1,721,045 research outputs found
Etiology, Clinical Approach, and Therapeutic Consequences of Hyponatremia
No full textA perturbation in the water balance rather than any change in salt content is the main cause of hyponatremia, the most frequent electrolyte abnormality, defined as a serum sodium concentration <135 mEq/L. Hyponatremia may be divided between mild (Na > 120 mEq/L) or severe (Na < 120 mEq/L) hyponatremia, and is most frequently observed in elderly ICU hospitalized patients. Based on tonicity, hyponatremia may be hypotonic (a decreased concentration of the solute), isotonic, and hypertonic (falsely low sodium). According to the volume of extracellular fluid (ECF), hyponatremia is further divided among hypovolemic, euvolemic, or hypervolemic hyponatremia. Finally, hyponatremia may develop rapidly as acute (<48 h), usually with severe symptoms, or slowly as chronic hyponatremia, usually being asymptomatic or with mild symptoms. Acute severe hyponatremia presents with severe CNS problems, increased hospitalization rates, and mortality. The treatment with 3% sodium chloride and a 100 mL IV bolus based on severity and persistence of symptoms needs careful monitoring. A non-severe hyponatremia may be treated with oral urea. In asymptomatic mild hyponatremia, an adequate solute intake with an initial fluid restriction of 500 mL/d adjusted according to the serum sodium levels is preferred. Vaptans could be considered in patients with high ADH activity regardless of whether they are euvolemic or hypervolemic. In general, the treatment of hyponatremia should be based on the underlying cause, the duration and degree of hyponatremia, the observed symptoms, and volume status of patient
A Review of Sevelamer Hydrochloride in End-Stage Renal Disease Patients on Dialysis
No full text It is known that in the presence of even subtle kidney dysfunction an intensive prevention of cardiovascular risk is required. Apart from the conventional factors which contribute to cardiovascular disease (CVD), there are also some specific conditions of the chronic kidney disease (CKD) population such as oxidative stress of uremia and dialysis (D). However, hyperphosphatemia, hypercalcemia, and elevated calcium-phosphorus product remain as major contributors to the development of vascular calcification (VC) in this population, as part of the systemic complication known as mineral and bone disorders (MBD) in CKD patients. Importantly, the retention of phosphate remains as main culprit in the pathogenesis of CKD–-MBD. Over the years, various treatment options for phosphate removal and controlling mineral metabolism, bone health, VC and CVD have failed, mainly through an over-suppression of PTH, development of ABD and promotion of VC and mortality. Although KDOQI and KDIGO published CKD–-MBD guidelines has clearly stated where calcium-based phosphate binders should not be used in D patients (hypercalcemia and low PTH) and where non calcium-containing phosphate binders are preferred (patients with severe vascular and/or other soft tissue calcifications), the greatest controversy and disagreements within the nephrological community still exists upon the cost-effectiveness of non calcium binder (sevelamer) use. Indeed, despite the evidence and recognised trend towards both a decrease in VC and CVD associated with sevelamer use, it is still an ongoing matter of debate. The magnitude of this controversy is increased when the issue of advanced medical and/or budgetary evaluation related to the implementation of clinical guidelines for CKD–-MBD treatment is considered. Despite advocated use of sevelamer across a range of common clinical scenarios in CKD, its widespread utilization is challenged as exceeding what would usually be considered good value for money. If so, it is questionable whether the recommendations and suggestions from the guidelines should be followed, and further, do we need guidelines and innovative drugs for treatment of hyperphosphatemia? While awaiting the answer, as clinicians we should proceed with a treatment to “do no harm”, trying to at least limit the calcium exposure of our dialysis patients. </jats:p
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Transforming Diabetes Care: The Molecular Pathways through Which GLP1-RAs Impact the Kidneys in Diabetic Kidney Disease
No full textDiabetic kidney disease (DKD) is a substantial complication of type 2 diabetes (T2D), presenting challenges in chronic kidney disease (CKD) management. In addition to traditional and recent therapies, including angiotensin, converting enzyme (ACE) inhibitors, angiotensin receptor blockers, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and mineralocorticoid receptor antagonists, the evolution of antihyperglycemic treatments has introduced a promising agent, glucagon-like peptide-1 receptor agonist (GLP-1RA) for the management of DKD. GLP-1RAs enhance insulin release and reduce glucagon release, offering a novel approach to DKD management. This review analyzes the molecular pathways through which GLP1-RAs confer renal protection in T2D and DKD, which are complex and multifaceted. They include modulation of renal hemodynamics, antioxidative and anti-inflammatory actions, metabolic regulation, and direct cellular effects. These mechanisms highlight GLP1-RA’s potential as a therapeutic option for glycemic control and direct or indirect renal function protection in diabetic patients, emphasizing the potentiality of GLP-1RAs for dual therapy, with cardiovascular and renal protection as a holistic approach. Clinical evidence supports GLP-1RAs in reducing albuminuria and enhancing kidney outcomes, highlighting their value in a comprehensive DKD management strategy
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