The effect of netilmicin and other aminoglycosides on renal function. A survey of the literature on the nephrotoxicity of netilmicin.
The antibiotics of the aminoglycoside group are all potentially nephrotoxic. Aminoglycosides are exclusively excreted via the kidneys by glomerular filtration. On passing the proximal tubular cells of the nephron, an active reabsorption and intracellular concentration, 10-20 times the serum concentration, take place. Aminoglycosides are trapped in the lysozymes and inhibit cell metabolism. Functional changes are at first discrete, comprising polyuria, slight proteinuria, enzymuria and glycosuria. With more progressive changes the glomerular filtration rate decreases, followed by increased blood urea and serum-creatinine. The urine contains protein, casts and shedded tubular cells. Ultimately, but rarely, oligo-anuric renal failure may be encountered. Compared with gentamicin, the newer aminoglycosides, amikacin, tobramycin and netilmicin show in animal experiments a decreasing nephrotoxicity in the mentioned order. Extensive studies have demonstrated that netilmicin may be the drug with the least nephrotoxic potential. Clinical studies confirm that netilmicin is less nephrotoxic than gentamicin and compares favourably with tobramycin and amikacin. A survey of the literature is given.
D058186:Acute Kidney Injury / Q000139:chemically induced; D000617:Aminoglycosides / Q000009:adverse effects*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005839:Gentamicins / Q000009:adverse effects* / Q000633:toxicity; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D007678:Kidney Glomerulus / Q000648:ultrastructure; D007684:Kidney Tubules / Q000648:ultrastructure; D009428:Netilmicin / Q000009:adverse effects*; D014031:Tobramycin / Q000633:toxicity
D000617:Aminoglycosides; D005839:Gentamicins; D009428:Netilmicin; D014031:Tobramycin