Biomedical subjects
Publications and source records attributed to A Bensman.
2 brothers with identical HLA antigens presented an idiopathic membranous glomerulonephritis. This is, to our knowledge, the first report of familial membranous glomerulonephritis. The fact that both brothers had identical HLA antigens suggests a genetic predisposing background.
A hemolytic-uremic syndrome is reported in a 9 month-old girl. It was remarkable because of the severity of the renal lesions, which ended in terminal renal failure; there were also neurologic changes, responsible for a coma of 3 month-duration and for right-sided hemiplegia. Two CT scan examinations showed a left hemispherical hypodensity, resulting from a largely extended infarction in the sylvian area. After a 3 year's follow-up, the magnitude of the clinical improvement shows the possibility of neurologic recovery in children.
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Based on a personal series of 310 observations, the authors have studied the presenting signs, the etiology, the urinary bacteriology and the localization of the stone in children with urolithiasis. Urinary tract infection is the presenting sign in 55% of the cases, hematuria in 23% and abdominal pain in 20%. Urinary malformation is associated in 26% of cases, whatever the age at diagnosis. The urinary bacteria found in 55% of cases is Proteus. Localization was in the kidney in 228 cases, in the ureter in 71 cases, the bladder in 45 cases and in the urethra in 5 cases.
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Previous reports concerning children with Cockayne syndrome had described decreased T cell proliferative responses and renal anomalies which could be associated with immunologic disturbances. Herein, the thymic function was evaluated by measuring the serum level of thymic hormone. This serum level was found to be undetectable or decreased in seven cases of Cockayne syndrome. Active serum concentrations varied between 0 and 1/8, whereas normal children of the same age show activity in the range between 1/16 and 1/64. In contrast, T cell function, explored by phytohemagglutinin and Concavalin A responses, and mixed lymphocyte cultures was normal. Whether or not this premature sign of immunological aging is primary or secondary to other manifestations of the syndrome is still difficult to assess.
A 2-year-old boy with familial extramembranous glomerulonephritis was unfortunately treated with corticosteroids (1 to 0.5 mg/kg/day) and Chlorambucil (cumulative dose: 2.5 g) over a period of 7 years. Three years later, after recovery from the renal affection, he developed fatty diarrhoea from exocrine pancreatic deficiency, followed 5 years later by the onset of diabetes with hypochlorhydric gastritis. The diagnosis of non-calcifying chronic pancreatitis was suggested by scintigraphic and ultrasonographic investigations and confirmed by the marked increase in lactoferrin levels and the lactoferrin/lipase ratio (greater 0.1 p. cent) in pancreatic juice. The etiology was more likely to be direct toxicity of corticoids and/or immunosuppressors on the pancreas than an immunologically-mediated disease.
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A massive haemothorax occurring acutely during haemodialysis in a child of 8 1/2 years is reported. The pleural effusion occurred synchronously with a round, dense shadow in the parenchyma similar to an intra-pulmonary haematoma. The density became bullous in six weeks and disappeared in three months. The suggested cause of this haemothorax is a pulmonary embolism whose site of origin was the arteriovenous fistula. This would have been responsible for the adjacent pleural and parenchymal haemorrhage in the lung. The heparin given intravenously at the beginning of the haemodialysis session probably contributed to the size of the haemorrhage.
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In 14 children with nephrotic syndrome the mean blood zinc level (10.6 +/- 2.2 micromol/l) was found to be significantly lower than that of 113 control children (24.7 +/- 7.3 micromol/l). The blood albumin/zinc ratio was also lower in nephrotic children (1.80 +/- 0.57) than in healthy children (2.87 +/- 0.49). There was no correlation between blood albumin and blood zinc levels. The abnormally low zinc levels are partly due to deficient zinc uptake and may explain some of the disorders described in children with persistent nephrotic syndrome.
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Experimental models of urinary tract infection caused by a group D Streptococcus sp. in rabbits are described: retrograde pyelonephritis was induced by injecting 10(9) group D streptococci into the renal pelvis and obstructing the ureter by ligature for 24 h; cystitis was induced by injecting 5.10(9) group D streptococci through a transurethral catheter. The animals were observed for 3 months. Microbiological data from the urine and from the renal parenchyma were well correlated in 12 of 14 animals. A hemagglutination test for titration of serum antibodies in these infected rabbits is described. Before the beginning of experimentation, hemagglutination titers for all animals were below 160. During experimentation, titers for rabbits with cystitis were always below 640; in those with pyelonephritis, the highest titer was much greater than 640. These results show a positive correlation between serum antibody levels and the localization of urinary tract infection.
The assay of humoral antibodies during urinary tract infections of children is performed by passive haemagglutination. In gram negative bacilli infections (176 children) the antigens are derived from the patients' bacteria. For streptococcus D infections the antigen is a phenol extract, specifically tested and used for all streptococcus D urinary tract infections (40 children). The humoral antibodies assay is of first interest to distinguish between high urinary tract infections with renal parenchym bacterial involvement and low urinary tract infections. In high urinary tract infections the antibodies are significantly elevated and almost surely indicate renal infection for a 1/2 560 titre; they raise both in gram negative bacteria and in streptococcus D infections. There is however a difference in a rather higher number of cases of streptococcus D infections where it is impossible of connect high sera titres and clinical symptoms of pyelonephritis, contrary to gram negative bacilli infections. It seems to be due to aetiological differences in urinary tract infections by streptococcus D, which are more often secondary infections, during severe urologic diseases. In such cases the symptomatology of infections is less typical than in E. Coli urinary tract infections. Another interest is the capacity of survey by this method. Three kinds of courses of antibody titres are observed: the first is a clean break of titre lower than 1/160 after three months; the second is the continuance of the same high levels over three months; the third is continuance of high significative level after a first incomplete fall. In the last two cases it is highly probable that a pyelonephritis processes is engaged. This may be useful for treatment and survey of children with urologic diseases.
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Forty infants with a uropathy diagnosed during the first two months of life were studied. Presenting signs were urinary tract infection in one-half of the cases, disorders of micturition, pelvic or abdominal wall malformations, abdomino-pelvic mass, and macroscopic hematuria. Obstructive uropathy was observed in 17 children and vesicoureteric reflux in 29. We noted a high incidence of extrarenal malformations (14 of the 40 cases) in this series of uropathies diagnosed during the neonatal period. Despite early diagnosis, the course was not favorable in 11 cases with congenital anomalies of the renal parenchyma.
Urine specimens from 88 children with urinary tract infections were tested by direct immunofluorescence for the presence of antibody coated bacteria and were positive. They were further tested to determine the classes of antibody complexed with the bacteria: 75% were coated with IgA, 62% with IgG and 9% with IgM. In 47 children, C1q, C3 and C4 coated bacteria were also studied: negative results were found in 30 children and positive in 17. The ACB test may be positive without any IgG present; therefore it must be used a antihuman globulin and not only a antihuman IgG.