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Nephrology›Condition·Updated Jul 11, 2026·v1

Hyponatremia

Hyponatremia is a common electrolyte disorder with significant morbidity and mortality. Safe management requires accurate volume status assessment, controlled correction (≤8 mEq/L/24h in chronic cases), and targeted therapy based on etiology. First-line treatments include hypertonic saline for severe symptoms, fluid restriction and urea for SIADH, and volume repletion for hypovolemia.

High Evidence270 references·10,046 words·41 min read·v1
HyponatremiaSIADHElectrolyte disorderNephrologyOsmotic demyelination syndrome

Quick Reference

RxDrug of choice3% hypertonic saline (for severe symptomatic hyponatremia); oral urea 30 g/day (for chronic SIADH)
AltAlternativesTolvaptan 15-60 mg/day (vaptan); empagliflozin 25 mg/day (SGLT2 inhibitor); desmopressin (for overcorrection rescue)
⊘AvoidThiazide diuretics in hyponatremic patients; vaptans in hypovolemic hyponatremia and liver disease; non-dihydropyridine CCBs (no direct role, but avoid in heart failure)
DxTest of choicePlasma osmolality, spot urine osmolality and urine sodium, volume status assessment (including PoCUS)
ScKey scoreSHOR score (Severe Hyponatremia Overcorrection Risk) to predict rapid correction; MELD-Na for liver disease prognosis
→When to referPersistent or severe hyponatremia (Na <120 mEq/L), suspected adrenal insufficiency, need for dialysis, ODS, or unclear etiology
Hyponatremia is common and dangerous; management hinges on accurate volume status and controlled correction (≤8 mEq/L/24h in chronic cases) to prevent osmotic demyelination.
Hyponatremia, defined as serum sodium <135 mmol/L, is the most common electrolyte disorder in hospitalized patients, affecting up to 47% of admissions in some populations. It independently increases mortality, fracture risk, and neurocognitive deficits, yet it is often underrecognized. Management hinges on accurate volume status assessment and controlled correction to prevent osmotic demyelination syndrome (ODS). First-line therapy for severe symptomatic hyponatremia is 3% hypertonic saline; for chronic euvolemic hyponatremia, fluid restriction and oral urea are preferred. Vasopressin receptor antagonists (vaptans) and SGLT2 inhibitors are second-line options. The key to safe management is limiting the 24-hour sodium rise to ≤8 mEq/L in chronic cases.

Overview and Recommendations

Background

  • •Hyponatremia (serum sodium <135 mmol/L) is the most common electrolyte disturbance among hospitalized patients, affecting up to 47% of admissions in cancer centers and 6.9% of community-dwelling adults. It is independently associated with increased morbidity and mortality across diverse clinical settings, including heart failure, cirrhosis, and chronic kidney disease.
  • •Classification by duration (acute <48 hours, chronic ≥48 hours) and severity (mild 130-135, moderate 120-129, severe <120 mmol/L) guides management. Volume status, hypovolemic, euvolemic, or hypervolemic, is the cornerstone of diagnostic classification and dictates treatment. Key causes include (euvolemic), renal salt wasting (hypovolemic), thiazide diuretics, heart failure, cirrhosis, and adrenal insufficiency.
  • •Pathophysiology centers on impaired renal water excretion due to persistent arginine vasopressin (AVP) secretion despite hypotonicity. In health, plasma osmolality <285 mOsm/kg suppresses AVP; in hyponatremia, baroreceptor-mediated or ectopic AVP release sustains water reabsorption via aquaporin-2 channels in the collecting duct. The brain adapts to chronic hyponatremia by exporting organic osmolytes over 48-72 hours, rendering it vulnerable to osmotic injury if correction exceeds 8 mEq/L in 24 hours, the mechanism behind (ODS).
  • •Epidemiology: prevalence is 6.9% in the community (Dallas Heart Study) and up to 47% in hospitalized cancer patients. Women have twice the rate of severe hyponatremia compared with men, and the elderly are disproportionately affected due to age-related declines in urinary dilution and polypharmacy. Thiazide diuretics confer a 5-fold risk (HR 4.95), and second-generation antidepressants increase 30-day hospitalization risk by 5.46-fold. High ambient temperature (>20°C) markedly increases prevalence in those >80 years.
  • •Key syndromes: (euvolemia, urine osmolality >100 mOsm/kg, urine sodium >40 mmol/L, low uric acid); renal salt wasting (hypovolemia, high urine sodium, persistent hypouricemia after correction); thiazide-associated hyponatremia (older age, female sex, low BMI, often with hypokalemia); and primary polydipsia (urine osmolality <100 mOsm/kg). Accurate differentiation is critical because treatment is opposite: fluid repletion for hypovolemia versus fluid restriction for SIADH.

