Thiazide-induced hyponatremia
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Abstract
Drug-induced hyponatremia is the most encountered problem especially diuretics because of its common use for treatment hypertension and extracellular volume expansion. Thiazides comprise drugs which potentially cause hyponatremia in susceptible patients despite understanding several potential risk factors of patients such as elderly age, female sex, low body mass, multiple comorbidities, polydipsia, hypokalemia, and concomitantly used drugs associated with impaired water excretion. Once hyponatremia developed, usually within two to three weeks after initiation, significant morbidity was observed of thiazide-induced hyponatremia among patients, while this condition could not be predicted individually. Mechanisms of thiazide-induced hyponatremia include excessive water intake, impaired free-water excretion with AVP dependence and AVP independence in the inner medullary portion and solute depletion. The SLCO2A1 allele was recently discovered with an encoding prostaglandin transporter suggesting the role of renal prostaglandins via increased water reabsorption through prostaglandin E receptor (EP4) signaling. Another uncertain mechanism involved the causal pathway of thiazides and renal prostaglandin. However, understanding these mechanisms and potential risk factors to the patients may identify those more likely to develop hyponatremia from thiazide use. Treatment of thiazide-induced hyponatremia must be avoid overcorrecting chronic hyponatremia by correct hypokalemia, correct solute depletion, continuous monitoring of urine output, and never repeating use.
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