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Clinical Management of Hyponatremia
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Clinical Management of Hyponatremia

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Nephrology & Urology".

Deadline for manuscript submissions: closed (25 May 2023) | Viewed by 51941

Special Issue Editor

Dr. John K. Maesaka

E-Mail Website
Guest Editor
NYU Langone Hospital Long Island, Mineola, NY, USA
Interests: nephrology; hyponatremia; cerebral/renal salt wasting; uric acid metabolism and renal physiology; sodium balance

Special Issue Information

Dear Colleagues,

Hyponatremia is the most common electrolyte disorder that is caused by a multitude of conditions that activate a unique set of physiologic responses. The application of these physiologic responses has improved our understanding and treatment of hyponatremia, which can have dire consequences, including death. The reports of deaths due to acute hyponatremia after a modest intake of water in athletes after strenuous physical activity raises questions about the importance of limiting water-intake in other hyponatremic conditions. We will address the effects of acute hyponatremia and its effects on the brain. This issue will focus on the pathophysiology and methods to treat some of the common causes of hyponatremia, discuss new approaches to identifying the cause of hyponatremia, how to differentiate the syndrome of inappropriate secretion of antidiuretic hormone from cerebral/renal salt wasting, and implications and clinical applications of the newly identified novel natriuretic protein that may cause salt wasting.

Dr. John K. Maesaka
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • clinical management of hyponatremic conditions
  • understanding causes of hyponatremia
  • consequences of hyponatremia

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Published Papers (6 papers)