Evaluation

  • •Suspect hyponatremia in any patient with headache, nausea, vomiting, confusion, seizures, or coma, especially if on thiazides, SSRIs, or with underlying heart failure, cirrhosis, or malignancy. Even mild chronic hyponatremia (130-135 mmol/L) can cause subtle gait instability and cognitive impairment, increasing fall risk.
  • •Confirm hypotonic hyponatremia by measuring plasma osmolality: <275 mOsm/kg confirms hypotonicity. If osmolality ≥295 mOsm/kg, consider hypertonic hyponatremia (hyperglycemia, mannitol); if 275-295, consider pseudohyponatremia from hyperlipidemia or paraproteinemia.
  • •Assess extracellular fluid volume status through history (orthostasis, vomiting, diarrhea, edema), physical exam (jugular venous pressure, skin turgor, mucous membranes, edema), and consider point-of-care ultrasound (lung B-lines, IVC collapsibility, VExUS score) to improve accuracy over exam alone.
  • •Order spot urine osmolality and urine sodium before any therapy. Urine osmolality <100 mOsm/kg suggests primary polydipsia or low solute intake (beer potomania); >100 mOsm/kg indicates inappropriate ADH activity (SIADH, hypovolemia, hypervolemia).
  • •Interpret urine sodium: <30 mEq/L suggests hypovolemia (extrarenal losses) or hypervolemia (heart failure, cirrhosis); >30 mEq/L suggests SIADH, renal salt wasting, diuretic use, or hypocortisolism. Caveat: diuretics can elevate urine sodium regardless of volume status.
  • •Measure serum cortisol (8 AM) and TSH to exclude adrenal insufficiency and hypothyroidism. Low cortisol with high ACTH suggests primary adrenal insufficiency; low cortisol with low/normal ACTH suggests secondary. Hypothyroidism is an uncommon cause but should be ruled out.
  • •Consider fractional excretion of urate (FEurate) to differentiate SIADH from renal salt wasting: in SIADH, FEurate is elevated during hyponatremia but normalizes after correction; in RSW, it remains persistently elevated. Hypouricemia is present in ~70% of SIADH patients.
  • •In unclear cases, plasma copeptin (surrogate for AVP) measured after hypertonic saline infusion (target Na ≥150 mmol/L) can distinguish primary polydipsia from partial central diabetes insipidus with high accuracy (96.5%), though not yet routine.
  • •Imaging: chest CT to screen for causing SIADH; brain MRI if CNS pathology suspected (e.g., multiple system atrophy, pituitary lesions). Adrenal CT if primary adrenal insufficiency from infection or malignancy is considered.
  • •Diagnostic criteria for SIADH (Bartter-Schwartz): euvolemia, plasma osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg, urine sodium >40 mmol/L, normal thyroid and adrenal function, no recent diuretic use. Reset osmostat is a variant where ADH secretion is regulated at a lower set point.
  • •Red flags requiring urgent intervention: respiratory compromise (PaO2 <70 mm Hg), autonomic instability (hypotension, bradycardia), seizures, or coma. These mandate immediate hypertonic saline and ICU admission.
  • •Common pitfall: misclassifying hypovolemic hyponatremia as euvolemic SIADH. A spot urine sodium <30 mEq/L with clinical signs of volume depletion should prompt volume repletion, not fluid restriction. Always check volume status before diagnosing SIADH.

