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

Male adult Sprague-Dawley rats were treated for 14 days with either rapamycin (RAP, 1.5 mg/kg/d i.p.) in carboxymethylcellulose (RAP/CMC) or polyethyleneglycol (RAP/PEG), cyclosporine (CsA, 15 mg/kg/d by gavage) or with the appropriate drug vehicles. Biochemical indices of renal function and integrity were determined throughout the experimental period, at the end of which the rats were killed and kidneys examined histologically. All animals gained weight at a similar rate to untreated animals except those treated with RAP; RAP/PEG animals were lighter on day 14 compared with day 0 values, whilst RAP/CMC animals were lighter only in comparison with CMC-only controls on day 14. Significant increases in urinary flow rate (UFR) were found in each drug treatment group. RAP/CMC, RAP/PEG and CsA caused mild renal functional impairment, but only with CsA was there a significant reduction in 51Cr-EDTA clearance. Significant enzymuria, resulting from drug but not vehicle administration, was observed only in the CsA-treatment group. Increased plasma and urinary glucose levels, elevated in all drug-treatment groups, were related to increased UFR. Kidneys of RAP-treated rats appeared normal, whereas mild, focal, acute tubular necrosis was evident in all CsA-tested animals. Pancreases of all drug-treated animals were histologically normal.
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PMID:The effect of rapamycin on renal function in the rat: a comparative study with cyclosporine. 168 33

A dog with oliguric acute renal failure presumed to have been caused by ethylene glycol ingestion was treated by hemodialysis for 1 month. Hemodialysis was effective in controlling azotemia, hyperphosphatemia, and hyperkalemia when performed on a daily or alternate-day basis. The major complications during treatment were infection and severe weight loss. Serial renal biopsies disclosed a progression from initial acute tubular necrosis to severe diffuse interstitial fibrosis and mononuclear cell inflammation. Infection, cachexia, development of end-stage renal lesions, and terminal hyperkalemia contributed to the eventual death of the dog.
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PMID:Hemodialysis of a dog with acute renal failure. 401 97

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

A young man presented to the emergency department with mental status changes, severe metabolic acidosis, and oliguria. Acute ethylene glycol intoxication was diagnosed. The patient suffered clinical brain death three days after admission despite intensive care and continuous hemodiafiltration. The patient died one month after admission. Autopsy revealed acute tubular necrosis of the kidneys with significant calcium oxalate depositions. The brain was markedly softening and with chronic meningoencephalitis and dural sinus thrombosis. We considered that the amount and the persistence of the calcium oxalate deposition in the kidney may afford a best clue to the postmortem diagnosis of ethylene glycol poisoning even in the chronic stage.
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PMID:Brain death with calcium oxalate deposition in the kidney: clue to the diagnosis of ethylene glycol poisoning. 1769 92

Calcium oxalate (CaOx) crystal deposition within the tubules is often a perplexing finding on renal biopsy of both native and transplanted kidneys. Understanding the underlying causes may help diagnosis and future management. The most frequent cause of CaOx crystal deposition within the kidney is hyperoxaluria. When this is seen in native kidney biopsy, primary hyperoxaluria must be considered and investigated further with biochemical and genetic tests. Secondary hyperoxaluria, for example due to enteric hyperoxaluria following bariatric surgery, ingested ethylene glycol or vitamin C overdose may also cause CaOx deposition in native kidneys. CaOx deposition is a frequent finding in renal transplant biopsy, often as a consequence of acute tubular necrosis and is associated with poorer long-term graft outcomes. CaOx crystal deposition in the renal transplant may also be secondary to any of the causes associated with this phenotype in the native kidney. The pathophysiology underlying CaOx deposition is complex but this histological phenotype may indicate serious underlying pathology and should always warrant further investigation.
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PMID:Calcium oxalate crystal deposition in the kidney: identification, causes and consequences. 3271 90