What type of hyponatremia is related to solute deficiency?

Solute Deficiency Hyponatremia

Solute deficiency causes euvolemic (or sometimes hypovolemic) hyponatremia, most commonly manifesting as "beer potomania" or "tea and toast" syndrome, where inadequate dietary solute intake impairs the kidney's ability to excrete free water despite normal or near-normal total body sodium. 1

Pathophysiology of Solute Deficiency Hyponatremia

• The mechanism involves inadequate solute intake (typically <250 mOsm/day) limiting the kidney's capacity to generate solute-free water excretion, even when ADH is appropriately suppressed 1, 2
• The kidney requires adequate solute delivery to the distal tubule to excrete free water—without sufficient dietary protein, sodium, and potassium intake, maximum urine dilution cannot be achieved even with complete ADH suppression 2
• This creates a situation where continued water intake (even modest amounts) leads to progressive hyponatremia because the kidneys cannot excrete the water load 1, 2

Clinical Presentation and Diagnosis

• Beer potomania classically occurs in patients consuming primarily beer (low solute content) with minimal food intake, while "tea and toast" syndrome affects elderly or malnourished patients with extremely limited dietary variety 1
• These patients typically present as euvolemic on examination, though some degree of volume depletion may coexist if caloric intake is severely restricted 1, 3
• Urine osmolality is typically low (<100 mOsm/kg) once solute intake improves, distinguishing this from SIADH where urine remains inappropriately concentrated (>300 mOsm/kg) 1, 2
• Serum uric acid is usually normal or elevated (>4 mg/dL), contrasting with SIADH where it is typically <4 mg/dL 4, 1

Critical Management Principles

• Discontinuing alcohol consumption and implementing adequate dietary solute intake (particularly protein and sodium) results in dramatic improvement, often within 24-48 hours 4
• Extreme caution is required during refeeding, as rapid restoration of solute intake can trigger dangerously rapid sodium correction—these patients are at exceptionally high risk for osmotic demyelination syndrome 4, 2
• The correction rate must not exceed 4-6 mmol/L per day in these malnourished, high-risk patients, with absolute maximum of 8 mmol/L in 24 hours 4
• Implementing dietary sodium restriction (2000 mg per day [88 mmol per day]) alongside gradual nutritional rehabilitation prevents overly rapid correction 4

Distinguishing from SIADH

• Unlike SIADH, solute deficiency hyponatremia resolves with nutritional rehabilitation alone, without requiring fluid restriction 1, 2
• Urine sodium may be low initially (<30 mmol/L) due to poor intake, but increases appropriately with dietary improvement, whereas SIADH maintains elevated urine sodium (>20-40 mmol/L) despite hyponatremia 4, 1
• The key diagnostic feature is the clinical context of severe dietary restriction combined with improvement upon nutritional rehabilitation 1

High-Risk Populations Requiring Vigilance

• Patients with alcoholism, advanced liver disease, or severe malnutrition require correction rates of only 4-6 mmol/L per day due to dramatically elevated risk of osmotic demyelination syndrome 4
• Monitoring serum sodium every 4-6 hours during initial refeeding is essential to prevent overcorrection 4
• If overcorrection occurs (>8 mmol/L in 24 hours), immediately discontinue nutritional advancement, switch to D5W, and consider desmopressin to relower sodium levels 4