Management

  • •For severe symptomatic hyponatremia (seizures, coma, respiratory arrest): administer 3% hypertonic saline IV, 100-150 mL bolus over 20 minutes; repeat every 20 minutes until symptoms improve or serum sodium rises by 4-6 mEq/L. Goal is to abate symptoms, not normalize sodium. Monitor sodium every 2 hours.
  • •For acute hyponatremia (<48 hours duration): can correct more rapidly; target 1-2 mEq/L per hour until symptoms resolve, then slow correction. The risk of ODS is low because brain adaptation has not occurred.
  • •For chronic hyponatremia (≥48 hours or unknown duration): limit correction to ≤8 mEq/L in the first 24 hours and ≤18 mEq/L in 48 hours. In high-risk patients (alcoholism, liver disease, malnutrition, hypokalemia), consider even stricter limits (≤6 mEq/L in 24 hours).
  • •Monitor serum sodium every 2 hours during active correction, then every 4-6 hours once stable. Use point-of-care testing if available. Document the rate of correction in the medical record.
  • •If overcorrection occurs (rise >8 mEq/L in 24 hours): re-lower serum sodium by administering desmopressin (DDAVP) 1-2 mcg IV or SC and 5% dextrose in water (10 mL/kg over 1 hour). This can reduce sodium by 2-9 mEq/L. Consider minocycline 200 mg orally twice daily for 5 days to prevent ODS (animal data, limited human evidence).
  • •For asymptomatic or mildly symptomatic euvolemic hyponatremia (SIADH): first-line therapy is fluid restriction ≤1 L/day. Assess adherence and response after 24-48 hours. If sodium does not rise by ≥2 mEq/L, consider adding pharmacotherapy.
  • •Add oral urea 30 g/day (range 15-60 g) in divided doses, mixed with flavored liquid or juice to improve palatability. Urea increases sodium by ~8 mEq/L on average, with overcorrection in only 3% of cases. It is inexpensive and well-tolerated long-term.
  • •Second-line: vasopressin V2-receptor antagonists (vaptans). Start tolvaptan 15 mg orally once daily; titrate to 30-60 mg based on response. Monitor sodium every 6-8 hours for the first 24 hours. Avoid in hypovolemic hyponatremia and in patients with liver disease (risk of hepatotoxicity). Limit use to 30 days due to cost and safety concerns.
  • •Alternative: empagliflozin 25 mg daily (SGLT2 inhibitor) for SIADH. In trials, it increased sodium by 4-10 mmol/L over 4 days and improved cognitive scores. No hypoglycemia or hypotension reported. Emerging evidence; not yet guideline-endorsed.
  • •For hypovolemic hyponatremia: replete volume with isotonic saline (0.9% NaCl) or balanced crystalloid (e.g., Plasma-Lyte). Correct the underlying cause (discontinue diuretics, treat vomiting/diarrhea). Monitor sodium and potassium; hypokalemia often coexists and should be corrected simultaneously.
  • •For hypervolemic hyponatremia (heart failure, cirrhosis): treat the underlying condition with loop diuretics, fluid restriction, and sodium restriction. Consider vaptans only if refractory and in patients without liver disease (tolvaptan is FDA-approved for hypervolemic hyponatremia but contraindicated in cirrhosis due to hepatotoxicity).
  • •Avoid thiazide diuretics in patients with hyponatremia; discontinue if they are the suspected cause. Thiazides impair urinary dilution and can cause severe hyponatremia, especially in elderly women with low BMI.
  • •In dialysis patients with severe hyponatremia: use concurrent dialysate flow (blood and dialysate flow in same direction) to slow correction, or use continuous venovenous hemofiltration (CVVH) with low-sodium replacement fluid. Monitor sodium every 2-4 hours; aim for rise <8 mmol/L in 24 hours. Avoid citrate-based anticoagulation if rapid correction is a concern.
  • •For drug-induced hyponatremia (SSRIs, carbamazepine, TMP/SMX, etc.): discontinue the offending drug if possible. If the drug cannot be stopped (e.g., essential antidepressant), manage with fluid restriction and consider switching to an agent with lower risk (e.g., mirtazapine).
  • •When to refer: to nephrology for persistent or severe hyponatremia (Na <120 mEq/L), recurrent hyponatremia, or if dialysis is needed; to endocrinology if adrenal insufficiency or hypothyroidism is suspected; to oncology if SIADH from malignancy is suspected; to neurology if ODS develops.
  • •Discharge criteria: serum sodium >130 mEq/L and stable for 24-48 hours, symptoms resolved, underlying cause identified and addressed, follow-up plan for monitoring sodium and adjusting therapy. Educate patient on symptoms of hyponatremia and when to seek care.

Board Review — High Yield

  • •SIADH diagnostic criteria, euvolemia, plasma osmolality <275, urine osmolality >100, urine Na >40, normal thyroid/adrenal.
  • •Osmotic demyelination syndrome (ODS), occurs when chronic hyponatremia is corrected >8 mEq/L in 24 hours; risk factors: alcoholism, liver disease, hypokalemia, malnutrition.
  • •Thiazide-associated hyponatremia, 5-fold risk; elderly women with low BMI; often with hypokalemia and metabolic alkalosis.
  • •Renal salt wasting vs SIADH, RSW: hypovolemia, persistent hypouricemia after correction, high renin/aldosterone; SIADH: euvolemia, hypouricemia normalizes after correction.
  • •First-line for severe symptomatic hyponatremia, 3% hypertonic saline 100-150 mL bolus; goal is to raise Na by 4-6 mEq/L to abate symptoms.
  • •First-line for chronic SIADH, fluid restriction ≤1 L/day; add oral urea 30 g/day if inadequate response.
  • •Overcorrection rescue, desmopressin 1-2 mcg IV/SC + 5% dextrose in water; can lower Na by 2-9 mEq/L.
  • •Empagliflozin for SIADH, SGLT2 inhibitor; increases Na by 4-10 mmol/L; improves cognitive scores; emerging therapy.
  • •SHOR score, predicts overcorrection risk; includes decreased consciousness, vomiting, severe hypokalemia, hypotonic urine, volume overload, chest tumor, age, initial Na <110.
  • •Hyponatremia in heart failure, independent predictor of mortality (HR 1.90); treat with fluid restriction, loop diuretics, consider vaptans if refractory (avoid in cirrhosis).

Deep Dive — Evidence Details

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