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Review

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11 pages, 730 KiB  
Review
Adaptation of the Brain to Hyponatremia and Its Clinical Implications
by Fabrice Gankam Kengne
J. Clin. Med. 2023, 12(5), 1714; https://doi.org/10.3390/jcm12051714 - 21 Feb 2023
Cited by 12 | Viewed by 11116
Abstract
Hyponatremia is the most common electrolyte disorder, occurring in up to 25% of hospitalized patients. Hypo-osmotic hyponatremia when severe and left untreated invariably results in cell swelling, which can lead to fatal consequences, especially in the central nervous system. The brain is particularly [...] Read more.
Hyponatremia is the most common electrolyte disorder, occurring in up to 25% of hospitalized patients. Hypo-osmotic hyponatremia when severe and left untreated invariably results in cell swelling, which can lead to fatal consequences, especially in the central nervous system. The brain is particularly vulnerable to the consequences of decreased extracellular osmolarity; because of being encased in the rigid skull, it cannot withstand persistent swelling. Moreover, serum sodium is the major determinant of extracellular ionic balance, which in turn governs crucial brain functions such as the excitability of neurons. For these reasons, the human brain has developed specific ways to adapt to hyponatremia and prevent brain edema. On the other hand, it is well known that rapid correction of chronic and severe hyponatremia can lead to brain demyelination, a condition known as osmotic demyelination syndrome. In this paper, we will discuss the mechanisms of brain adaptation to acute and chronic hyponatremia and the neurological symptoms of these conditions as well as the pathophysiology and prevention of osmotic demyelination syndrome. Full article
(This article belongs to the Special Issue Clinical Management of Hyponatremia)
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13 pages, 1580 KiB  
Review
New Approach to Hyponatremia: High Prevalence of Cerebral/Renal Salt Wasting, Identification of Natriuretic Protein That Causes Salt Wasting
by John K. Maesaka, Louis J. Imbriano, Candace Grant and Nobuyuki Miyawaki
J. Clin. Med. 2022, 11(24), 7445; https://doi.org/10.3390/jcm11247445 - 15 Dec 2022
Cited by 5 | Viewed by 6390
Abstract
Our understanding of hyponatremic conditions has undergone major alterations. There is a tendency to treat all patients with hyponatremia because of common subtle symptoms that include unsteady gait that lead to increased falls and bone fractures and can progress to mental confusion, irritability, [...] Read more.
Our understanding of hyponatremic conditions has undergone major alterations. There is a tendency to treat all patients with hyponatremia because of common subtle symptoms that include unsteady gait that lead to increased falls and bone fractures and can progress to mental confusion, irritability, seizures, coma and even death. We describe a new approach that is superior to the ineffectual volume approach. Determination of fractional excretion (FE) of urate has simplified the diagnosis of a reset osmostat, Addison’s disease, edematous causes such as congestive heart failure, cirrhosis and nephrosis, volume depletion from extrarenal salt losses with normal renal tubular function and the difficult task of differentiating the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from cerebral/renal salt wasting (C/RSW). SIADH and C/RSW have identical clinical and laboratory parameters but have diametrically opposite therapeutic goals of water-restricting water-loaded patients with SIADH or administering salt water to dehydrated patients with C/RSW. In a study of nonedematous patients with hyponatremia, we utilized FEurate and response to isotonic saline infusions to differentiate SIADH from C/RSW. Twenty-four (38%) of 62 hyponatremic patients had C/RSW with 21 having no clinical evidence of cerebral disease to support our important proposal to change cerebral to renal salt wasting (RSW). Seventeen (27%) had SIADH and 19 (31%) had a reset osmostat. One each from hydrochlorothiazide and Addison’s disease. We demonstrated natriuretic activity in the plasma of patients with neurosurgical and Alzheimer diseases (AD) in rat clearance studies and have now identified the natriuretic protein to be haptoglobin related protein without signal peptide (HPRWSP). We introduce a new syndrome of RSW in AD that needs further confirmation. Future studies intend to develop HPRWSP as a biomarker to simplify the diagnosis of RSW in hyponatremic and normonatremic patients and explore other clinical applications that can improve clinical outcomes. Full article
(This article belongs to the Special Issue Clinical Management of Hyponatremia)
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22 pages, 753 KiB  
Review
Exercise-Associated Hyponatremia in Marathon Runners
by Mark Klingert, Pantelis T. Nikolaidis, Katja Weiss, Mabliny Thuany, Daniela Chlíbková and Beat Knechtle
J. Clin. Med. 2022, 11(22), 6775; https://doi.org/10.3390/jcm11226775 - 16 Nov 2022
Cited by 13 | Viewed by 7161
Abstract
Exercise-associated hyponatremia (EAH) was first described as water intoxication by Noakes et al. in 1985 and has become an important topic linked to several pathological conditions. However, despite progressive research, neurological disorders and even deaths due to hyponatremic encephalopathy continue to occur. Therefore, [...] Read more.
Exercise-associated hyponatremia (EAH) was first described as water intoxication by Noakes et al. in 1985 and has become an important topic linked to several pathological conditions. However, despite progressive research, neurological disorders and even deaths due to hyponatremic encephalopathy continue to occur. Therefore, and due to the growing popularity of exercise-associated hyponatremia, this topic is of great importance for marathon runners and all professionals involved in runners’ training (e.g., coaches, medical staff, nutritionists, and trainers). The present narrative review sought to evaluate the prevalence of EAH among marathon runners and to identify associated etiological and risk factors. Furthermore, the aim was to derive preventive and therapeutic action plans for marathon runners based on current evidence. The search was conducted on PubMed, Scopus and Google Scholar using a predefined search algorithm by aggregating multiple terms (marathon run; exercise; sport; EAH; electrolyte disorder; fluid balance; dehydration; sodium concentration; hyponatremia). By this criterion, 135 articles were considered for the present study. Our results revealed that a complex interaction of different factors could cause EAH, which can be differentiated into event-related (high temperatures) and person-related (female sex) risk factors. There is variation in the reported prevalence of EAH, and two major studies indicated an incidence ranging from 7 to 15% for symptomatic and asymptomatic EAH. Athletes and coaches must be aware of EAH and its related problems and take appropriate measures for both training and competition. Coaches need to educate their athletes about the early symptoms of EAH to intervene at the earliest possible stage. In addition, individual hydration strategies need to be developed for the daily training routine, ideally in regard to sweat rate and salt losses via sweat. Future studies need to investigate the correlation between the risk factors of EAH and specific subgroups of marathon runners. Full article
