Hypertonicity: Clinical entities, manifestations and treatment

Table 3 Clinical states causing excessive water loss

Extrarenal water loss

Gastrointestinal losses

Vomiting

Nasogastric drainage

Ileostomy

Pancreatobiliary fistula

Diarrhea (non-secretory)

Laxatives, e.g., lactulose

Skin

Excessive sweating

Respiratory airways

Hyperpnea

Tracheal intubation

Mechanical ventilation

Excessive renal water losses

Osmotic (solute) diuresis

Osmotic diuretics, e.g., mannitol

Glucosuria, e.g., hyperglycemia, sodium-glucose transporter 2 (SGLT2) inhibitors

Urea diuresis, e.g., diuresis post-acute tubular necrosis, post- obstructive diuresis, use of catabolic medications (corticosteroids, tetracyclines, etc.), high protein intake, urea treatment for hyponatremia

Salt diuresis, e.g., intravenous infusion of saline, high salt intake

Water diuresis

Central diabetes insipidus

Idiopathic (most common)

Genetic: Familial (mutation causing misfolding of vasopressin), congenital hypopituitarism, Wolfram syndrome (diabetes insipidus, diabetes mellitus, optic atrophy, deafness)

Acquired: Neurosurgery, head trauma, brain tumors, infiltrative disorders (sarcoidosis, Langerhans cell histiocytosis, etc.)

Nephrogenic diabetes insipidus

Genetic: Inactivating mutations of V2 receptor gene (most common) or aquaporin 2 gene

Acquired:

Renal disease (chronic renal failure, post-acute tubular necrosis, obstructive nephropathy, sickle cell disease, autosomal dominant polycystic kidney disease)

Electrolyte disorders: Hypokalemia, hypercalcemia

Drugs: Lithium, amphotericin, demeclocycline, ifosfamide, V2 receptor antagonists

Gestation: Increased placental production of vasopressinase

Upward resetting of the osmostat (reset osmostat): Primary hyperaldosteronism (thought to be secondary to volume expansion and resulting in modest hypernatremia, up to 147 mmol/L)