Thiazide diuretics are more likely than loop diuretics to cause hyponatremia. Loop diuretics inhibit sodium (Na+) transport in the renal medulla and prevent the generation of a maximal osmotic gradient. Thus, urinary concentrating ability is impaired with loop diuretics. Alternatively, thiazide-type diuretics increase Na+ excretion and preclude maximal urine dilution, while preserving the kidney's innate concentrating capacity. When diuretic-related hyponatremia occurs, it is typically in elderly females and is usual seen shortly after therapy begins (within the first 2 weeks).[8] However, diuretic-related hyponatremia can occur on a delayed basis even after several years of therapy.[7] Multiple factors contribute to the penchant of females to diuretic-related hyponatremia, including age, reduced body mass, exaggerated natriuretic response to a thiazide diuretic, diminished capacity to excrete free water, and self-imposed low-solute intake. Independent of this constellation of risk factors, it has been suggested that the apparent female preponderance of thiazide-induced hyponatremic adverse events is related to overrepresentation of females in thiazide-treated cohorts, rather than intrinsic susceptibility to the electrolyte disturbance.[7]