Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute renal failure secondary to interstitial nephritis caused by therapeutic ingestion of sodium diphenylhydantoins has been reported recently. The interference of sodium diphenylhydantoins on Vitamin D metabolism causing or aggravating ricketts has also been reported. This communication deals with an infant girl who was admitted to the hospital due to seizures. Four months before, she had convulsions and she was treated with diphenylhydantoins until admission. She was found to have renal failure and ricketts. Histological diagnosis of interstitial nephritis was established by means of percutaneous renal biopsy. Clinical and radiological improvement of ricketts was observed after dehydrotachysterol treatment. Clinical and biochemical alterations of renal failure slowly subsided. She had a clear-cut history of vitamin D defficiency ricketts. Seizures were due to hypocalcemia tetany but was erroneusly treated as "grand mal" epilepsy, with diphenylhydantoins. Interstitial nephritis complicated with acute renal failure was probably caused by diphenylhydantoins administration.
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PMID:[Renal failure and rickets]. 46 92

An 81-year-old woman had chills, fever, nausea, vomiting, and epigastric pain. On day 3 she had hematuria and was treated with trimethoprim-sulfamethoxazole. On day 5 she had a cough, hypotension, anemia, azotemia, and elevated hepatic enzyme levels. Her condition deteriorated with thrombocytopenia, anuria requiring dialysis, edema, and hypoalbuminemia. Treatment with chloramphenicol and doxycycline was started on day 10. By day 11, she was in hypotensive shock; on day 12 she had seizures and died. Murine typhus was diagnosed by demonstration of antibodies to Rickettsia typhi by indirect immunofluorescence. Necropsy revealed interstitial pneumonia, pulmonary edema, hyaline membranes, alveolar hemorrhages, petechiae and vasculitis in the central nervous system, interstitial myocarditis, multifocal interstitial nephritis and hemorrhages, splenomegaly, portal triaditis, and mucosal hemorrhages in urinary tract. Immunofluorescent R. typhi were demonstrated in the lungs, brain, kidneys, liver, and heart. This unusual death occurred in an elderly patient without rash who was treated too late with antirickettsial drugs.
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PMID:Histopathology and immunohistologic demonstration of the distribution of Rickettsia typhi in fatal murine typhus. 249 81

A 5-year-old Chinese girl had had absence seizures and received sodium valproate (VPA) treatment which provided good control. Six months later, she developed interstitial nephritis with proteinuria and microhematuria. Renal biopsy revealed interstitial nephritis with granular deposition of immunoglobulin G (IgG) and C3 in the renal tubular basement membrane (TBM). Ultrastructurally, dilated smooth endoreticular cisternae with mitochondrial degeneration in the tubular cells and scattered electron-dense deposits within the TBM were also noted. Serum circulating immune complexes were detectable, ACH50 and properdin factor B increased. Mononuclear cells (MNC) from the patient after in vitro incubation with VPA (100 micrograms/ml) induced interleukin-2 (IL-2) production and lymphoproliferative response. However, there was no response in controls. The serum VPA level ranged from 84 to 92 micrograms/ml. After VPA was stopped, the microhematuria and proteinuria disappeared. These observations indicate that VPA-induced interstitial nephritis represents a sequence of interrelationships among multiple immunologic factors.
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PMID:Sodium-valproate-induced interstitial nephritis. 312 10

Male Fischer rats received daily intraperitoneal injections of cyclosporine (IV preparation containing CsA + cremophor) diluted in NaCl or in NaCl + cremophor. At the dose of 100 mg and 50 mg/kg/day the animals developed seizures, motor weakness and died at 4-7 days. Light microscopy at 7 days in these rats showed diffuse vacuolization of all segments of the proximal tubules which was very extensive in the outer stripe. At the dose of 25 mg and 15 mg/kg/day animals were free of symptoms and were sacrificed at day 15 for functional and histological studies. Light and electron microscopy showed cytoplasmic vacuolization in all segments of the proximal tubules. Crystal structures were observed in the experimental animals as well as in the control group that received cremophor + NaCl. The CsA blood levels were at the range of 134-236 ng/ml. Reduction of the glomerular filtration rate was observed in experimental animals as compared with the controls. We concluded that CsA is not the cause of an interstitial nephritis in the Fischer rats and that CsA is nephrotoxic to all segments of the proximal tubules. The cremophor is the cause of the crystal structures seen in the proximal tubules.
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PMID:Cyclosporine nephrotoxicity in the Fischer rat. 370 42

A severely handicapped 14-year-old Japanese girl had epilepsy and was treated with sodium valproate (SV) from the age of 7 years. Although the epileptic seizures were well controlled, she sometimes had a fever and hypokalemia from the age of 13 years. Laboratory examinations revealed metabolic acidosis, hypouricemia, hypophosphatemia, glycosuria, proteinuria and aminoaciduria, thus suggesting Fanconi syndrome. Gallium scanning showed marked renal uptake. A renal biopsy revealed interstitial nephritis without immuno-deposition. SV was replaced since it was considered to be the most probable cause of the renal involvement. Thereafter, she showed marked improvement of the clinical symptoms and the laboratory data gradually, and she never had a fever. Although SV is an effective anti-epileptic drug, we have to pay attention to adverse renal effects such as Fanconi syndrome and interstitial nephritis.
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PMID:Tubulo-interstitial nephritis caused by sodium valproate. 1189 Nov 2

