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)

Seventy-seven children with chronic renal failure were examined at one hospital in the province of Quebec between 1970 and 1975; this represents an incidence of 2.5 per million population per year. The entities responsible for chronic renal failure were urinary tract malformation (in 36%), chronic glomerulonephritis (in 22%), congenital renal parenchymal malformation (in 21%) and hereditary nephropathy (in 13%). The evolution of chronic renal failure in children with either vesicoureteral reflux or a posterior urethral valve seemed to be related more to the initial severity of the disease than to the age at the time of diagnosis. Hence any screening program designed to detect kidney disease in schoolchildren would not prevent chronic renal failure, since at that age renal parenchymal damage seems to be irreversible. The manner in which chronic glomerulonephritis evolved depended on whether the nephrotic syndrome was present and on the type of histologic lesion. Children with congenital renal hypoplasia or dysplasia often presented with seizures due to hypertensive encephalopathy without obvious symptoms or signs of pre-existing renal disease. Among patients with familial nephropathy many of those with cystinosis underwent successful renal transplantation early in life.
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PMID:Chronic renal failure in children. 64 61

Two children, 1 with idiopathic nephrotic syndrome and 1 with endo-extracapillary glomerulonephritis, presented an episode of seizures and transient blindness at different times after i.v. pulse methylprednisolone (IVPMP) treatment. Neurological manifestations in patient 1 could be due to hypertension secondary to IVPMP, while the pathogenesis of such manifestations remained difficult to clarify in patient 2. The severity of uremia in patient 2 could be one of the conditions that, in association with the abrupt changes obtained with IVPMP, predispose to neurological manifestations. Careful clinical and biochemical monitoring seems necessary in children with primary glomerulonephritis, other than those transplanted, after IVPMP, and factors predisposing to neurologic sequelae should be further defined.
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PMID:Seizures and transient blindness following intravenous pulse methylprednisolone in children with primary glomerulonephritis. 186 81

A 3-year-old child with minimal change nephrotic syndrome (MCNS) developed an acute hypertensive encephalopathy characterized by coma, focal seizures, right hemiparesis, global aphasia and cortical blindness. Episodic hypertension and seizures persisted for 24 h despite intervention with antihypertensive and anticonvulsant therapy. Clinical suspicion of cortical blindness was confirmed by visual-evoked potential studies. CT scans performed 14 and 21 days after the acute episode demonstrated symmetric occipital white matter lucencies compatible with ischemia and/or associated edema. Hypertensive encephalopathy with cortical blindness and symmetric white matter hypodense lesions visualized on CT scan have recently also been described in eclampsia of pregnancy. This report documents an unusual acute hypertensive encephalopathy in childhood MCNS, unassociated with membranoproliferative glomerulonephritis, or progressive focal glomerulosclerosis.
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PMID:Acute hypertensive encephalopathy in minimal change nephrotic syndrome. 225 60

Two cases of idiopathic arterial calcification of infancy that occurred in sisters are reported. One patient died at age 14 months after a protracted course characterized by the nephrotic syndrome, blood chemistry abnormalities, hypertension, seizures, and a microangiopathic hemolytic anemia. Her sister died at age 3 weeks after a precipitous illness that initially was misinterpreted at autopsy as Reye's syndrome.
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PMID:Idiopathic arterial calcification of infancy with unusual clinical presentations in sisters. 321 7

Chlorambucil (CHL) was used in combination with prednisolone in the treatment of nine children with frequently relapsing nephrotic syndrome. Serial electroencephalograms were obtained to evaluate CHL central nervous toxicity, before, during and after treatment with this agent. EEG abnormalities were observed in two of the nine children during chlorambucil therapy. EEG changes were diffuse spike and wave complexes and disappeared after discontinuation of therapy. There were no other neurological abnormalities and more particularly, no seizures or myocloni were observed. According to the literature, chlorambucil central nervous toxicity is found almost exclusively in childhood nephrotic syndrome. Strict neurological supervision of patients treated with chlorambucil is recommended.
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PMID:Chlorambucil central nervous toxicity: a significant side effect of chlorambucil therapy in childhood nephrotic syndrome. 405 70

