Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A significant increase in S-urate was found postictally in 17 patients with two or more grand mal seizures within 24 h. In six patients S-urate was above the level at which hyperuricemic renal failure may develop. Impaired renal function was observed in two patients who had extremely high S-urates. It is proposed that prophylactic procedures against hyperuricemic renal failure should be carried out in all patients with repetitive convulsions.
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PMID:Grand mal-provoked hyperuricemia. 10 41

A case of fatal viscerotropic Rocky Mountain spotted fever with virtual absence of cutaneous lesions was diagnosed at autopsy by specific immunofluorescent demonstration of Rickettsia rickettsii in spleen, kidney, epididymis and skin. The clinical presentation was that of insidious onset of fever, renal failure, hypotension, hyponatremia and obtundation over a 10 day period. The patient had respiratory insufficiency, hypocalcemia, increases in creatinine phosphokinase (CPK), serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), lactic dehydrogenase (LDH), alkaline phosphatase, billirubin and serum phosphate, grand mal seizure, myalgia and unremitting shock with death occurring on day 12 of illness. Postmortem examination revealed severe vasculitis with interstitial nephritis and multifocal tubular necrosis, pericholangitis with bile stasis, glial nodules in the brain, multifocal rhabdomyonecrosis, interstitial pneumonitis and mild interstitial myocarditis. Risk factors which this patient shared with other patients with fatal Rocky Mountain spotted fever were failure to recognize a rash, failure to obtain a tick bite history, male sex, black race and age greater than 30 years.
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PMID:Fatal viscerotropic Rocky Mountain spotted fever. Report of a case diagnosed by immunofluorescence. 34 5

Phenylbutazone is a potent nonsteroidal, anti-inflammatory drug often used by veterinarians to treat racetrack animals. Its use in human beings is limited because of significant adverse effects and the availability of newer, safer drugs. We report the case of a 24-year-old man who ingested 17 g of equine phenylbutazone over a 24-hour period to treat the pain of a toothache. He developed grand mal seizures, coma, hypotension, respiratory and renal failure, and hepatic injury. Serum phenylbutazone concentration obtained approximately eight hours after presentation was 900 micrograms/mL. The patient recovered during six weeks of intensive supportive care and repeated hemodialysis.
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PMID:Poisoning with equine phenylbutazone in a racetrack worker. 199 8

Although neurological signs and symptoms are well described in leptospiral infections, cerebral edema has not been reported previously. We have encountered two patients with severe leptospiral infection, associated with multisystem involvement, who developed cerebral edema. Both patients were in acute oligoanuric renal failure, one being treated by acetate hemodialysis and the other by hemofiltration. Grand mal seizures developed in both patients, followed by respiratory, then cardiac arrest, as a consequence of dialytic therapy. Only one patient could be resuscitated and he was left with a hemiparesis. Cerebral edema may develop in patients with severe leptospiral infections consequent to treatments used in the management of renal failure.
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PMID:Morbidity and mortality due to cerebral edema complicating the treatment of severe leptospiral infection. 238 55

A male with an atypical adrenomyeloneuropathy is described, who developed spastic paraparesis at the age of 37. Because his gait deteriorated further and he had a bladder dysfunction, he was admitted to National Sanatorium Hyogo Central Hospital at the age of 51. A diagnosis of adrenomyeloneuropathy was supported by increased level of very long chain fatty acids in plasma. He became demented and suffered from grand mal seizures during the last one year of his life. CT scan showed symmetrical hypodense lesions in the centrum semiovale. He died of pneumonia and renal failure at the age of 53. Autopsy revealed symmetrical degeneration throughout the corticospinal tracts from cerebral white matter to lumbar spinal cord. Degeneration of the optic radiation, posterior half of the corpus callosum, thalamus, cerebellar white matter, and gracile tract in high cervical segments were also observed. In these area, there was a loss of myelin and axon with marked gliosis and foamy macrophages, as well as mild perivascular cuffing. In our case, symmetrical and well-defined lesion in cerebral white matter is atypical for adrenomyeloneuropathy, while destruction of the gracile tracts is not a feature of adrenoleukodystrophy. In addition, well-demarcated "pseudosystemic" type of fiber tract degeneration appears to be different from a feature of primary demyelination which has been considered to be an essential alteration of adrenoleukomyeloneuropathy-complex. We propose another hypothesis, therefore, that neurons are primarily altered, thereby leading to the degeneration of myelins in this disease.
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PMID:[A case of adrenomyeloneuropathy with localized cerebral white matter degeneration]. 261 1