The number of medications used to treat different types of seizures has increased over the last 10-15 years. Most of the newer antiepileptic drugs (AEDs) are likely to be unfamiliar to many nephrologists. For both the older and newer AEDs, basic pharmacokinetic information, recommendations for drug dosing in patients with reduced kidney function or who are on dialysis, and adverse renal and fluid-electrolyte effects are reviewed. Newer AEDs are less likely to have significant drug-drug interactions than older agents, but are more likely to need dosage adjustment in patients with reduced kidney function. The most common renal toxicities of these drugs include metabolic acidosis, hyponatremia, and nephrolithiasis; interstitial nephritis and other adverse effects are less common. Little is known about the clearance of most of the newer AEDs with high-efficiency hemodialyzers or with peritoneal dialysis. Monitoring of drug levels when available, careful clinical assessment of patients taking AEDs, and close collaboration with neurologists is essential to the management of patients taking AEDs.
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PMID:Use of antiepileptic drugs in patients with kidney disease. 1697 Jul 41

A 56 year old aromatherapist presented with advanced renal failure following chronic coal tar creosote vapour inhalation, and a chronic tubulo-interstitial nephritis was identified on renal biopsy. Following dialysis dependence occult inhalation continued, resulting in seizures, ataxia, cognitive impairment and marked generalised cerebral atrophy. We describe for the first time a case of creosote abuse by chronic vapour inhalation, resulting in significant morbidity. Use of the polycyclic aromatic hydrocarbon-containing wood preservative coal tar creosote is restricted by many countries due to concerns over environmental contamination and carcinogenicity. This case demonstrates additional toxicities not previously reported with coal tar creosote, and emphasizes the health risks of polycyclic aromatic hydrocarbon exposure.
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PMID:Coal tar creosote abuse by vapour inhalation presenting with renal impairment and neurotoxicity: a case report. 1789 38

We report what we believe to be the first two cases of acute interstitial nephritis associated with vancomycin and ceftriaxone therapy in adults. A 40-year-old man with a medical history of traumatic brain injury and tonic-clonic seizure disorder was admitted to the hospital with a seizure episode and temperature of 103 degrees F. He was administered ceftriaxone, vancomycin, and acyclovir for suspected bacterial and/or viral meningitis. On day 4, the patient was noted to have diffuse erythematous plaques on the neck, chest, arms, abdomen, and back, as well as an elevated serum creatinine level of 3.1 mg/dl (baseline 0.9 mg/dl) and an elevated eosinophil count (6%). Dermatology and renal consultations were obtained, and a diagnosis of suspected acute interstitial nephritis was made. After a 3-day course of antibiotic treatment (day 4 of hospitalization), all antibiotics were discontinued and topical triamcinolone 0.1% ointment and hydrocortisone 2.5% cream were begun for the rash. The patient was discharged 5 days later with improvement in the rash, serum creatinine level (1.0 mg/dl), and eosinophil count (0.9%). A 59-year-old woman with a medical history of diabetes mellitus was admitted to the hospital with a serum creatinine level of 3.7 mg/dl, eosinophil count of 8.4%, and fractional excretion of sodium of 2.94%. The patient had been receiving treatment with vancomycin and ceftriaxone for osteomyelitis for 28 days before this hospital admission. Her baseline serum creatinine level (before antibiotic therapy) was 1.0 mg/dl. Renal consultation was obtained, and a diagnosis of probable acute interstitial nephritis was made. Ceftriaxone and vancomycin were discontinued, and her serum creatinine level gradually decreased to 3.3 mg/dl and then further to 1.5 mg/dl over the next 3 months. Use of the Naranjo adverse drug reaction probability scale revealed that the adverse reaction was possible in the first case and probable in the second case. Health care professionals need to be cognizant that drug-induced acute interstitial nephritis can be associated with concomitant administration of ceftriaxone and vancomycin therapy. Early detection of this rare adverse reaction is paramount in order to prevent acute renal insufficiency.
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PMID:Acute interstitial nephritis associated with coadministration of vancomycin and ceftriaxone: case series and review of the literature. 1789 1

A 17-year-old girl who had started on levetiracetam because of new onset partial complex seizures developed acute renal failure and biopsy-confirmed interstitial nephritis 10 days after starting the drug. She made a complete and rapid recovery after discontinuation of levetiracetam and administration of oral corticosteroids. Levetiracetam, known to be predominantly excreted by the kidneys, has not previously been reported to cause significant renal complications in children. Children taking levetiracetam who present with abdominal pain, malaise, vomiting, oliguria, rash, or urticaria may require screening laboratory evaluation for potential renal adverse effects.
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PMID:Levetiracetam induced interstitial nephritis and renal failure. 1952 Feb 78

A 45-year-old man with a new diagnosis of low grade glioma was started on an escalating dose of levetiracetam (Lev) for seizure management. He gradually developed intractable nausea/vomiting and a high creatinine concentration due to acute renal failure which was attributed to Lev-induced interstitial nephritis. The medication was changed and his renal function rapidly improved to his baseline.
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PMID:Levetiracetam-induced interstitial nephritis in a patient with glioma. 2207 60


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