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)

Djenkolic acid was extracted from djenkol beans with 70% ethanol and water and was quantitatively determined by paper chromatography. Djenkol beans contained 0.3-1.3 gm% djenkolic acid and about 93% of this acid occurred in the free state. The toxicity of djenkol beans was studied in 5 rhesus monkeys, 9 albino rats and 22 mice fed with 70% ethanol extracts. The total urinary output decreased. There was an increase in specific gravity of the urine during the period of feeding monkeys with djenkol beans. Urinary samples of the experimental animals were turbid and contained some red cells, white cells, epithelial cells, albumin and amorphous particles. One of 22 mice excreted sharp needle-shaped crystals in the urine on day 3 after feeding. Histological examination of kidneys of rats and mice showed mild to severe acute tubular necrosis with some glomerular cell necrosis.
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PMID:Studies on djenkol bean poisoning (djenkolism) in experimental animals. 82 79

Techniques applied in SEM studies of a solid organ such as the kidney are reviewed. The tissue can be prepared by razor sectioning, ethanol cryofracture and ultraplanning of polyethylene glycol embedded tissue. Tissues embedded in paraffin can also be used. Glomeruli and tubuli can be isolated from renal biopsies. A new procedure for tubular isolation is based on sequential digestion by trypsin, pepsin and Pronase E. SEM examination has proved useful in a number of renal diseases, such as glomerular diseases, hypertensive renal disease, an tubular diseases, including medullary cystic disease, adult polycystic disease, and acute tubular necrosis. Particularly in human acute tubular necrosis, SEM was helpful. SEM has also contributed to the study of the physiologically important basal-lateral surfaces of human, dog, rat, rabbit and frog renal tubules, and in particular allowed the elucidation of patterns of processes on the basal-lateral surfaces of proximal S1, S2, and S3 tubular segments, thin limbs, distal ascending and convoluted limbs and collecting ducts in human tubules.
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PMID:The complementary role of scanning electron microscopy in renal pathological diagnosis. 641 8

Due to a combination of ingested ethanol and inhaled trichloroethylene (Tri) a 28 year old man developed toxic hepatitis and acute oliguric renal failure, both of which had a favorable evolution. Tri has been described as a cause of hepatic disfunction and acute renal failure due to acute tubular necrosis, although some of the cases described are controversial, because Tri was either contaminated by other dissolvents or could not be proven pure, with the exception of one case. In many there was ethanol ingestion. The Tri inhaled by our patient was found to contain less than 1% of carbon tetrachloride (C-Tchl). This would suggest the C-Tchl to be responsible for the clinical picture although the combination Tri/ethanol cannot be discarded as the causal agent, due to the small amount of contaminant present.
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PMID:[Toxic hepatitis and acute renal failure after inhalation of chloride solvents: report of one case (author's transl)]. 732 30

Acute nephrotoxicity due to nonsteroidal anti-inflammatory drugs is usually observed in clinical situations in which renal perfusion is compromised as in volume contraction. We report a case of a 20 year-old woman who suffered from acute tubular necrosis after concomitant ingestion of nonsteroidal anti-inflammatory drugs and binge drinking. This acute tubular necrosis is likely to have an hemodynamic origin due to nonsteroidal anti-inflammatory drugs in a patient with volume contraction secondary to binge drinking. The risk appears to be even more important since ethanol has been implicated in tubular necrosis by direct toxicity. This observation underlines the danger in associating nonsteroidal anti-inflammatory drugs and ethanol.
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PMID:[Tubular necrosis after non-steroidal anti-inflammatory agents and acute alcoholic intoxication]. 929 32

A 38-year old man presented with drowsiness 14 hours after ingesting about 1200 mls (40 ounces) of antifreeze in a suicide attempt. He was successfully treated with an ethanol enriched, bicarbonate based-dialysate. With a concomitant peripheral intravenous infusion of ethanol, this enrichment of the dialysate helped maintain the intradialytic ethanol concentration between 97-135 mg/dl over an 8 hour dialysis session. The patient developed acute tubular necrosis and required further dialysis. He made a complete recovery after three weeks and was discharged with a serum creatinine of 1.4 mg/dl.
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PMID:Survival after massive ethylene glycol poisoning: role of an ethanol enriched, bicarbonate-based dialysate. 1061 1

Ethylene glycol intoxication is a rare but dangerous type of poisoning. It causes a severe acidosis with high anion and osmolal gaps. Clinical manifestations of the ethylene glycol intoxication can be divided in three phases: a neurologic stage, with hallucinations, stupor and coma; the second stage is cardiovascular with cardiac failure. Renal failure characterizes the third stage, due to acute tubular necrosis. After aggressive gastric emptying, the main treatment is ethanol or 4-methypyrazole, which can be given either orally or intravenous, with supportive measures for all symptoms or diseased organ.
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PMID:Diagnosis and treatment of an unusual cause of metabolic acidosis: ethylene glycol poisoning. 1103 83

