Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphocytes from patients with neoplastic disease were tested for sensitization to encephalitogenic factor (EF) by the macrophage migration inhibition test. Sensitization to EF was demonstrated in 71% of patients with various forms of neoplastic disease. Sensitization to EF was also demonstrated for 31% of subjects with no evidence of neoplastic disease; these included patients with warts, chronic bronchitis and hernias. In contrast, healthy subjects showed no sensitization to myelin basic protein. These observations suggest that sensitization to EF may not be confined to patients with neoplastic disease. Lymphocytes from hamsters bearing a transplanted virus induced tumour were sensitized to EF prepared from both human and hamster brain. Sensitization was also seen in hamsters infected with influenza virus but not in animals with acute tubular necrosis produced by glycerol treatment. The development of an animal model system provides a method for the investigation of possible mechanisms of sensitization.
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PMID:Cellular immunity to myelin basic protein in man and in animal model systems as measured by the macrophage migration inhibition test. 5 Aug 55

This review concerns the present state of accomplishments in the study of SEM of human and experimental renal disease. Critical techniques of specimen preparation reviewed include perfusion fixation, razor tissue sectioning, alcohol cryofracture, microtome sectioning of paraffin or styrene embedded tissue, ultraplaning with glass knives of hard carbowax embedded tissues and glomerular isolation. Gold-palladium coating and heavy metal impregnation with osmium, uranium, and silver are discussed. A compendium of SEM observations of human glomerular, vascular and tubular disease is presented. Techniques for SEM of experimental renal disease are reviewed. These include latex vascular injection, freeze drying, x-ray microanalysis and use of backscattered electron imaging. Experimental models previously investigated by SEM are puromycin aminonucleoside nephrosis, daunomycin nephrosis, and N,N1-Diacetylbenzedine glomerulopathy, nephrotoxic serum nephritis, and protamine perfusion glomerulopathy. Reviewed are acute tubular necrosis caused either by angiotensin, hypotension, norepinephrine, glycerol, mercury, and unilateral renal artery occlusion, also potassium depletion nephropathy, alloxan diabetes and diphenylamine-induced polycystic disease.
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PMID:SEM of human and experimental renal disease. 52 33

Renal tubular function was evaluated in vitro by kidney slice uptakes of p-aminohippurate (PAH) and tetraethylammonium (TEA) at 24 and 48 h in water-drinking rats and at 24 h in chronic saline-loaded rats after induction of acute tubular necrosis (ATN) by HgCl2 and glycerol injection. Significant correlations between decrease tubular uptake of PAH and TEA and elevated serum creatinine levels were noted in both models of ATN in water- and saline-drinking rats. However, with the same degree of impairment of PAH and TEA uptakes the creatinine was significantly lower in saline-loaded rats than in water-drinking rats in both forms of ATN. The correlation between impaired tubular function and elevated creatinine suggests that tubular damage and glomerular filtration reduction might be pathophysiologically related in ATN.
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PMID:The role of tubular necrosis in the pathophysiology of acute renal failure. 94 Jun 26

Metabolic and morphologic changes occurred in the kidneys of rats within 3 hours after inciting acute tubular necrosis by completely clamping the renal blood supply, by intramuscular injections of glycerol, and by subcutaneous injections of HgC12. Although the initial trend was for p-aminohippurate and tetraethylammonium transport to decrease and for oxygen consumption, ammonia production, and gluconeogenesis to increase after glycerol, all of these parameters changed in opposite directions after renal pedicle clamping and after subcutaneous HgC12 (4.7 mg. per kg;). In addition, early morphologic changes in glycerol-injected rats differed from those seen with pedicle clamping and low dose HgC12. With high dose HgC12 (25 mg. per kg.), the metabolic and morphologic changes were somewhere in between those seen with the other insults. Coinciding with early metabolic and morphologic changes, cardiac output and renal blood flow decreased soon after the glycerol was given. On the basis of our findings, we cannot ascribe all of the early metabolic and morphologic changes in the glycerol model to ischemia, and we postulate that the circulating heme proteins may be nephrotoxic to ischemic renal tissue.
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PMID:Early events in various forms of experimental acute tubular necrosis in rats. 112 11

Male Sprague-Dawley rats, weighing 180-250 g and depleted with water for 16 h, were injected with glycerol (im) to induce acute tubular necrosis, and then divided into groups given blood-activating and stasis-removing drug, Hirudo solution (GH) tap water (GW), verapamil (GV) and none (GSDW) in incipient stage separately. It was observed that levels of BUN increased at 24th and 48th h after administration of glycerol and levels of Bcr increased at 3rd, 24th and 48th h after injecting glycerol in GH were significantly lower than those increased in GW and GSDW (P less than 0.05-P less than 0.001), but roughly similar to those in GV (P greater than 0.05-P greater than 0.5). Renal histopathological damage under light microscope and electron-microscope in GH at 3rd and 24th h after administration of glycerol were also less severe than those in GW and GSDW. The results suggested that Hirudo could exert a preventive and therapeutic effects on incipient acute tubular necrosis induced by glycerol in rats.
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PMID:[Preventive and therapeutic effects of hirudo on incipient acute tubular necrosis in rats]. 139 83

The effects of intramuscular glycerol on ischemic acute renal failure was investigated in dogs. Anesthetized dogs received a bilateral 120-min renal artery obstruction (RAO) alone, RAO plus 5 ml/kg of 50% glycerol or RAO plus 5 ml/kg of 75% glycerol. Control groups received the glycerol injection, but not RAO. Renal histopathology was minimal in dogs receiving glycerol alone. In RAO dogs, those receiving 50% glycerol showed diffuse acute tubular necrosis (ATN), while those receiving 75% glycerol had severe ATN with extreme mortality. Changes in serum creatinine, creatinine clearance, and fractional excretion of sodium were consistent with the histopathologic changes. We conclude that myoglobinuria, of a degree insufficient to cause renal failure itself, can interact with renal ischemia to significantly exacerbate the renal damage produced.
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PMID:Myoglobinuria exacerbates ischemic renal damage in the dog. 279 46

