|
|
|||||||||||||||||||||||
Go back to clinical information and images Diagnosis: Acute tubular damage asociated to antibiotics (colistin?) In this patient was notorious as the renal function was altered just after sepsis started to improve. Although it is not possible to know with certainty if antibiotics were the cause of tubular damage, the temporal relationship suggests this hypothesis. Antibiotics linked to acute renal failure include: aminoglycosides, beta lactams (cephalosporins, penicillins, penems), rifampicin, vancomycin, sulfonamides, fluoroquinolones, tetracyclines and others. Aminoglycosides and beta lactams predominate the literature regarding nephrotoxicosis. Research indicates that aminoglycosides cause renal failure primarily through proximal tubular necrosis and beta lactams initiate both acute tubulointerstitial nephritis and proximal tubular necrosis. Colistin has been very involved in nephrotoxicity. Colistin belongs to the polymyxin class of cationic polypeptide antibiotics. During the 1970s, the popularity of colistin rapidly faded because of reports of significant renal and neurological toxicity and it was progressively supplanted by less toxic antibiotics with a comparable or broader antibacterial spectrum. However, the mounting prevalence worldwide of infections due to multidrug-resistant Gram-negative bacilli has renewed interest into colistin but also revived the discussion about its toxicity. Renal toxicity is the most common adverse effect of colistin treatment because the drug is excreted primarily by the kidneys and elevated blood levels may further impair renal function (Spapen H, etl. Renal and neurological side effects of colistin in critically ill patients. Ann Intensive Care. 2011;1(1):14. [PubMed link] [Free full text link]). Little information is available on the mechanism of toxicity but probably are related to tubular damage. Our case is very interesting because the particular vacuolation of the tubular epithelium, mainly in proximal tubuli. Note that in figures 2 and 5 there are distal tubules no involved (or not vaculolated). In addition there is arteriolar hyalinosis, not related to antibiotics (Figure 9). Go back to clinical information and images References
|
||||||||||||||||||||||||