[Severe Amanita phalloides poisoning in a 7-year-old girl]. / Tezká otrava muchomurkou hlízovitou u sedmileté dívky.

Authors describe a case of a very severe poisoning, the prothrombin-time was less than 10% of the normal value and the child developed hepatic coma. We suppose, the favourable outcome may have been influenced by the treatment with Silymarin in combination with high doses of G-Penicillin.

[Acute interstitial nephritis with uveitis in children and adolescents]. / Akutní intersticiální nefritida s uveitidou u detí a mladistvých.

Acute non-suppurative tubulointerstitial nephritis was recorded within a five-month interval in 1988 in one girl and two boys aged 15, 16 and 12 years. The common feature was non-selective proteinuria, slight glycosuria, anaemia, a sedimentation rate of more than 100 mm/2 hrs hyperatotaemia not calling for dialyzation treatment (268, 354 and 266 mumol/l plasma creatinine resp.), a markedly impaired concentrating capacity (540, 593 and 520 mOsm/kg urine resp.). In all patients circulating serum immunocomplexes were elevated (PEG-IKEM). One patient developed acute uveitis at the onset of the disease, the remainder after 5 and 6 months resp. and in all there was a tendency of a protracted course and relapses resp. In two patients uveitis was diagnosed by an aimed examination by means of a slit lamp at a time when there were not yet any clear signs of affection of the eyes. All patients were subjected to percutaneous renal biopsy which revealed an interstitium with uneven lymphoplasmacytic cellulization with infrequent eosinophil and neutrophil polynuclear cells. Electron microscopy revealed sections of varying size with fibrotization of the tubular basal membrane; the glomerular changes were not typical. All patients had prednisone treatment and their renal functions were gradually restored. Despite extensive serological examinations, the aetiology was not cleared, however before the onset of the disease the patients had penicillin, cotrimoxazol and erythromycin resp.

[Familial hematuria and Alport's syndrome]. / Familiární hematurie a Alportuv syndrom.

In their review the authors discuss the history of Alport's syndrome, its nomenclature, incidence, genetics, clinical diagnosis. The authors emphasize electron microscopic findings and criteria of the diagnosis (haematuria or renal failure in the family, progressive nervous deafness, typical changes of the basal glomerular membrane (GBM) and ophtalmological findings of lenticonus or perimacular spots. Familial haematuria (FH) is according to the authors defined as haematuria in several members of the family. Based on data in the literature and the authors' experience, the authors discuss the differential diagnosis of FH where Alport's syndrome is relatively rare. A far more frequent unit is benign familial haematuria characterized morphologically as isolated thinning of the GBM. In some cases these patients are threatened by iatrogenic damage from unnecessary and invasive diagnostic method. The finding of thinned GBM and normal renal function in the parents and grandparents suggest a favourable prognosis also in child patients. Cases of familial glomerulonephritis or idiopathic syndrome with glomerulosclerosis or familial IgA nephropathies are relatively rare. Familial haematuria is are relatively rare. Familial haematuria is relatively frequent (according to the authors 20% of all obscure haematurias) and their diagnosis is based on systematic examination of the urine in other members of the patient's family who also suffer from haematuria.

Relation between the chemical structure and acute toxicity of 1-phenyl-3-methyltriazenes as activated metabolites during the carcinogenic action of 1-phenyl-3,3-dimethyltriazenes.

The mol LD50 values were correlated with Hammett sigma constants in terms of the Hansen empiric equation 6 for para substituted derivatives of 1-phenyl-3-methyltriazene. Good agreement was achieved and the line slope of the correlation, 0.3, is the same as that found during an identical experiment with derivatives of 1-phenyl-3,3-dimethyltriazene [1]. This is an indirect evidence that the considered mechanism of the interaction with biological substrate goes through the "activated carcinogen" - derivatives of 1-phenyl-3-methyltriazene, formed through the oxidative N-demethylation of the initial 1-phenyl-3,3-dimethyltriazenes.