the cause that has lead to the failure and medical treatment to avoid the worsening of the renal function while the cause is being resolved. On the other hand, there are more typical pictures of the oncology patient. These are tumor lysis syndrome and hepatorenal syndrome. These are also reviewed in this protocol.

Isolated aldosterone deficiency in two infants: Mistakes and dilemmas in the diagnosis and treatment of a rare disease

In this article, we describe the clinical picture and follow-up of two children diagnosed as suffering from pseudohypoaldosteronism when they were infants, and it was later recognized as isolated aldosterone deficiency in both. We illustrate the clinical differences between the two patients in terms of hydroelectrolytic balance, laboratory data and growth. In fact, while the growth and hematological parameters of the electrolytes and acid-base balance were normal in the first patient, and also without treatment with fludrocortisone thanks to very high renin activity, in the second patient, this treatment was vitally necessary to maintain normal growth and biochemical data. Despite the absence of a molecular analysis which could have confirmed this diagnosis, we believe that the description of the clinical evolution of these two cases from the moment of the incorrect diagnosis until the correct diagnosis and action taken, could be useful to highlight the extreme clinical variability of this rare disease.

Physiological Demands and Changes Resulting from Effort in Low Handicap Polo Horses

In order to understand the physiological demands and possible changes resulting from effort in horses and determine the type and intensity of exercise performed in equestrian polo of low handicap, we analyzed the negative logarithm of the activity of hydrogen ions (pH), carbon dioxide partial pressure (pCO2), oxygen partial pressure (pO2), the concentration of plasma bicarbonate ions (HCO3-) and serum concentrations of Na+, Cl- and K+ of seven healthy horses after a polo match of low handicap. Variables pCO2, pO2 and HCO3- were the only parameters that were significantly different before and after the match, and there were no significant hydroelectrolytic changes. It was possible to classify the low handicap polo as an exercise of short duration and varying intensity, considering the lack of change in the hydroelectrolytic balance. The exercise to which the animals were subjected is compatible with their athletic fitness.

Hydroelectrolytic Balance and Cerebral Relaxation with Hypertonic Isoncotic Saline versus Mannitol (20%) During Elective Neuroanesthesia

Cerebral relaxation during intracranial surgery is necessary, and hiperosmolar therapy is one of the measures used to this end. Frequently, neurosurgical patients have sodium imbalances. The objective of the present study was to quantify and determine cerebral relaxation and duration of hydroelectrolytic changes secondary to the use of mannitol versus hypertonic isoncotic solution (HIS) during neurosurgery. Cerebral relaxation and hydroelectrolytic changes were evaluated in 29 adult patients before de beginning of infusion, and 30 and 120 minutes after the infusion of equiosmolar loads of approximately 20% mannitol (250 mL) or HIS (120 mL). The volume of intravenous fluids infused and diuresis were recorded. A p < 0.05 was considered significant. A statistically significant difference in cerebral relaxation between both groups was not observed. Although several changes in electrolyte levels and acid-base balance with mannitol or HIS reached statistical significance only the reduction in plasma sodium 30 minutes after infusion of mannitol, mean of 6.42 ± 0.40 mEq.L(-1), and the increase in chloride, mean of 5.41 ± 0.96 mEq.L(-1) and 5.45 ± 1.45 mEq.L(-1) 30 and 120 minutes after infusion of HIS, caused a transitory dislocation of serum ion levels from normal range. The mannitol (20%) group had a significantly greater diuresis at both times studied compared with HIS group. A single dose of hypertonic isoncotic saline solution [7.2% NaCl/6% HES (200/0.5)] and mannitol (20%) with equivalent osmolar loads were effective and safe in producing cerebral relaxation during elective neurosurgical procedures under general anesthesia.

Aldosterone Postnatally, but not at Birth, Is Required for Optimal Induction of Renal Mineralocorticoid Receptor Expression and Sodium Reabsorption

Sodium wasting during the neonatal period is the consequence of a physiological aldosterone resistance, related to a low renal mineralocorticoid receptor (MR) expression at birth, both in humans and mice. To investigate whether aldosterone is involved in the neonatal regulation of MR expression, we compared aldosterone and corticosterone levels and renal MR expression by quantitative real-time PCR, between aldosterone synthase (AS) knockout, heterozygous, and wild type (WT) mice, at birth and postnatal d 8. Analysis of MR transcripts showed a similar expression profile in all genotypes, demonstrating that the lack of aldosterone does not modify either the low renal MR expression at birth or its postnatal induction. However, mRNA levels of the α-subunit of the epithelial sodium channel, a MR target gene, were significantly higher in WT compared with AS knockout mice, both at birth and postnatal d 8, despite high corticosterone levels in AS knockout mice, indicating that aldosterone is required for optimal renal induction of the epithelial sodium channel. Using organotypic cultures of newborn WT kidneys, we confirmed that aldosterone does not regulate MR expression at birth, but is instead capable of increasing MR expression in mature kidneys, unlike dexamethasone. In sum, we demonstrate both in vivo and in vitro, that, whereas aldosterone has no significant impact on renal MR expression at birth, it is crucial for optimal MR regulation in postnatal kidneys and for appropriate hydroelectrolytic balance. Understanding of MR-regulatory mechanisms could therefore lead to new therapeutic strategies for the management of sodium loss in preterms and neonates.

Etiopathology of chronic tubular, glomerular and renovascular nephropathies: Clinical implications

Chronic kidney disease (CKD) comprises a group of pathologies in which the renal excretory function is chronically compromised. Most, but not all, forms of CKD are progressive and irreversible, pathological syndromes that start silently (i.e. no functional alterations are evident), continue through renal dysfunction and ends up in renal failure. At this point, kidney transplant or dialysis (renal replacement therapy, RRT) becomes necessary to prevent death derived from the inability of the kidneys to cleanse the blood and achieve hydroelectrolytic balance. Worldwide, nearly 1.5 million people need RRT, and the incidence of CKD has increased significantly over the last decades. Diabetes and hypertension are among the leading causes of end stage renal disease, although autoimmunity, renal atherosclerosis, certain infections, drugs and toxins, obstruction of the urinary tract, genetic alterations, and other insults may initiate the disease by damaging the glomerular, tubular, vascular or interstitial compartments of the kidneys. In all cases, CKD eventually compromises all these structures and gives rise to a similar phenotype regardless of etiology. This review describes with an integrative approach the pathophysiological process of tubulointerstitial, glomerular and renovascular diseases, and makes emphasis on the key cellular and molecular events involved. It further analyses the key mechanisms leading to a merging phenotype and pathophysiological scenario as etiologically distinct diseases progress. Finally clinical implications and future experimental and therapeutic perspectives are discussed.