What is the impact of Furosemide (Lasix) on sodium levels?

From the Guidelines

Lasix significantly impacts sodium levels in the body by increasing its excretion in the urine, and its use should be carefully monitored to avoid excessive sodium loss and potential hyponatremia. As a loop diuretic, Lasix blocks the sodium-potassium-chloride cotransporter in the ascending loop of Henle, preventing sodium from being reabsorbed back into the bloodstream, which is supported by the guidelines on the management of ascites in cirrhosis 1. This causes increased sodium excretion in the urine, along with water and other electrolytes. Typically, Lasix can eliminate a significant amount of filtered sodium, making it valuable for treating conditions with fluid overload such as heart failure, liver cirrhosis, and kidney disease.

Some key points to consider when using Lasix include:

• Monitoring for diuretic adverse events, such as electrolyte imbalance, worsening hypokalaemia, hyperkalaemia, serum creatinine, hepatic encephalopathy, and muscle cramps 1
• Temporarily discontinuing diuretics if electrolyte imbalance (Na < 125 mmol) occurs 1
• Adjusting diuretic doses to achieve optimal response, with maximal doses often not achieved in clinical practice 1
• Considering the use of other diuretics, such as spironolactone, in combination with Lasix for optimal management of fluid retention 1

It is essential to note that excessive sodium loss can lead to hyponatremia, which may cause confusion, muscle weakness, seizures, or coma in severe cases. Patients taking Lasix should be monitored for electrolyte imbalances, especially when starting treatment or adjusting dosages, as recommended by the 2013 ACCF/AHA guideline for the management of heart failure 1. Sodium levels should be checked periodically, and patients should be aware of symptoms of hyponatremia such as headache, confusion, fatigue, and muscle cramps.

From the FDA Drug Label

Investigations into the mode of action of Furosemide tablets have utilized micropuncture studies in rats, stop flow experiments in dogs and various clearance studies in both humans and experimental animals It has been demonstrated that Furosemide tablets inhibits primarily the absorption of sodium and chloride not only in the proximal and distal tubules but also in the loop of Henle.

The impact of Lasix (furosemide) on sodium is that it inhibits the absorption of sodium in the proximal and distal tubules, as well as in the loop of Henle, leading to increased excretion of sodium in the urine 2. This effect can lead to electrolyte depletion, including hyponatremia, especially in patients receiving higher doses and a restricted salt intake 2.

• Key points:
  • Inhibition of sodium absorption
  • Increased excretion of sodium in the urine
  • Risk of electrolyte depletion, including hyponatremia
  • Monitoring of serum electrolytes is recommended, especially in patients with restricted salt intake or those receiving higher doses of furosemide 2 2.

From the Research

Lasix Impact on Sodium

• Lasix, also known as furosemide, is a potent loop diuretic that inhibits the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle, leading to increased urinary water and sodium excretion 3.
• The inhibition of NKCC2 by furosemide results in a decrease in extracellular water and body weight, with a positive correlation between the decrease in extracellular water and the decrease in body weight 3.
• Furosemide also increases intracellular water, which may be explained by an extracellular sodium loss 3.
• The use of furosemide can lead to undesirable consequences, such as worsening of kidney function and unpredictable effects on sodium balance, highlighting the need for careful evaluation of its effects on renal and cardiovascular physiology 4.

Mechanism of Action

• Furosemide's mechanism of action involves the inhibition of NKCC2, which leads to a decrease in sodium reabsorption and an increase in sodium excretion 3, 4.
• The increase in urinary excretion of NKCC2 after furosemide administration correlates with an increase in urine output and a decrease in extracellular water 3.
• Furosemide's effects on sodium balance are complex and involve multiple mechanisms, including modulation of the intrarenal renin-angiotensin system and changes in venous compliance 4.

Clinical Implications

• Furosemide is frequently used in the treatment of acute kidney injury, but its clinical roles remain uncertain 5.
• The severity of acute kidney injury has a significant effect on the diuretic response to furosemide, and a good 'urinary response' may be considered as a 'proxy' for having some residual renal function 5.
• Furosemide may be useful in achieving fluid balance in patients with acute lung injury without haemodynamic instability, but its effects on mortality in patients with acute kidney injury are unclear 5.