Gentamicin and sisomicin - induced renal tubular damage

Insights

Aminoglycoside antibiotics like gentamicin can cause early kidney damage. Monitoring urinary low molecular weight proteins (LMWP) and enzymes offers a sensitive method to detect this tubular impairment.

Area of Science:

  • Nephrology
  • Pharmacology
  • Biochemistry

Background:

  • Aminoglycosides are potent antibiotics used to treat severe bacterial infections.
  • Nephrotoxicity is a significant concern with aminoglycoside therapy, potentially leading to kidney damage.
  • Early detection of renal tubular damage is crucial for managing aminoglycoside-induced side effects.

Purpose of the Study:

  • To investigate early renal tubular damage induced by gentamicin and sisomicin.
  • To evaluate the utility of urinary low molecular weight proteins (LMWP) and enzyme activity as biomarkers for aminoglycoside nephrotoxicity.
  • To compare the renal toxicity profiles of gentamicin and sisomicin.

Main Methods:

  • Measurement of urinary excretion of beta 2 microglobulin, retinol binding protein, and lysozyme (LZM) in patients receiving gentamicin or sisomicin.
  • Assay of urinary alanine aminopeptidase and N-acetyl-beta-glucosaminidase activity.
  • Monitoring of serum creatinine and urinary transferrin to assess glomerular function.

Main Results:

  • Increased urinary LMWP elimination, particularly lysozyme (LZM), was observed in patients treated with gentamicin.
  • Elevated urinary enzyme activities (alanine aminopeptidase, N-acetyl-beta-glucosaminidase) correlated with gentamicin administration.
  • Sisomicin induced less pronounced changes in urinary markers compared to gentamicin, suggesting potentially lower nephrotoxicity.
  • Glomerular function remained unaffected, as indicated by stable serum creatinine and urinary transferrin levels.

Conclusions:

  • Urinary LMWP and enzyme measurements are sensitive and reliable indicators of early aminoglycoside-induced renal tubular damage.
  • Lysozyme (LZM) excretion is a particularly sensitive marker for gentamicin-induced tubular impairment.
  • Differences in renal toxicity between gentamicin and sisomicin may be linked to their varying accumulation in the renal cortex.

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