In a sibship of four, Friedreich's ataxia and minimal lesion nephrotic syndrome occurred in two siblings, a third sibling had Friedreich's ataxia, but no evidence of nephrotic syndrome; the fourth sibling had neither condition. The chance of Freidreich's ataxia and minimal lesion nephrotic syndrome occurring in two siblings is small, and suggested a common immunological abnormality. High dose prednisone and antimetabolites given for the nephrotic syndrome did not appear to affect the course of Friedreich's ataxia. The two siblings with Friedrich's ataxia and nephrotic syndrome developed epilepsy at age 15 years. All three children with Friedreich's ataxia had abnormal electroencephalograms (EEGs). These epileptiform EEG abnormalities were probably inherited from the mother, who had spike wave epilepsy. The neurologic deficits of Friedreich's ataxia, in turn, may have allowed the EEG trait to be expressed as a seizure disorder. The progressive ataxia and epileptic, sometimes myoclonic, seizures in these patients and the dentate nucleus changes in the autopsied patient were consistent with the diagnosis of dyssynergia cerebellaris myoclonica. This suggested that the latter disorder may represent a coincidence of two genetic entities: Friedreich's ataxia and spike wave epilepsy.
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PMID:Friedreich's ataxia with nephrotic syndrome and convulsive disorder: clinical and neurophysiological studies with renal and nerve biopsies and an autopsy. 722 58

Chlorambucil neurotoxicity was observed in two children treated for frequently relapsing minimal change nephrotic syndrome. In the first child the drug was overdosed. Myoclonic jerks were observed, followed by a generalized tonic-clonic seizure. Concomitant EEG abnormalities disappeared after discontinuation of therapy, but reappeared 6 months later without further seizures. In the second child chlorambucil treatment was started twice, but had to be interrupted each time; the first time because of sudden collapse, bradycardia and respiratory arrest, and the second time because of myoclonic jerks. EEG changes were limited to generalized slowing and improved after discontinuation of therapy. According to the literature chlorambucil neurotoxicity is found almost exclusively in children, after overdosage or in the nephrotic syndrome. Strict neurologic supervision of patients treated with this drug is recommended.
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PMID:Chlorambucil neurotoxicity: report of two cases. 741 Jan 14

A 23-year-old woman, who had nonbullous congenital ichthyosiform erythroderma since her childhood, was diagnosed as nephrotic syndrome caused by systemic lupus erythematosus (SLE). She was pregnant but experienced fetal loss at the age of 25. Although 10 mg/day of oral prednisolone was administered, low levels of serum complement, proteinuria, thrombocytopenia (6.0 x 10(4)/mm3) and biological false positive for STS continued. When she was 27 years old, right hemichorea developed. She was admitted to our hospital at the age of 28 because of low levels of serum complement, high titers of anti ds-DNA antibody, profuse proteinuria, gingival bleeding and thrombocytopenia (1.5 x 10(4)/mm3). The nephrotic syndrome gradually improved after 1 g/day of methylprednisolone for 2 days and the oral prednisolone dosage was then increased up to 40 mg/day, and was tapered to 10 mg/day. Epileptic attack (minor seizure) occurred at the age of 29. Continuous low levels of serum complement and high titers of anti ds-DNA antibody were improved by adding 50 mg/day of cyclophosphamide. However, high levels of beta 2 GPI dependent anticardiolipin antibody and lupus anticoagulant activity were observed throughout the study. Our patient was a very rare case of congenital ichthyosis with typical antiphospholipid antibody syndrome and SLE. A few cases of acquired ichthyosis associated with SLE has been reported, and ichthyosis developed only in active stage of SLE. However, our patient's ichthyosiform lesions were not changed throughout the course.
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PMID:[Systemic lupus erythematosus and antiphospholipid antibody syndrome in a patient with congenital ichthyosiform erythroderma]. 748 67

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The syndrome of inappropriate secretion of antidiuretic hormone. 861 39

A 14-year-old girl with sickle cell disease and nephrotic syndrome developed bone pain, followed by pulmonary edema, seizures, coma, and bilateral flaccid paralysis. Fat embolism syndrome was diagnosed by cranial magnetic resonance imaging and an exchange transfusion was performed. Within 3 months, all symptoms had resolved. It is concluded that fat embolism syndrome must be considered as a possible cause of acute neurologic deterioration in patients with sickle cell anemia.
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PMID:Nontraumatic fat embolism syndrome in sickle cell anemia. 774 67


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