nephrosis/seizures

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Congenital nephrotic syndrome presenting with cerebral venous thrombosis, hypocalcemia, and seizures in the neonatal period.

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Congenital nephrotic syndrome, a rare form of nephrosis, presents during the first year of life. We describe the case of a patient seen on the fifth day of life with seizures, hypocalcemia, hypothyroidism, and cerebral deep venous thromboses. Whereas these are generally long-term complications of

Non-ketotic hyperosmolar coma complicating steroid treatment in childhood nephrosis.

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Two nephrotic children treated with prednisone developed steroid-induced diabetes and non-ketotic hyperosmolar coma (NKHC). Both patients presented with convulsions, coma and shock. The glucose concentration of the cerebrospinal fluid was 425 mg/dl and 622 mg/dl, respectively. Both patients had no

Cerebral thrombosis in childhood nephrosis.

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Sinovenous thrombosis is an uncommon but serious complication associated with nephrotic syndrome in children. We describe a 9-year-old Caucasian boy who presented with dehydration, vague neurological symptoms and seizures. A diagnosis of nephrotic syndrome was made during the course of

Central neurotoxicity of cyclosporine in two children with nephrotic syndrome.

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The central neurotoxicity of cyclosporin A (CsA) has been abundantly documented in pediatric and adult recipients of bone marrow or organ transplants, with variations in the rate of occurrence from 0.5% to 35%. We report two cases of central neurotoxicity ascribable to CsA in children with nephrotic

Brain morphology in the Galloway syndrome.

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The Galloway syndrome is a rare autosomal recessive disease consisting of congenital microencephaly associated with congenital nephrotic syndrome, and in some cases with hiatus hernia [Galloway and Mowatt, 1968]. The case presented is that of a microencephalic infant with the nephrotic syndrome who

Ethylene glycol: an estimate of tolerable levels of exposure based on a review of animal and human data.

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Upon ingestion ethylene glycol (EG, monoethylene glycol) is rapidly absorbed from the gastrointestinal tract, and depending on the severity of exposure signs of toxicity may progress through three stages. Neurological effects characterize the first step consisting of central nervous depression

[Case report of a recurrent nephrotic syndrome patient with sudden onset of blindness during treatment with cyclosporin A].

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We report a case of recurrent nephrotic syndrome with transient blindness after taking cyclosporin A (CsA). Renal biopsy showed minimal change of nephrotic syndrome and the patient was treated with predonisolone (PSL) and cyclophosphamide leading to remission of nephrosis. CsA was given to the

A child with phenylketonuria and focal segmental glomerulosclerosis, the bright side of proteinuria.

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Phenylketonuria (PKU) is the most common inborn error of amino acid metabolism. Phenylalanine hydroxylase is the underlying deficient enzyme. If left untreated, growth failure, microcephaly, global developmental delay, seizures and severe intellectual impairment would characterize the clinical

Ammonia toxicity from urea in a Brazilian dairy goat flock.

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A flock of goats received a diet with 1% urea for at least 1 y. A new batch of concentrate was offered increasing the level of urea to 4.2%. Eighteen of 54 goats showed acute signs of ammonia toxicosis. Ten goats died within 60 min; 4 goats and a buck with convulsions recovered when treated by

Disease versus disease: how one disease may ameliorate another.

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Systemic disease, either genetic or acquired, may prevent or decrease the severity of another disease. These observations have led to important therapeutic advances. The best-known examples are Edward Jenner's use in 1798 of cowpox to prevent smallpox and J.B. Haldane's 1942 observation that

Acute lead arsenate poisoning in beef cattle in Uruguay.

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We describe and illustrate lesions in an outbreak of lead arsenate poisoning in beef cattle that ingested pesticide residues stored in an abandoned building of a former orange orchard. Of 70 exposed cattle, 14 had diarrhea, paresis, ataxia, recumbency, and/or seizures. Ten of the affected animals

NTP Toxicology and Carcinogenesis Studies of n-Butyl Chloride (CAS No. 109-69-3) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

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Toxicology and carcinogenesis studies of n-butyl chloride (greater than 99.5% pure), a solvent as well as an alkylating agent, were conducted by exposing groups of F344/N rats and B6C3F1 mice to n-butyl chloride in corn oil by gavage for 14 days, 13 weeks, and 2 years. In the 14-day studies, no

Toxicology of selected pesticides, drugs, and chemicals. Boric acid.

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With the advent of boric acid insecticides, accidental ingestion of the compound can be encountered in animals. Toxic levels of boric acid most commonly cause vomiting, depression, and, occasionally, diarrhea. Boric acid is, however, cytotoxic to all cells. If a sufficiently high level is ingested,

[Fatal complications in pre-eclampsia and eclampsia].

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OBJECTIVE Analysis of preeclampsia and eclampsia--one of the major contributor to life-threatening maternal morbidity frequently leading to maternal mortality in the Czech Republic till late 70's. Our goal was to mention major causal links in clinical courses of individual maternal death and to

The pathology of peracute experimental Clostridium perfringens type D enterotoxemia in sheep.

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The pathological findings in sheep with peracute experimental Clostridium perfringens type D enterotoxemia are described. Of 16 animals inoculated intraduodenally with a whole culture of this microorganism and a starch solution in the abomasum, 12 developed clinical signs including increased

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