Twenty-two patients who had been bitten by a Russell's viper were studied. Neurological manifestations and generalized myalgia were observed, respectively, in 86.4% and 72.7%. Renal failure did not occur in three patients who received antivenin within 5 hours of the bite, and it is suggested that administration of antivenin within the first few hours following the bite could prevent renal failure. Of 19 patients who were in acute renal failure, seven responded to conservative management while 12 needed peritoneal dialysis. Nine patients developed pulmonary edema and four had grand mal seizures. Five patients died. Autopsy revealed massive pulmonary edema, thought to be the immediate cause of death, in four of them and extensive cortical and tubular necrosis in three.
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PMID:Russell's viper bite in Sri Lanka. A study of 22 cases. 673 82

Three cases of generalized seizures in patients with high cerebrospinal fluid (CSF) concentrations of cefazolin are reported. Patient 1, a 60-year-old woman with impaired renal function and a Klebsiella pneumoniae infection, was treated with 70 mg every eight hours of i.v. gentamicin sulfate and 1.5 g every four hours of i.v. cefazolin sodium. Gentamicin was discontinued on day 11. On day 12, the patient had a generalized tonic-clonic seizure. Serum and CSF concentrations of cefazolin one day later were 470 and 64 micrograms/ml, respectively. Patient 2, a 70-year-old man with impaired renal function, was given i.v. cefazolin, 1 g every 12 hours; the dosage interval was shortened later to every six hours. Two days later, the patient had two tonic-clonic seizures. Serum and CSF concentrations eight hours after the last dose of cefazolin were 360 and 34 micrograms/ml, respectively. Patient 3, a 67-year-old woman with renal vein thrombosis, received 55 mg every eight hours of i.v. gentamicin and 2 g every six hours of i.v. cefazolin. The antibiotics were discontinued after eight days when the patient had two tonic-clonic seizures. Serum and CSF concentrations of cefazolin measured 28 hours later were 1000 and 106 micrograms/ml, respectively. Previous reports of cefazolin-associated seizures are reviewed. In patients with renal failure, cefazolin may obtain high CSF concentrations. To avoid seizures, cefazolin doses should be adjusted in these patients.
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PMID:Seizures associated with high cerebrospinal fluid concentrations of cefazolin. 736 4

Meperidine is a widely prescribed opioid analgesic used in a variety of clinical situations. The parent compound has central nervous system depressant effects. However, the sole active metabolite, normeperidine, is a central nervous system excitatory agent and has the ability to cause seizures, especially in patients with renal failure. Patients with normal renal function rarely manifest seizure activity when given meperidine, but if the drug is used in large doses at frequent dosing intervals, seizures may occur. Reported here is the case of a man with normal renal function who had a tonic-clonic seizure due to meperidine that was administered for the pain of underlying chronic pancreatitis.
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PMID:Meperidine-induced generalized seizures with normal renal function. 916 82

Normeperidine, a major metabolite of meperidine, is half as potent as meperidine as an analgesic but two to three times more potent as a convulsant. Renal failure significantly increases the plasma half-life of normeperidine. The intensity of the central nervous system excitation is highly correlated with the plasma concentration of normeperidine. Moreover, normeperidine toxicity is not reversed by naloxone, which may exacerbate it. We report a patient with end-stage renal disease undergoing maintenance continuous cycler peritoneal dialysis who had been receiving meperidine for pain control. The patient subsequently developed myoclonic contractions and a grand mal seizure. The patient was successfully treated with hemodialysis (using an F8 dialyzer) for presumed normeperidine-induced seizure. During hemodialysis, normeperidine average blood clearance was 73 mL/min, average plasma clearance was 50 mL/min, and average percentage of plasma extraction was 24%. There also was a 26% reduction in plasma concentration of normeperidine over 3 hours of hemodialysis. In conclusion, our findings suggest that hemodialysis may be used effectively for treating patients with suspected normeperidine-induced neurotoxicity.
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PMID:Successful treatment of normeperidine neurotoxicity by hemodialysis. 1062 May 57

In 1986 Andermann et al. described a syndrome presenting with renal failure, myoclonus, cerebellar symptoms, and epilepsy. They presumed a hereditary cause. We describe the first appearance of this syndrome in Europe, affecting three family members with comparable symptoms. Two of these patients were treated by us, and the third, already decreased, is described according to the available reports. The first clinical symptoms were manifested between the ages of 14 and 20. A female patient suffered from compensated kidney insufficiency and her two brothers aged 18 and 26 required dialysis. Biopsy of kidney tissue revealed nonspecific nephritis. All cases showed a cerebellar syndrome and action myoclonus. Two of them were diagnosed with epilepsy and grand mal seizures, and all suffered from demyelinizing or mixed polyneuropathy. Anamnesis of the family seems to indicate autosomal recessive inheritance.
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PMID:[Familial myoclonus-renal failure syndrome]. 1151 6


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