Fluid, electrolyte and acid-base disorders associated with antibiotic therapy

Area of Science:

• Nephrology
• Pharmacology
• Toxicology

Background:

• Antibiotics are widely prescribed, but can cause kidney toxicity.
• Renal toxic effects often manifest as decreased glomerular filtration rate.
• However, some antibiotics cause tubular dysfunction with near-normal filtration.

Purpose of the Study:

• To review antibiotic-associated fluid, electrolyte, and acid-base disorders.
• To focus on tubular dysfunction not significantly impacting glomerular filtration.
• To elucidate the mechanisms of antibiotic-induced renal tubular damage.

Main Methods:

• Review of existing literature on antibiotic nephrotoxicity.
• Integration of renal physiology with antibiotic effects on nephron segments.
• Discussion of affected receptors, transporters, channels, and pores.

Main Results:

• Antibiotics affect proximal tubules (e.g., Fanconi syndrome with tetracyclines, aminoglycosides).
• Aminoglycosides and capreomycin can cause Bartter-like syndrome affecting the loop of Henle.
• Collecting duct dysfunction includes hyponatremia, hypokalemia, hyperkalemia, renal tubular acidosis, and nephrogenic diabetes insipidus.

Conclusions:

• Antibiotics disrupt renal tubular function through various mechanisms.
• Understanding these specific disruptions aids in pathophysiology-directed treatment.
• Targeted therapies can mitigate antibiotic-induced kidney disorders.