The statural growth of 85 patients with steroid-responsive idiopathic nephrotic syndrome, attending the Pediatric Nephrology Unit, Children's Institute, Hospital das Clínicas School of Medicine, University of São Paulo, with a minimum follow-up of 3 years, was evaluated. Analysis of the patient population as a group did not show any significant alterations in the height Z score and the mean height percentile between the first (-0.59 and 33.9, respectively) and last consultation (-0.57 and 34.8, respectively). Analysis of each individual patient allowed the definition of two subgroups. Subgroup A, which achieved growth improvement, was composed of 47 children-initial Z score and mean initial height percentile of -0.91 and 24.0, respectively; final Z score and mean height percentile of -0.30 and 40.7, respectively ( P=0.00). Subgroup B, which showed growth retardation, was composed of 38 children-initial Z score and mean initial height percentile of -0.19 and 46.2, respectively; final Z score and mean height percentile of -0,9 and 27.5, respectively ( P=0.00). The following factors were significantly different when both subgroups were compared: (1) total duration of prednisone therapy and total prednisone dose were greater in subgroup B; (2) the final chronological age of patients using prednisone was higher in subgroup B; (3) the pubertal growth spurt in subgroup B showed attenuation and retardation.

Objective: To review the various mechanisms of glucocorticoid action and the ability of these agents to induce osteoporosis and growth deficits. Sources:A review of the scientific literature was conducted on the basis of a MEDLINE search using the keywords and descriptors "glucocorticoids," "bone mineralization," "growth," and "side effects" and limited to articles published in the last decade. The references cited by these articles were used to identify relevant older publications, with an emphasis on landmark studies essential to an understanding of the topic. Summary of the findings:Emphasis was placed on the actions of glucocorticoids on the hormones and cytokines that modulate linear growth. The end effects of glucocorticoids on the skeletal system are the result of systemic effects on bone metabolism and of direct actions on bone cells, which alter bone cell counts and predispose to bone loss. The mechanisms underlying catch-up growth and bone mass recovery after discontinuation of glucocorticoid treatment are discussed, followed by a review of diagnostic methods available for assessment of bone metabolism and mineralization and of measures for prevention and management of glucocorticoid-induced bone changes. Conclusion:Patient monitoring on a case-by-case basis plays an essential role in detection and, potentially, reversal of the damage associated with chronic glucocorticoid therapy. J Pediatr (Rio J). 2011;87(1):4-12:Glucocorticoids, steroids, growth, bone mineralization, growth retardation, child growth, children, adolescents, densitometry, bone mineral density, bone mineralization markers, bone. ResumoObjetivo: Revisar os mecanismos de ações dos glicocorticoides e sua capacidade de induzir osteoporose e déficits de crescimento. Fontes dos dados:A revisão bibliográfica de artigos científicos foi realizada na base de dados MEDLINE e utilizou as palavras-chave agrupadas nas sintaxes "glicocorticoides", "mineralização óssea", "crescimento" e "efeitos colaterais", nos últimos 10 anos, e das referências destes nos reportamos para as publicações mais antigas, mas com os estudos fundamentais para a compreensão do assunto. Síntese dos dados:Destacam-se ações dos glicocorticoides sobre hormônios e citocinas responsáveis pelo crescimento longitudinal. Os efeitos finais dos glicocorticoides sobre o esqueleto são determinados por ações sistêmicas no metabolismo ósseo e por ações diretas desses esteroides nas células ósseas, levando a mudanças no número e função das mesmas e favorecendo a perda óssea. Discutem-se os mecanismos indutores da recuperação dos canais de crescimento e recuperação da massa óssea após a descontinuação dos glicocorticoides; os métodos diagnósticos do metabolismo e mineralização óssea; assim como medidas terapêuticas e preventivas das alterações óssea induzidas pelos glicocorticoides.Conclusão: A monitorização de cada paciente é essencial para identificação e potencial reversão dos danos associados ao uso crônico de glicocorticoides. J Pediatr (Rio J). 2011;87(1):4-12:Glicocorticoide...

The aim of this study was to evaluate the final stature of adults with childhood-onset steroid-responsive idiopathic nephrotic syndrome (INS) and the influence of disease-related issues on the achievement of their target heights. We analyzed 60 (41 male) patients and/or their records, with a minimum age of 19 years or at a Tanner's pubertal stage 4 for boys or status postmenarche for girls, and normal glomerular filtration rate. Mean age at first and last consultation was 5.3+/-2.4 years and 20.5+/-3.1 years, respectively. Mean follow-up period was 15.10 years. Mean cumulative dose of prednisone was 1254+/-831.40 mg/kg. Mean initial and final height Z scores (HtZ) were, respectively, -0.60+/-1.0 and -0.64+/-0.92 (p=0.72). The final HtZ showed a significant correlation only with the initial HtZ and the target HtZ (THZ). Six patients achieved a final HtZ below -2, which in male patients correlated strongly to the initial HtZ and THZ. A strong correlation was demonstrated between final HtZ, initial HtZ, and THZ. INS-related issues did not prevent the final stature to reach the predicted target height.

IntroduçãoAs doenças renais, por terem repercussões crô-nicas, se revestem de importância clínica e econômica, sendo por isso, um problema de saúde pública. Dessa forma, todos os fatores que predispõem a uma diminuição ou perda da função renal, mesmo que indiretamente, devem ser investigados, possibilitando a prevenção e/ou a correta intervenção terapêutica. Neste contexto, a disfunção do trato urinário inferior, que indica um padrão miccional anormal gerando a perda da capacidade coordenada de armazenamento e eliminação de urina, ocupa um lugar de destaque, pois pode lesar o trato urinário superior gerando cicatrizes ou atrofias do parênquima renal 1,2 .A disfunção do trato urinário inferior, por ser uma desordem funcional, nem sempre é evidente e o diagnóstico pode não ser feito caso não haja um grande nível de suspeição, muitas vezes só sendo detectada após lesões renais irreversíveis. A dificuldade de abordagem dos pacientes com disfunção do trato urinário inferior fomentou o desenvolvimento de instrumentos de aferição 3,4,5 , com intuito de detectar potenciais portadores desta e estabelecer critérios universalmente aceitos, que possam ser aplicados em diferentes países, culturas, idiomas e faixas etárias. Entretanto foram desenvolvidos em países de língua inglesa, muitas vezes apenas traduzidos do original para a língua portugue-ARTIGO ARTICLE

Some infections can be the cause of secondary nephrotic syndrome. The aim of this study was to describe the experience of a Renal Disease Reference Clinic from Central Brazil, in which serological markers of some infectious agents are systematically screened in children with nephrotic syndrome. Data were obtained from the assessment of medical files of all children under fifteen years of age, who matched nephrotic syndrome criteria. Subjects were tested for IgG and IgM antibodies against T. gondii and cytomegalovirus; antibodies against Herpes simplex, hepatitis C virus and HIV; and surface antigen (HBsAg) of hepatitis B virus. The VDRL test was also performed. 169 cases were studied. The median age on the first visit was 44 months and 103 (60.9%) patients were male. Anti-CMV IgG and IgM were found in 70.4% and 4.1%, respectively. IgG and IgM against Toxoplasma gondii were present in 32.5% and 5.3%, respectively. Two patients were positive for HBsAg, but none showed markers for HIV, hepatitis C, or Treponema pallidum. IgG and IgM against herpes simplex virus were performed on 54 patients, of which 48.1% and 22.2% were positive. IgM antibodies in some children with clinical signs of recent infection suggest that these diseases may play a role in the genesis of nephrotic syndrome.