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At least 163 records · Page 9Linked to original sources
PubMed1988

Effects of unilateral ureteric occlusion on renal necrosis occurring in rats fed a methyl-deficient diet.

Wistar male rats were fed from weaning a methyl-deficient diet (groups I and II) or a standard commercial diet (groups III and IV). At the day 3 the left ureter was tied and divided in animals of groups I and III, while those in groups II and IV were sham operated. Rats of all groups were killed on days 8 and 10 to evaluate the incidence and extent of tubular necrosis (day 8) and tubular and cortical necrosis (day 10). The results of this study show that unilateral ureteric obstruction diminishes the incidence, severity and extent of necrosis in the same kidney.

Acute Kidney Injury↗
PubMed1975

Histochemical examination of lysosomal exzymes in necrotic proximal renal tubules of albino rats.

The lysosomal enzymatic activity of the necrotic proximal tubules was examined by light microscopy and electron microscopy in 24- and 48-h focal renal cortical necrosis induced by administration of oestrogen and posterior pituitary extract in rats. Organelles exhibiting acid phosphatase activity can also be seen in the necrotic cells but these differ in size and structure from the lysosomes of normal cells. The cytoplasmic nonspecific esterase and thioacetic acid hydrolase activities decrease considerably or disappear, although some morphologically damaged, but active, lysosomes can be observed. The role of thelysosomal enzymes is seen not in the development of the necrosis but rather in the breaking down of the already necrotic cell constituents.

Acid Phosphatase↗
PubMed1976

[Renal toxicity of contrast media. Experimental study on dogs (author's transl)].

Experiments injecting Indian ink have confirmed the theory that postangiographic renal damage is due primarily to ischaemia. Cortical ischaemia is due to vascular spasm and sludging caused by contrast medium. Current and previous experimental findings suggest the following course in the pathomechanism: vasospasm reduced blood velocity--aggregation of erythrocytes--further deterioration in the circulation--microemboli--irreversible sludge formation--arterial and venous thromboses--ischaemic foci--necrosis or infarction. It is not possible to prevent this damage by alpha blocking sympathicolytic drugs.

Acetrizoic Acid↗
PubMed1977

Unilateral Shwartzman reaction: cortical necrosis in one kidney following in vivo perfusion with endotoxin.

Unilateral renal cortical necrosis was selectively induced by in situ perfusion of the rabbit kidney with a perfusate containing 50 microgram of endotoxin followed by the i.v. administration of 250 microgram of endotoxin 24 hr later. The results strongly support the idea that the initial event in the genesis of renal cortical necrosis during the Shwartzman reaction is a specific local effect of endotoxin on the vascular endothelium.

Animals↗
PubMedDate not supplied

CT findings in acute renal cortical necrosis.

Acute renal cortical necrosis has three characteristic findings on contrast enhanced CT: (a) lack of enhancement of the renal cortex, (b) enhancement of the renal medulla, and (c) absent renal excretion.

Adult↗
PubMed2004

Influence of spironolactone treatment on gentamicin-induced nephrotoxicity in rats.

The effect of treatment of rats with gentamicin (80 mg/kg/day for 6 days), oral doses of spironolacatone (20 mg/kg/day for 6 days), and the combined treatment (spironolactone + gentamicin) on renal histology and reduced glutathione (GSH) concentration, and some serum constituents indicative of kidney function were studied. The serum concentrations of creatinine and urea were not significantly affected by spironolactone treatment, but were significantly elevated (P<0.05) by gentamicin administration. The antibiotic treatment also reduced GSH concentration and caused a moderate renal cortical necrosis. However, rats exposed to spironolactone + gentamicin revealed drastic increases in the serum urea and creatinine concentrations amounting to about 1.8 and 2.1 times those of rats treated with gentamicin alone, respectively. The histological examination of slides of the renal cortex of rats exposed to the combined drugs exhibited more extensive necrosis in the tubules when compared to those treated with gentamicin alone. The reduction in GSH induced by gentamicin was unaffected by the concomitant treatment of gentamicin and spironolactone. The concentration of gentamicin accumulated in the renal cortex was significantly larger (twofold) in rats treated concomitantly with spironolactone + gentamicin than in rats treated with gentamicin alone. The present results indicate that spironolactone aggravates gentamicin-induced nephrotoxicity in the rat.

Administration, Oral↗
PubMed1978

Chronic renal insufficiency from cortical necrosis induced by arsenic poisoning.

A 39-year-old man had anuria and azotemia and was found to be suffering from acute arsenic poisoning. After two peritoneal dialyses, partial renal function returned, and the patient has survived for five years without dialysis. Renal cortical necrosis was demonstrated by renal biopsy and renal calcification. We suggest that arsenic be added to the list of substances capable of causing renal cortical necrosis and recommend consideration of this complication in cases of arsenical poisoning.

Acute Disease↗
PubMed1974

Failure of cobra venom factor to prevent the generalized Shwartzman reaction and loss of renal cortical fibrinolytic activity.

Previous studies have shown that renal cortical fibrinolytic activity is absent in rabbits given one or two injections of endotoxin. Using a fibrin slide technic, we have studied the effect of endotoxin on cortical fibrinolytic activity in rabbits depleted of terminal complement components (C3-C9) by cobra venom factor. The loss of cortical fibrinolytic activity induced by endotoxin is not prevented by pretreatment with cobra venom factor. Additionally, this complement depletion did not prevent development of glomerular fibrin deposition, cortical necrosis or thrombocytopenia in the generalized Shwartzman reaction.

Animals↗