Patient on a thiazide diuretic has serum sodium 101 mmol/L, urine sodium 90 mmol/L, and urine osmolality 310 mOsm/kg. Is this thiazide‑induced hyponatraemia?

Thiazide-Induced Hyponatremia: Diagnostic Confirmation

Yes, this clinical picture is entirely consistent with thiazide-induced hyponatremia and represents a medical emergency requiring immediate discontinuation of the thiazide diuretic. 1, 2

Why This Is Thiazide-Induced Hyponatremia

The laboratory constellation you describe—serum sodium 101 mmol/L, urine sodium 90 mmol/L, and urine osmolality 310 mOsm/kg—is pathognomonic for thiazide-induced hyponatremia 1, 3:

• Severe hyponatremia (serum Na 101 mmol/L) places this patient in the highest-risk category, with thiazides responsible for 94% of severe diuretic-induced hyponatremia cases (defined as serum sodium <115 mmol/L) 3
• Inappropriately elevated urine sodium (90 mmol/L) indicates ongoing renal sodium wasting despite profound hyponatremia, which is the hallmark of thiazide action at the distal convoluted tubule 1, 4
• Urine osmolality 310 mOsm/kg demonstrates impaired urinary dilution—thiazides preserve concentrating ability but abolish the kidney's capacity to excrete maximally dilute urine, trapping patients in a state where they cannot excrete free water 1

Mechanism of Thiazide-Induced Hyponatremia

Thiazides cause hyponatremia through multiple synergistic mechanisms 1:

• Direct inhibition of sodium-chloride cotransport in the cortical diluting segment prevents generation of free water
• Stimulation of vasopressin (ADH) release through volume depletion, creating an SIADH-like state 4
• Reduction in glomerular filtration rate with enhanced proximal tubular water reabsorption, reducing distal delivery to diluting sites 1
• Possible direct effect on collecting duct water permeability 1

The combination of impaired water excretion plus ongoing cation depletion (sodium and potassium) produces the severe hypotonicity seen in your patient 4.

Critical Immediate Management Steps

1. Discontinue the Thiazide Immediately

Stop the thiazide diuretic now—this is the single most important intervention 2, 3. Thiazide-induced hyponatremia can develop within 1–14 days of starting therapy, and most cases occur within the first two weeks 3.

2. Assess for Severe Neurological Symptoms

• If the patient has seizures, altered mental status, or focal neurological deficits, administer 3% hypertonic saline immediately with a target correction of 6 mmol/L over 6 hours or until symptoms resolve 5, 4
• If the patient is asymptomatic or mildly symptomatic, implement fluid restriction to <1 L/day and allow spontaneous correction after thiazide discontinuation 5, 1

3. Correct Hypokalemia Aggressively

Check serum potassium and replace deficits before correcting sodium 3. Hypokalemia is present in the majority of thiazide-induced hyponatremia cases and increases susceptibility to osmotic demyelination syndrome 1, 3. Potassium replacement itself will raise serum sodium as potassium shifts into cells 1.

4. Limit Sodium Correction Rate

The maximum correction must not exceed 8 mmol/L in any 24-hour period 5, 3. For thiazide-induced hyponatremia, this is especially critical because:

• Rapid correction (>20 mmol/L in 24 hours) is significantly associated with mortality or demyelinating syndrome 3
• Inadvertent overcorrection is common in thiazide-induced hyponatremia because urinary diluting ability is restored immediately when the diuretic is stopped and volume deficits are repaired 1

5. Monitor Serum Sodium Every 2–4 Hours

Check serum sodium every 2 hours during the first 6–8 hours, then every 4 hours 5. The rapidity of correction after thiazide discontinuation can be unpredictable, and close monitoring prevents overcorrection 1, 3.

Distinguishing Thiazide-Induced Hyponatremia from SIADH

Your patient's presentation mimics SIADH but is caused by the thiazide 1, 4:

• Both conditions show elevated urine sodium (>20 mmol/L) and inappropriately concentrated urine relative to serum osmolality 6, 1
• The key difference is volume status: thiazide-induced hyponatremia typically involves mild volume depletion (though patients may appear euvolemic), whereas SIADH is truly euvolemic 1, 4
• Thiazides can also exacerbate underlying SIADH in patients with other causes of inappropriate ADH secretion 1

In your patient, the history of thiazide use combined with the laboratory findings makes thiazide-induced hyponatremia the primary diagnosis 2, 3.

High-Risk Features in This Patient

• Serum sodium 101 mmol/L represents life-threatening hyponatremia with a 60-fold increase in hospital mortality (11.2% vs 0.19% in normonatremic patients) 7
• Women are four times more likely than men to develop severe thiazide-induced hyponatremia 3
• Rapid onset (within 1–14 days) is typical for thiazide-induced cases, distinguishing them from furosemide-induced hyponatremia, which takes longer to develop 3

Common Pitfalls to Avoid

• Do not administer isotonic saline (0.9% NaCl) as initial therapy unless the patient is profoundly hypovolemic with hemodynamic instability—isotonic saline can worsen hyponatremia in thiazide-induced cases because the urine osmolality (310 mOsm/kg) exceeds that of normal saline (308 mOsm/kg), leading to net free water retention 7
• Do not correct sodium faster than 8 mmol/L in 24 hours—rapid correction (>20 mmol/L in 24 hours) is associated with osmotic demyelination syndrome, which manifests 2–7 days later with dysarthria, dysphagia, oculomotor dysfunction, and quadriparesis 5, 3, 8
• Do not overlook hypokalemia—potassium deficits must be corrected to prevent arrhythmias and reduce the risk of osmotic demyelination 1, 3
• Do not restart the thiazide until serum sodium has normalized and the patient has been counseled about the risk of recurrence 2

Prognosis and Follow-Up

• Mortality is directly related to hyponatremia in 12 of 129 reported cases of severe diuretic-induced hyponatremia 3
• Neurological recovery is possible even after severe hyponatremia (serum sodium 104 mmol/L) if correction is managed carefully, though extrapontine myelinolysis can occur despite appropriate correction rates 8
• Rechallenge with thiazides should be avoided in patients who have experienced severe thiazide-induced hyponatremia, as recurrence is likely 4