(This article belongs to the Special Issue Clinical Management of Hyponatremia)
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17 pages, 2763 KiB  
Review
Pathophysiology of Drug-Induced Hyponatremia
by Gheun-Ho Kim
J. Clin. Med. 2022, 11(19), 5810; https://doi.org/10.3390/jcm11195810 - 30 Sep 2022
Cited by 39 | Viewed by 18385
Abstract
Drug-induced hyponatremia caused by renal water retention is mainly due to syndrome of inappropriate antidiuresis (SIAD). SIAD can be grouped into syndrome of inappropriate antidiuretic hormone secretion (SIADH) and nephrogenic syndrome of inappropriate antidiuresis (NSIAD). The former is characterized by uncontrolled hypersecretion of [...] Read more.
Drug-induced hyponatremia caused by renal water retention is mainly due to syndrome of inappropriate antidiuresis (SIAD). SIAD can be grouped into syndrome of inappropriate antidiuretic hormone secretion (SIADH) and nephrogenic syndrome of inappropriate antidiuresis (NSIAD). The former is characterized by uncontrolled hypersecretion of arginine vasopressin (AVP), and the latter is produced by intrarenal activation for water reabsorption and characterized by suppressed plasma AVP levels. Desmopressin is useful for the treatment of diabetes insipidus because of its selective binding to vasopressin V2 receptor (V2R), but it can induce hyponatremia when prescribed for nocturnal polyuria in older patients. Oxytocin also acts as a V2R agonist and can produce hyponatremia when used to induce labor or abortion. In current clinical practice, psychotropic agents, anticancer chemotherapeutic agents, and thiazide diuretics are the major causes of drug-induced hyponatremia. Among these, vincristine and ifosfamide were associated with sustained plasma AVP levels and are thought to cause SIADH. However, others including antipsychotics, antidepressants, anticonvulsants, cyclophosphamide, and thiazide diuretics may induce hyponatremia by intrarenal mechanisms for aquaporin-2 (AQP2) upregulation, compatible with NSIAD. In these cases, plasma AVP levels are suppressed by negative feedback. In rat inner medullary collecting duct cells, haloperidol, sertraline, carbamazepine, and cyclophosphamide upregulated V2R mRNA and increased cAMP production in the absence of vasopressin. The resultant AQP2 upregulation was blocked by a V2R antagonist tolvaptan or protein kinase A (PKA) inhibitors, suggestive of the activation of V2R-cAMP-PKA signaling. Hydrochlorothiazide can also upregulate AQP2 in the collecting duct without vasopressin, either directly or via the prostaglandin E2 pathway. In brief, nephrogenic antidiuresis, or NSIAD, is the major mechanism for drug-induced hyponatremia. The associations between pharmacogenetic variants and drug-induced hyponatremia is an area of ongoing research. Full article
(This article belongs to the Special Issue Clinical Management of Hyponatremia)
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11 pages, 1625 KiB  
Opinion
Hyponatremia Associated with Congestive Heart Failure: Involvement of Vasopressin and Efficacy of Vasopressin Receptor Antagonists
by San-e Ishikawa and Hiroshi Funayama
J. Clin. Med. 2023, 12(4), 1482; https://doi.org/10.3390/jcm12041482 - 13 Feb 2023
Cited by 5 | Viewed by 3244
Abstract
Hyponatremia is frequently found in patients with congestive heart failure. A reduction in effective circulatory blood volume in a volume-expanded patient with decreased cardiac output is linked to a baroreceptor-mediated non-osmotic release of arginine vasopressin (AVP). The increased production of AVP and salt [...] Read more.
Hyponatremia is frequently found in patients with congestive heart failure. A reduction in effective circulatory blood volume in a volume-expanded patient with decreased cardiac output is linked to a baroreceptor-mediated non-osmotic release of arginine vasopressin (AVP). The increased production of AVP and salt and water retention in the proximal and distal tubules of the kidney by humoral, hemodynamic, and neural mechanisms increase circulatory blood volume and contribute to hyponatremia. Recent studies have indicated that hyponatremia predicts the short-term and long-term prognosis of heart failure by increasing cardiac death and rehospitalization. In addition, the early development of hyponatremia in acute myocardial infarction also predicts the long-term prognosis of worsening heart failure. AVP V2 receptor antagonism may relieve water retention, but it is unknown whether the V2 receptor inhibitor, tolvaptan, improves the long-term prognosis of congestive heart failure. The newly identified natriuretic factor in renal salt wasting has the potential of improving clinical outcomes when combined with a distal diuretic. Full article
(This article belongs to the Special Issue Clinical Management of Hyponatremia)
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8 pages, 1104 KiB  
Opinion
Morbidity Associated with Chronic Hyponatremia
by Guy Decaux
J. Clin. Med. 2023, 12(3), 978; https://doi.org/10.3390/jcm12030978 - 27 Jan 2023
Cited by 13 | Viewed by 4216
Abstract
This article will discuss the consequences of chronic hyponatremia. In conditions such as cancer, heart failure, liver cirrhosis, or chronic kidney disease, the presence and magnitude of hypotonic hyponatremia are considered to reflect the severity of the underlying disease and are associated with [...] Read more.
This article will discuss the consequences of chronic hyponatremia. In conditions such as cancer, heart failure, liver cirrhosis, or chronic kidney disease, the presence and magnitude of hypotonic hyponatremia are considered to reflect the severity of the underlying disease and are associated with increased morbidity as well as mortality. Hyponatremia can be acute (<48 h) or chronic (>2–3 days). Chronic hyponatremia is associated with attention deficit, dizziness, tiredness, gait disturbance, falls, sarcopenia, bone fractures, osteoporosis, hypercalciuria (in the syndrome of inappropriate antidiuresis—SIADH), and kidney stones. In vitro studies have shown that cells grown in a low concentration of extracellular sodium have a greater proliferation rate and motility. Patients with chronic hyponatremia are more likely to develop cancer. We will not review the clinical consequences of respiratory arrest and osmotic demyelination syndrome (ODS) of the too-late or excessive treatment of hyponatremia. Full article
(This article belongs to the Special Issue Clinical Management of Hyponatremia)
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