ABSTRACT
In this study, thirty adult male albino rats were used. They were classified into three groups; one control and two experimental groups [10 rats each]. Rats of the first experimental group [group I] had received 5.5 mg of the broad-spectrum antifungal Nizoral every day for two weeks. While rats of the second experimental group [group II] had received the same dose for four weeks. At the end of drug administration, animals of both control and experimental groups were anaesthetized and the kidneys were enucleated and processed for histological and ultrastructural studies. Light microscopic examination of all specimens of control rats was similar and had revealed normal structure for the kidney. Specimens of group I experimental rats showed hyper cellularity and hypertrophy of the capillary tuft of renal corpuscles, mild degree of degeneration affecting cells of the convoluted tubules, obliteration of tubular lumens, vascular congestion, presence of few scattered haemorrhagic spots and mild thickening of the basement membranes of the glomeruli and convoluted tubules as a result of deposition of extraordinary amount of collagen fibers. As regards group II experimental rats, the histological examination of rat kidney had revealed marked hyper cellularity and proliferation of glomerular capillary tuft, marked hydropic degeneration of the cellular cytoplasm of the convoluted tubules, partial destruction of the brush border, hyaline red casts, massive tubulo-interstitial haemorrhage and marked deposition of extraordinary amount of collagen fibers around glomerular and tubular basement membrane. At the electron microscopic level specimens of the control group revealed normal structure of the rat kidney. In group I experimental rats. It was observed that the ultrastructural changes were not symmetrical, the basement membrane thickening was the prominent finding as well as fusion of some minor foot processes with, obliteration of the filtration slits, and cellular degeneration of the convoluted tubules as evidenced from the presence of large number of degenerated mitochondria. Most of them lost their internal cristae. But few of them clarified a destruction of a local area of the outer membrane. In-group II experimental rats, focal widened areas of the glomerular basement membranes were observed with fusion of some minor and major foot processes which occurred at the expense of the filtration slits which were markedly reduced or completely obliterated. In conclusion, long-term administration of Nizoral induced variable degrees of renal damage
ABSTRACT
This study was performed using adult male albino rats and acute tubular necrosis was induced by glycerol injection into the hind limbs. Inhibitors for angiotensin converting enzyme [ACE], prostaglandins [PG] and nitric oxide [NO] synthase were injected intraperitonealy before and after glycerol injection to study their roles in acute renal failure and the possibility of their interaction in the kidney in a similar pattern to that takes place in the heart. Tubular damage occurring was semi-quantified in kidneys of different groups. ACE inhibitor [perindopril] was found to reduce the glycerol-induced acute tubular necrosis establishing the injurious role of angiotensin converting enzyme in the pathogenesis of this condition. Injection of either PG synthesis inhibitor [voltaren] or NO synthase inhibitor [L-NAME] has caused increase of the glycerol-induced acute tubular necrosis indicating that both prostaglandins and NO has renoprotective effects. Injection of either PG synthesis inhibitor [voltaren] or the NO synthase inhibitor [L-N AME] together with the ACE inhibitor impairs its renoprotective effect denoting that prostaglandins and NO may mediate this renoprotection