Nefrotoxicidad Por Antibioticos

reviews
Fluid, electrolyte and acid–base disorders
associated with antibiotic therapy
R. Zietse, R. Zoutendijk and E. J. Hoorn
Abstract | Antibiotics are among the most frequently prescribed drugs in medicine. Their use, however,
is often limited by associated renal toxic effects. The most common manifestation of these toxic effects is
decreased glomerular filtration rate. However, they canalso occur while renal function remains near to normal.
This review focuses on antibiotic-associated fluid, electrolyte and acid–base disorders that do not greatly
reduce glomerular filtration. renal tubules can be affected by antibiotics at various locations. in the proximal
tubule, toxic effects of tetracyclines and aminoglycosides can result in complete proximal tubular dysfunction,
alsoknown as Fanconi syndrome. Aminoglycosides (and capreomycin) can also affect the loop of Henle and
lead to a Bartter-like syndrome. in the collecting ducts, antibiotics can cause a diverse range of disorders,
including hyponatremia, hypokalemia, hyperkalemia, renal tubular acidosis, and nephrogenic diabetes
insipidus. Causative antibiotics include trimethoprim, amphotericin B, penicillins,ciprofloxacin, demeclocycline
and various antitubercular agents. Here, we describe the mechanisms that disrupt renal tubular function.
integrated with the physiology of each successive nephron segment, we discuss the receptors, transporters,
channels or pores that are affected by antibiotics. This insight should pave the way for pathophysiologydirected treatment of these disorders.
Zietse, r. etal. Nat. Rev. Nephrol. 5, 193–202 (2009); doi:10.1038/nrneph.2009.17

Introduction

the introduction of antibiotic treatment counts as one
of the great medical achievements of the 20th century.
Compared to early treatments with chemical compounds,
antibacterial antibiotics are highly effective and have a
favorable adverse-effect profile.
renal clearance of a drug, and/or its metabolites, isan
important mechanism for the elimination of antibiotics.
this pharmacokinetic property determines the risk of
adverse effects to the kidneys and, therefore, kidney
function should be monitored in patients who receive
high doses of these drugs. Despite the large therapeutic
window for most of these agents, renal impairment often
occurs, as revealed by an impaired glomerular filtrationrate. even when little impairment in this rate is seen,
however, antibiotic-associated renal damage might still
b e present. additionally, renal failure due to tubular
necrosis or interstitial nephritis has been described
as a consequence of treatment with several classes of
antibiotics, such as aminoglycosides and vancomycin.
However, antibiotic-induced acute renal failure is not
discussedfurther in this article because that topic has
been extensively reviewed elsewhere.1,2
the nature of the damage depends on the renal handling of the drug. although most antibiotics are cleared
by glomerular filtration, tubular function can be disrupted in any part of the entire nephron; consequently,
most renal toxic effects occur further downstream, in
Competing interests
The authorsdeclared no competing interests.

the tubules. For instance, treatment with aminoglycosides is associated with contraction and proliferation
of glomerular mesangial cells, 3 but most histological
abnormalities associated with administration of these
agents occur in the proximal tubule.4 Gentamicin is the
best-studied of this class of drugs, but several studies have
documented similar effects oftobramycin on proximal
tubular histology.
Following glomerular filtration, the renal tubules
determine the ultimate composition of the urine according to physiological demands. vast amounts of water
and solutes are reabsorbed along the nephron, and substances that are not readily filtered are added to urine
by active tubular secretion. subtle abnormalities in
tubular reabsorption or...