Poisonings with industrial products represent approximately 7% of the cases reported to the poison centres. Ingestion of petroleum distillates induces irritation of the gastrointestinal tract, central nervous system depression and aspiration pneumonitis which may be severe; treatment is mainly supportive. Ethylene and diethylene glycol poisonings produce central nervous system depression, anion gap metabolic acidosis, osmolar gap and acute tubular necrosis; in severe cases, hypocalcaemia, cerebral oedema and heart failure may be observed; treatment often associates supportive measures, haemodialysis and administration of competitive inhibitors of alcohol dehydrogenase (ethanol or 4-methylpyrazole). Glycol ethers induce central nervous system depression and metabolic acidosis; in addition, ethylene glycol monobutyl ether produces haemolysis; monomethyl and monoethyl ethers are responsible for bone marrow and lymphoid organ toxicity, they adversely affect spermatogenesis and are teratogens.
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PMID:[Acute poisoning with industrial products]. 1074 68

Recent clinical and experimental studies have demonstrated that the habitual consumption of large amounts of ethanol has deleterious effects on the kidney. A variety of tubular defects have been described in patients with chronic alcoholism. Evidence is emerging that tubular dysfunction has an important pathophysiological role in a wide range of electrolyte and acid-base disturbances commonly observed in these patients, and possibly in alcohol-induced bone disease. These renal abnormalities are often reversible, disappearing with abstinence. However, since 1990 a few cases of a syndrome of acute tubular necrosis due to binge drinking of ethanol in the absence of other evident nephrotoxic mechanisms, or in association with the use of nonsteroidal anti-inflammatory drugs, have been reported. A link between glomerulonephritis and alcoholism has become evident. IgA nephropathy has been demonstrated at autopsy in 64% of chronic alcoholics and, more recently, the association between alcoholism and postinfectious glomerulonephritis has been described. Structural and functional abnormalities of the kidney are reported with increasing frequency in the fetal alcohol syndrome seen in children who have been prenatally exposed to ethanol. In addition, over the last few years experimental studies in vitro or in animal models have provided information about the biochemical and molecular basis of alcohol-induced injury to kidney. It is hoped that future experimental and clinical research will provide us with a more comprehensive knowledge of the mechanisms of renal damage in alcohol misuse.
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PMID:Alcohol misuse and renal damage. 1289 83

Calcineurin inhibitors exacerbate ischemic injury in transplanted kidneys, but it is not known if sirolimus protects or exacerbates the transplanted kidney from ischemic injury. We determined the effects of sirolimus alone or in combination with cyclosporin A (CsA) on oxygenated and hypoxic/reoxygenated rat proximal tubules in the following in vitro groups containing 6-9 rats per group: sirolimus (10, 50, 100, 250, 500, and 1000 nanog/mL); CsA (100 microg/mL); sirolimus (50 and 250 nanog/mL) + CsA (100 microg/mL); control; vehicle (20% ethanol). For in vivo studies, 3-week-old Wistar rats (150-250 g) were submitted to left nephrectomy and 30-min renal artery clamping. Renal function and histological evaluation were performed 24 h and 7 days after ischemia (I) in five groups: sham, I, I + SRL (3 mg x kg(-1) x day(-1), po), I + CsA (3 mg x kg(-1) x day(-1), sc), I + SRL + CsA. Sirolimus did not injure oxygenated or hypoxic/reoxygenated proximal tubules and did not potentiate the tubular toxic effects of CsA. Neither drug affected the glomerular filtration rate (GFR) at 24 h. GFR was reduced in CsA-treated rats on day 7 (0.5 +/- 0.1 mL/min) but not in rats receiving sirolimus + CsA (0.8 +/- 0.1 mL/min) despite the reduction in renal blood flow (3.9 +/- 0.5 mL/min). Acute tubular necrosis regeneration was similar for all groups. Sirolimus alone was not toxic and did not enhance hypoxia/reoxygenation injury or CsA toxicity to proximal tubules. Despite its hemodynamic effects, sirolimus protected post-ischemic kidneys against CsA toxicity.
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PMID:Effects of sirolimus alone or in combination with cyclosporine A on renal ischemia/reperfusion injury. 2054 36

Renal cortical necrosis (RCN) is a rare cause of acute kidney injury secondary to ischemic necrosis of the renal cortex. Acute tubular necrosis after binge drinking is usually attributed to volume depletion, idiosyncratic reaction to alcohol, rhabdomyolysis or a combination with non-steroidal anti-inflammatory drugs. Binge drinking itself as a cause of RCN has not yet been reported. We report a case of a 25-year-old Asian male who developed bilateral RCN following binge drinking.
Alcohol Alcohol
PMID:Bilateral renal cortical necrosis following binge drinking. 2221 4


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