<b>Background/Objectives</b>: Potomania and beer potomania are rare but important causes of dilutional hyponatremia, resulting from excessive fluid intake combined with low solute consumption. This systematic review aimed to identify and describe the clinical presentations, underlying causes, complications, and management approaches in published case reports of these conditions. <b>Methods</b>: A systematic search was conducted in PubMed, Embase, Web of Science, and Scopus. Inclusion criteria were case reports and letters to the editor with confirmed diagnoses of potomania or beer potomania. The Joanna Briggs Institute (JBI) checklist was used to evaluate study quality. The SPIDER framework guided the selection process. A qualitative, narrative synthesis was performed. <b>Results</b>: Forty-four cases were included. Hyponatremia was the most frequent finding, commonly accompanied by neurological symptoms such as confusion and seizures. Beer potomania was more prevalent among male patients and associated with alcohol consumption and poor nutrition. Potomania was linked to restrictive diets, psychiatric disorders, or excessive intake of various non-alcoholic fluids. Management typically involved fluid restriction, correction of electrolytes, nutritional support, and psychiatric care. Five cases developed osmotic demyelination syndrome due to rapid sodium correction. <b>Conclusions</b>: Increased clinical awareness of potomania and beer potomania is essential to prevent severe outcomes. Early identification, individualized management, and cautious correction of serum sodium are crucial. Despite the limitations of case report evidence, this review provides meaningful insights into diagnosis and treatment.

If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ . Abstract Background Hyponatremia (serum sodium lower than 135 mmol/L) is the most frequent electrolyte alteration diagnosed in medical practice. It has deleterious clinical effects, being an independent predictor of mortality. Malnutrition encompasses pathological states caused by both nutrients excess and deficiency, being frequently documented in chronic kidney disease patients. In addition, chronic hyponatremia promotes adiposity loss and sarcopenia, while malnutrition can induce hyponatremia. This pathological interaction is mediated by four main mechanisms: altered electrolyte body composition (low sodium, low potassium, low phosphorus, or high-water body content), systemic inflammation (cytokines increase), hormonal mechanisms (renin–angiotensin–aldosterone system activation, vasopressin release), and anorexia (primary or secondary). Conclusion Malnutrition can induce hyponatremia through hydro-electrolytic, hormonal, inflammatory, or nutritional behavior changes; while hyponatremia per se can induce malnutrition, so there is a pathophysiological feedback between both conditions. Keywords: Hyponatremia, Malnutrition, Pathophysiology status released display-pdf yes is-in-collection-domain yes is-olf no is-manuscript no is-preprint no is-journal-matter no is-scanned no is-retracted no Received 2023 Jun 17; Accepted 2023 Aug 2; Issue date 2024. Introduction Hyponatremia, defined as natremia < 135 mmol/L, is the most frequent electrolyte alteration diagnosed in medical practice. Hyponatremia and malnutrition are frequently found associated, and they have been even reported as Precisely, hyponatremia secondary to low potassium body content can be documented in severe malnourished patients. Moreover, sarcopenia is a condition usually documented in this population, and since muscle mass is the main potassium body store, sarcopenia represents reduced body potassium content. Therefore, it has been hypothesized that sarcopenia per se, as a cause of low potassium body content, could cause hyponatremia [ 10 , 18 ]. These anions would then leave the cells together with potassium in order to maintain electroneutrality, generating an osmotic effect that would dilute the intravascular compartment, favoring the appearance of hyponatremia [ 6 , 19 , 20 ]. In the fifth place, reset osmostat (RO), a condition that has a low-normal plasma osmolality threshold which consequently induces vasopressin release at a lower plasma osmolarity, with normal water load excretion, and intact urine diluting ability, while maintaining normal sodium balance. RO has been documented in severely frail individuals [ 7 – 12 ]. Sixth, there is the combination of some of the abovementioned mechanisms, which is usually documented in this population, as is the typical case of a patient suffering from chronic diarrhea (high sodium loss) and hyporexia (low sodium income). Seventh, it has already been documented a positive association between decreased lean body mass and low serum sodium levels, as well as that serum sodium tends to be low in the malnourished individuals [ 7 , 8 , 13 , 14 ]. In this sense, Barsoney et al. have hypothesized based on animal studies that chronic hyponatremia can increase oxidative stress, promoting senescence manifestations, such as loss of adiposity, bone mass, and sarcopenia. Hormonal mechanisms RASS can be activated by real or effective hypovolemia. Regarding the former, this can be documented in malnourished patients who suffer from volume contraction due to a chronic low sodium diet (salt restriction) and/or sustained sodium loss induced by undeclared diuretics or cathartic drugs intake (anorexia nervosa). Regarding the latter, this can be induced by low serum oncosis due to significant hypoalbuminemia (serum albumin ≤ 2 mg/L) in malnourished patients or it could be secondary to advanced edematous states (heart failure, cirrhosis, etc.) which have already developed malnutrition [ 1 , 19 ]. In a particular sort of anorexia, the anorexia nervosa [ 14 , 22 ], which is the most life-threatening of all psychiatric diseases, medical complications due to malnutrition and/or purging behaviors are the main cause of mortality in these patients. In this sense, they are more susceptible to sodium and water depletion due to diuretic and/or laxative abuse, and vomiting in a context of inadequate intake of fluids and sodium in defect of sodium (long-term sodium restriction). This nutritional behavior of not adding salt to food is usually used as a method to control body weight in this population.