SUMMARY One hundred and fourteen children with primary nephrotic syndrome were followed up prospectively for periods of between 5 and 14 years. Urine samples from 94 of them became proteinfree during the initial 8-week course of prednisone, and the outcome for these children was good: 74 of them have been free of symptoms for at least 3 years, 18 have had relapses during the last 3 years, and only one child still has proteinuria. All these children have normal renal function and blood pressure. One child died accidentally. Twenty children did not respond to the initial prednisone treatment. Thirteen of them had remissions later, of whom 2 have had relapses during the last 3 years. Seven were totally resistant to prednisone 4 of whom died in renal failure, the remaining 3 have persistent proteinuria with normal levels of creatinine; one has high blood pressure too. Remission during the initial treatment indicated a good prognosis, but two-thirds of the initial non-responders also fared well.

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252 infants and children were followed for 2 years after their first urinary tract infection. Each symptomatic infection was determined by simple laboratory examinations as upper pyelonephritic or lower urinary tract infection. I.v. urography was done at the beginning of the follow-up and 2 years later; micturating cystourethrography was taken after the third infection at the latest. Urological abnormalities were found in 26 patients (10%), and 12 subjects (5%) developed renal scars during the study. Patients, who had their first upper urinary tract infection before the age of 12 months, numbered 93, and 19 of them had urological abnormalities and 10 scars. Two renal scars occurred among the 71 subjects with their first pyelonephritic infection after the age of 12 months. No renal injury was detected in the 88 infants and children with lower symptomatic urinary tract infection or asymptomatic bacteriuria. The determination of the level of the infection may be a useful aid in detecting the harmful scar-forming urinary tract infections. Infants with a pyelonephritic infection are at high risk, and in need of an early urological evaluation.

The scientific literature concerning alcohol intoxication is enormous. However, less is known of alcohol-induced disturbances in children and adolescents and most of those reports concern cases of hypoglycemia in children under five years of age. We studied the clinical status and chemistry, especially acid-base balance, in 36 young teenagers treated at hospital for alcohol intoxication. On physical examination 6 patients were somnolent, 18 were comatose and 12 were in deep coma. The impairment of consciousness was directly proportional to the blood ethanol concentration. Acidosis was a central finding, and it was caused by a combination of respiratory and metabolic factors (a high blood PCO2 and a low base excess; r = 0.97, p < 0.001); the finding of respiratory acidosis dominated. Base excess correlated negatively with beta-hydroxybutyrate and lactate, as expected. All the metabolic products measured--acetate, beta-hydroxybutyrate and lactate--were significantly elevated compared with the control patients. No hypoglycemia was found. Prior treatment with intravenous glucose decreased vomiting and normalized the serum lactate concentration and PO2. Hypokalemia was the most common abnormality in serum electrolytes. In four patients the rate of fall of blood ethanol concentration was 2.8-3.3 mmol/h (0.13-0.15 g/l-1 h-1) and the mean acetate concentration was 0.8 mmol/l (SE 0.3). Biochemical disturbances in young teenage alcohol intoxicants resemble those previously found in adults. The severe toxicity by ethanol, manifesting in coma, occurs in lower blood alcohol concentrations in children than in adults.

In diagnosing urinary tract infection (UTI) the symptoms of 477 infants and children and the findings in their clean-voided urine specimens were evaluated. 322 patients were considered infected, when a bacterial culture of suprapubic aspirate was used as a diagnostic reference. No diagnosis was attempted on the basis of symptoms only. Numerous bacteria or greater than or equal to 200 leuc./mm3 in an uncentrifuged clean-voided urine specimen or greater than or equal to 10(5) bact./ml in quantitative bacterial culture were found in 59%, 42% and 81% of the infected symptomatic patients. The diagnostic accuracies of these indices were 88%, 94% and 95%, respectively. In asymptomatic patients the accuracies were considerably lower. Among these infected patients normal or equivocal isolated findings in the clean-voided urine specimens were frequently seen, and could not markedly be reduced by the various related factors, such as technique of urine collection, urine specific gravity or pH of urine. None of the above mentioned indices of the clean-voided urine specimens seems to be alone accurate and sensitive enough for diagnosing UTI, and therefore these should be used in combination. The advantage of immediately obtaining results supports the use of urine microscopy as a primary diagnostic method in symptomatic UTI of childhood in particular.

Cases of alcohol intoxication in children are common; they are encountered every day in Finland. Studies other than case studies of alcohol intoxication in children are few. Metabolic acidosis was a frequent finding in juvenile alcohol intoxication. Capillary or arterial blood pH was below normal (less than 7.36) in 61.4% of patients and bicarbonate (less than 22) in 55.3% of patients. pCO2 was varied; the higher the blood alcohol concentration the higher the pCO2. Metabolic acidosis and blood pH correlated with the blood alcohol concentration and consciousness. The lower the blood pH the higher the serum glucose. Hypoglycemia is the most common reported symptom in children under 5 years of age. In the present study three patients were slightly hypoglycemic. Hypokalemia was the most important change (in 12.2%) in serum electrolytes. Alcohol intoxication causes metabolic acidosis and respiratory depression in children. Metabolic acidosis reduces consciousness.

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