Thiazides like chlorothiazideand hydrochlorothiazideinhibit the transport of Na+ and Cl- ions in the distal tubule. By blocking the Na+/Cl- co-transporter the NaCl concentration in the tubular fluid remains high and more water will be lost. The diuretic effect is not related with the antihypertensive effect, because this effect is mainly regulated by vasodilation.
for the treatment with thiazides are hypertension, edema (heart failure, hepatic cirrhosis, nephrotic syndrome), hypercalciuria and renal diabetes insipidus.
Adverse effects are hyponatremia (especially as result of disturbed dilution in elderly women drinking a lot of water), hypokalemia (low muscular mass), hyperuricemia, hypercalcemia. Dry mouth, fatigue, cramps, dizziness and gout may accompany these side effects. It is important that the electrolyte balance is monitored closely during treatment with loop diuretics. Moreover, a combination with potassium-rich diet is recommended. High dose thiazides also decrease insulin sensitivity.
These drugs interact with lithium, digoxin (hypokalemia), and ACE-inhibitors (see Kompas for further details). Interaction with quinidine can cause life-threatening arrhythmias.
What is NOT a cause of diuretic resistance?
Extra info: Diuretic resistance is very common in clinical practice and we should know these factors. E.g. a patient with end stage renal disease is given 80mg furosemide, and then 160 mg but still no urine! This is useless as the kidneys are already functionless.
Due to their potential to decrease glucose tolerance, thiazide diuretics may decrease the effect of:
Extra info: Thiazides may elevate blood glucose levels and thus antagonize the hypoglycemic effects of oral sulfonylureas and metformin. Tolbutamide’s main action is the stimulation of insulin secretion, and is independent of the glucose tolerance. Digoxin and omeprazol have no effect on glucose tolerance.