What are the signs and symptoms of aminoglycoside toxicity?

GENERAL FEATURES OF AMINOGLYCOSIDE NEPHROTOXICITY Nephrotoxicity induced by aminoglycosides manifests clinically as nonoliguric renal failure, with a slow rise in serum creatinine and a hypoosmolar urinary output developing after several days of treatment.

What should you monitor with aminoglycosides?

Background. Therapeutic drug monitoring (TDM) is essential to ensure that aminoglycoside peak concentrations are high enough for effective antimicrobial treatment and trough levels are low enough to minimise toxicity. Inappropriate utilisation of TDM may lead to suboptimal therapy, toxicity and waste of resources.

How do aminoglycosides affect renal function?

Chronic kidney disease. Regular courses of aminoglycoside antibiotics may cause subclinical kidney damage leading to chronic kidney disease (CKD). This can manifest at the level of the glomerulus (causing decreased glomerular filtration rate, GFR) and the tubules (causing altered excretion of electrolytes).

How does aminoglycosides cause renal toxicity?

They exert their main toxic effect within the tubular cell by altering phospholipid metabolism. In addition to their direct effect on cells, aminoglycosides cause renal vasoconstriction.

What is the most nephrotoxic aminoglycoside?

Choice of aminoglycoside The following rank order of nephrotoxicity has been reported, from most toxic to least toxic: neomycin > gentamicin ≥ tobramycin ≥ amikacin ≥ netilmicin > streptomycin [1].

What are two major side effects of aminoglycosides?

The major side effects of aminoglycosides are kidney injury, hearing impairment and vestibular toxicity.

What labs should be monitored when taking gentamicin?

Gentamicin is cleared by the kidney and accumulates in renal tubular cells. Nephrotoxicity is most closely related to the length of time that trough levels are >2 μg/mL. Creatinine levels should be monitored every two to three days as an indicator of impending renal toxicity.

How do you test for nephrotoxicity?

Nephrotoxicity can be diagnosed through a simple blood test. Evaluation of nephrotoxicity through blood tests includes the measurements of blood urea nitrogen (BUN), concentration of serum creatinine, glomerular filtration rate and creatinine clearance.

What is aminoglycoside toxicity?

The toxicities of aminoglycosides include nephrotoxicity, ototoxicity (vestibular and auditory) and, rarely, neuromuscular blockade and hypersensitivity reactions. Nephrotoxicity receives the most attention, perhaps because of easier documentation of reduced renal function, but it is usually reversible.

What are the major toxic effects of aminoglycosides?

What causes renal failure in aminoglycoside toxicity?

RENAL FAILURE. The hypoosmotic polyuria, characteristic of the aminoglycoside toxicity, has been shown to result from the decreased fluid reabsorption by proximal tubules, secondary to an impaired solute reabsorption ( 64, 105 ), evidenced by the ion-wasting phenomena described above.

Do drug monitoring services reduce aminoglycoside toxicity?

Therapeutic drug monitoring services have failed to reduce aminoglycoside toxicity over the years, although two pharmacological parameters are imperative. The first is that peak aminoglycoside levels correlate with efficacy, as these agents display concentration-dependent bacterial killing.

How do aminoglycosides exert their toxicity?

The first hypothesis assumes that aminoglycosides exert their toxicity in direct relation to their local concentration. This would therefore designate lysosomes as a key site and lysosomal alterations as a main cause of toxicity, since this is where the bulk of the tissue-bound drug is primarily stored.

What are the signs and symptoms of aminoglycoside toxicity?