Lasix, or furosemide, powerfully inhibits sodium-potassium-chloride co-transport in the thick ascending limb of the loop of Henle. This action directly increases sodium, potassium, chloride, and water excretion in the urine. Consequently, Lasix promotes diuresis – a significant increase in urine production.
While this diuretic effect is therapeutically beneficial for conditions like edema and hypertension, it also carries a risk of nephrotoxicity. Prolonged or high-dose Lasix use can cause hypokalemia (low potassium), hypomagnesemia (low magnesium), and dehydration – all factors contributing to kidney damage.
Here’s a table summarizing the key renal effects of Lasix:
| Increased Urine Output | Inhibition of Na+/K+/2Cl – co-transport | Reduces edema, lowers blood pressure |
| Hypokalemia | Increased potassium excretion | Cardiac arrhythmias, muscle weakness |
| Hypomagnesemia | Increased magnesium excretion | Muscle cramps, cardiac arrhythmias |
| Dehydration | Significant fluid loss | Decreased renal blood flow, acute kidney injury |
| Ototoxicity | Direct effect on inner ear | Hearing loss, tinnitus |
| Acute Kidney Injury | Dehydration, electrolyte imbalances | Reduced glomerular filtration rate |
Careful monitoring of serum electrolytes (potassium, magnesium) and renal function (creatinine, glomerular filtration rate) is crucial during Lasix therapy to minimize the risk of nephrotoxicity. Appropriate hydration and electrolyte supplementation may be necessary to mitigate these risks. Always consult a physician before starting or altering Lasix treatment.
