Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various tubules and the collecting duct. Solutes and water are selectively reabsorbed or secreted throughout this journey using passive and active transport mechanisms. This maintains optimal sodium levels. However, excessive sodium intake or impaired renal excretion can raise sodium concentration in the bloodstream, triggering osmosis and water retention, thereby increasing blood volume and pressure on vessel walls. Diuretics control this pressure by inhibiting ion transporters, promoting sodium and water excretion through increased urine output. This reduces arterial wall pressure and blood pressure. Diuretics effectively decrease blood pressure by 10-15 mmHg in most patients, serving as a standalone treatment for mild to moderate hypertension. However, they may cause side effects like hyperuricemia, characterized by elevated uric acid levels, leading to gout attacks with pain, swelling, and redness.