Review
Copyright ©The Author(s) 2017.
World J Nephrol. Jan 6, 2017; 6(1): 1-13
Published online Jan 6, 2017. doi: 10.5527/wjn.v6.i1.1
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)