The present study was designed to evaluate the effect of acute fall in plasma osmolality in three models of acute tubular necrosis in rats: (a) glycerol, (b) arterial clamping and (c) mercuric chloride. Plasma osmolality was reduced by a water loading during a mild anaesthesia from 305 +/- 7 to 270 +/- 12 mosmol/kg of water (P less than 0.01). In the ischaemic models of acute tubular necrosis (glycerol and arterial clamping), during the first 24 h in rats with reduced plasma osmolality, the respective creatinine clearance rates (CCR), 0.04 +/- 0.02 and 0.06 +/- 0.04 ml/min, were strikingly lower than those in rats with normal osmolality, 0.21 +/- 0.03 and 0.26 +/- 0.06 ml/min (P less than 0.001) respectively. The control CCR were 0.65 +/- 0.07 and 0.62 +/- 0.07 ml/min respectively. During the second day after induction of ischaemic (glycerol and arterial clamping) acute tubular necrosis, rats with reduced plasma osmolality exhibited a similar worsening in CCR as on the first day, when compared with that in rats with normal osmolality. In rats with acute tubular necrosis induced with mercuric chloride reduction in plasma osmolality did not aggravate the severity of renal failure. These results show that acute fall in plasma osmolality worsens the renal failure in the ischaemic but not in the nephrotoxic models of acute tubular necrosis.
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PMID:The effect of acutely reduced plasma osmolality on acute renal failure in rats. 388 36

An animal model is described in which mild transitory renal impairment is induced with glycerol and the nephrotoxic effects of cephalosporin antibiotics and furosemide studied. Cephaloridine and cephalothin were found to produce extensive acute tubular necrosis in rats when given in subnephrotoxic doses in combination with furosemide; this damage occurred at serum antibiotic levels not much higher than those obtained in clinical practice. No significant renal damage was found with cephalexin or Cephapirin given in equivalent dosage. It is suggested that the cephalosporin antibiotics should be used with caution in the presence of even minor transient renal impairment and particularly if furosemide is being given concurrently.
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PMID:Relative nephrotoxicity of cephalosporin antibiotics in an animal model. 507 52

Acute tubular necrosis (ATN) is associated with hyperkalemia. We have shown that the medulla is the main site of impaired sodium (Na+)/potassium (K+) pump activity in ATN. CHIF, a gene that evokes K+ conductance in oocytes, is regulated in the colon by aldosterone and in the kidney by K+ intake. It is assumed that CHIF has a role in K+ homeostasis. To characterize the impaired K+ handling in ATN, the effect of impaired renal function on CHIF mRNA expression in the kidney and colon was studied. Three groups of rats with glycerol-induced ATN were studied: (1) control group, (2) moderate-ATN group, and (3) severe-ATN group. Serum creatinine levels in the control group were 45+/-2.1 micromol/L; in the moderate-ATN group, 224.8+/-16.9 micromol/L; and in the severe-ATN group, 376.5+/-15.9 micromol/L. In the group with severe ATN, significant hyperkalemia (P < 0.001 v control group) was noted. The expression of CHIF mRNA in relative units (percentage of control) in the moderate-ATN group, in the medulla, papilla, and colon, was 16.3%+/-5.6% (P < 0.001), 94.2%+/-9.3% (P=not significant ), and 165.9%+/-11.1% (P < 0.001); and in the severe-ATN group was 11.1%+/-6.4% (P < 0.001), 73.7%+/-4% (P < 0.001), and 310.8%+/-27.3% (P < 0.001), respectively. These results show that (1) in both moderate and severe ATN, CHIF mRNA is dramatically reduced in the medulla, (2) in severe ATN, CHIF mRNA expression decreases in the papilla, and (3) CHIF mRNA is upregulated in direct relationship to the severity of ATN and to the levels of aldosterone in the colon. These results suggest that the hyperkalemia that occurs in severe ATN stems at least in part from the downregulation of CHIF mRNA in the kidney medulla and papilla. The compensatory increase in colonic CHIF mRNA is not sufficient to maintain normal serum K+ levels.
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PMID:Role of down-regulated CHIF mRNA in the pathophysiology of hyperkalemia of acute tubular necrosis. 977 21

Melatonin, the pineal hormone with antioxidative properties was administered to rats with glycerol-induced myoglobinuric acute renal failure (Gly-ARF). This model is characterized by acute tubular necrosis mediated by heme-iron oxidative stress. Rats received melatonin (20 mg/kg) concomitant and 3 h after glycerol injection. Gly-ARF rats showed at 24 h a 78% reduction in glomerular filtration rate, whereas this decrement was significantly reduced to 35% in the melatonin treated Gly-ARF rats. Tubular function evaluated by tubular reabsorption of sodium and lithium was also preserved in melatonin treated rats. The histologic analysis revealed extensive cortical tubular necrosis that was significantly reduced by melatonin treatment. The renal concentration of malondialdehyde (MDA) was increased 6 h after glycerol injection in Gly-ARF and this elevation was prevented when melatonin was administered. Renal concentration of reduced glutathione (GSH) was decreased at 6 h in Gly-ARF and melatonin did not reverse this decrease. It was concluded that melatonin administration attenuated the renal injury in the glycerol model of acute renal failure and reduced kidney oxidative stress through a GSH-independent mechanism.
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PMID:Effects of melatonin administration to rats with glycerol-induced acute renal failure. 1247 96


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