Consecutive renal biopsies were performed on native kidneys in 109 children and adolescents, aged 0.1-19.8 (mean 9.9) years (119 biopsies). Bleeding diatheses were excluded or treated pre-operatively with intravenous desmopressin acetate. Biopsies were performed by a radiologist under ultrasound imaging, using an automated spring-loaded device allowing selection of the length of the needle movement and score size. Diagnostically adequate tissue was retrieved in 118 of 119 (99.2%) biopsy procedures; 24-h post-biopsy ultrasonography disclosed a small haematoma of the biopsied kidney in 26% of the cases. No correlation was seen between the occurrence of haematoma and (treated) prolonged bleeding time or a decrease in the haemoglobin level. No major complications occurred. Newly developed macroscopic haematuria was reported by 7% and micturition pain by 7% of patients. Painful body movements were reported by 37%. We conclude that the use of ultrasound imaging and an automated gunshot technique is a safe and efficient method for performing renal biopsies in paediatric patients.

Reduced glomerular filtration rate (GFR), not due to hypovolemia, has been reported in patients in the proteinuric phase of the minimal change nephrotic syndrome (MCNS). A group of children with MCNS was studied to investigate the possible relationship between the fusion of glomerular epithelial foot processes and the reduction in GFR. The degree of foot process fusion was estimated as the harmonic true mean of foot process width and the length density of epithelial slit pores as determined by quantitative electron microscopic stereology. In the patients investigated GFR ranged between 40 and 127 ml/min/1.73 m2 body surface area, the filtration fraction between 6.9 and 22.5%, and the serum albumin concentration between 14 and 46 g/liter. The mean foot process width, which varied between 330 and 870 nm, showed a close correlation with GFR (r = -0.859) and the filtration fraction (r = -0.812), as well as with the serum albumin concentration (r = -0.756). As expected, a reduction of epithelial slit pore length occurred concomitant with the broadening of the foot processes. These results agree with the hypothesis that the reduction in the total length of glomerular epithelial slit pores, due to the fusion of foot processes, results in a reduced glomerular capillary permeability to water and small solutes.

Coreceptor use was determined for human immunodeficiency virus type 1 (HIV-1) isolates of various subtypes from 11 women during pregnancy and their infected children. Isolates from peripheral blood mononuclear cells (n=79) and from plasma (n=59) were available. The clinical and immunological stages of HIV-1 infection were recorded. Coreceptor use was tested on human cell lines expressing CD4 and different chemokine receptors. The R5 virus predominated, and only 9 isolates from 2 mothers used CXC chemokine receptor 4. All children carried the R5 virus at the time of diagnosis of HIV-1 infection. In 2 children of mothers carrying the X4 virus, the virus switched from R5 to X4 or to R5X4 by age 18 months (child no. 9) and age 48 months (child no. 10), whereas no children followed up to a similar age whose mothers were carrying the R5 virus experienced such a switch (P=.048). This points to a link between the presence of X4 virus in the mother and the emergence of X4 virus in her child.

This article describes the characteristics of children infected vertically with HIV surviving 10 years or more who were enrolled in the prospective European Collaborative Study. Thirty-four of 187 infected children were identified with a median age of 11.4 years (range, 10.1-15.9 years). Factors examined included clinical status, immunologic and virologic characteristics, type of antiretroviral therapy, and psychosocial characteristics. By 10 years of age, 6 (18%) children had progressed to Class A as determined by the system of the U.S. Centers for Disease Control and Prevention (CDC), 17 (52%) to class B, 7 (21%) to class C, and 3 (9%) had remained asymptomatic. At 73% (904 of 1234) of scheduled clinic visits, these children had no symptoms of HIV disease. Most children were in CDC immune categories 1 (18, 56%) or 2 (11, 34%) at their last visit. Three quarters (24 patients) were on combination therapy with three or more drugs, although 3 children had never received any antiretroviral therapy. Nineteen (56%) children were living with at least 1 parent and the mothers of 13 (38%) children had died. Most (77%) children had been told about their HIV infection. Children infected vertically with HIV who have survived their first 10 years are mainly free of serious symptoms. As they enter adolescence, additional services are needed including support with disclosure to others, therapy, and sexual health.

Previously, we found that emergence of the X4 viral phenotype in HIV-1-infected children was related to the presence of X4 in their mothers (C.H. Casper et al., J Infect Dis 2002; 186:914-921). Here, we investigated the origin of the X4 phenotype in the child, analyzing two mother-child pairs (Ma-Ca, Mb-Cb) where the mothers carried X4 and their children developed X4 after an initial presence of R5. We used nested polymerase chain reaction of the env V3 region to generate 203 HIV-1 clones for sequencing (Ma, n = 44; Ca, n = 73; Mb, n = 61; Cb, n = 25) from DNA of peripheral blood mononuclear cell (PBMC) lysates, altogether 167 clones, or from cDNA of plasma RNA, 36 clones. PBMC and plasma isolate sequences from each time point enabled us to assign the probable phenotype to clone sequences in a phylogenetic tree. The transmission and evolution were reconstructed using the maximum likelihood method. In mother-child pair Ma-Ca, one maternal R5 isolate clustered with the child's R5 sequences, at the earliest time when R5 was isolated in the child, confirming this as a likely source of the transmitted R5 phenotype. At age 3, an X4 population was present in the child that had evolved from the child's own R5-associated population, clearly distinct from the maternal X4 sequences. The second mother-child pair (Mb-Cb) displayed a similar pattern. Amino acid substitution patterns corroborated the conclusions from the phylogenetic tree. Thus, in both children, the X4 virus developed from their own R5 population, and was not caused by transmission of X4.