Histopathological changes in kidneys of dogs with gentamicin-induced acute renal failure

Abstract

If applied in high doses and for a longer period, aminoglycoside antibiotics are potential risk for renal tissue and may cause acute renal failure (ARF). ARF is a syndrome that develops from progressive nephron damage resulting in the loss of renal function. Our investigations were conducted to evaluate the histopathological changes in the structure of kidney, following application of 80 mg/kg/24 h gentamicin during 7 days. Functional capacity of kidneys was evaluated by endogenous creatinine clearance. Our results indicate that gentamicin, in doses 20 times higher than the therapeutic ones, cause progressive ARF starting from the 3rd day of application. Histopathological changes were characterized by cloudy swelling at the beginning of the observation period, followed by vacuolar and reticular dystrophy and later on necrosis of the tubulocytes in the proximal nephron segments. During the experiment, histopathological lesions were intensifying and were manifested by the appearance of lympho-histiocytic infiltrate in the interstitium and furthermore by hypercellularity of glomerules.

Ukoliko se primenjuju u većoj dozi ili tokom dužeg vremenskog perioda, aminoglukozidni antibiotici predstavljaju potencijalni rizik za oštećenje bubrežnog tkiva, što često dovodi do razvoja akutne renalne insuficijencije (ARI). ARI predstavlja sindrom koji se razvija usled propadanja većeg broja nefrona, što ima za posledicu gubitak bubrežne funkcije. Svrha naših istraživanja bila je da se utvrdi priroda i stepen histopatoloških promena u bubrezima pasa, nastalih kao posledica primene gentamicina u dozi od 80 mg/kg/24h tokom 7 dana. Funkcionalna sposobnost bubrega eksperimentalnih životinja ispitivana je izračunavanjem endogenog klirensa kreatinina. Naši rezultati ukazuju da gentamicin primenjen u dozi 20 puta većoj od terapijske, izaziva progresivnu ARI, počevši od 3. dana ogleda. Inicijalne histopatološke prornene karakteriše pojava mutnog bubrenja (3. dan), a tokom ogleda one se razvijaju u smislu pojave vakuolarne i rctikularne distrofije, sve do nekroze epitelnih ćelija proksimalnih bubrežnih kanalića. Tokom eksperimenta histopatološke lezije se pojačavaju i manifestuju pojavom limfohistiocitnog ćelijskog infiltrata u intersticijurnu kao i hipercelularnošću glomerula.