thiazideinduced

Thiazide-induced refers to adverse effects caused by thiazide diuretics, a class that includes hydrochlorothiazide, chlorthalidone, indapamide, and metolazone. These drugs inhibit the Na-Cl cotransporter in the distal convoluted tubule, producing natriuresis and mild diuresis. While effective for hypertension and edema, thiazides can provoke several electrolyte and metabolic disturbances, particularly in older adults or those with low solute intake or kidney impairment.

The most clinically important thiazide-related disturbances are hyponatremia, hypokalemia, hyperuricemia, and hyperglycemia. Hyponatremia arises from impaired free water excretion and potentiation of antidiuretic hormone activity, and may present with confusion, weakness, seizures, or falls, especially in the elderly. Management involves stopping the thiazide, assessing volume status, and correcting sodium gradually to avoid osmotic demyelination. Hypokalemia results from increased potassium loss in the distal nephron and can cause muscle cramps, arrhythmias, and QT changes; it is managed with potassium supplementation and monitoring, and by adjusting the diuretic dose. Thiazides can raise serum urate levels, increasing gout risk; those with prior gout should be monitored, and alternative therapies considered if urate burden is high. Hyperglycemia or impaired glucose tolerance can occur, contributing to worsened glycemic control in susceptible individuals.

Other potential effects include volume depletion with orthostatic symptoms, dehydration, and photosensitivity with some agents. Clinicians should monitor electrolytes, uric acid, and glucose as appropriate, particularly after initiation or dose changes. Rechallenge may be feasible after resolution of adverse effects, or patients may be shifted to alternative antihypertensive or diuretic therapies.