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We have examined, in a randomized crossover trial, the antiproteinuric effect of treatment with low- (0.2 mg/kg daily) and high-dose (0.6 mg/kg daily) enalapril in 25 consecutive patients with steroid-resistant nephrotic syndrome (SRNS). Patients in group A ( n=11) received enalapril at low doses for 8 weeks, followed by 2 weeks of washout and then at high doses for 8 weeks. Those in group B ( n=14) initially received enalapril at high and then low doses. Patients continued to receive treatment with tapering doses of prednisolone; none received concomitant therapy with daily oral or intravenous steroids, alkylating agents, cyclosporine, non-steroidal anti-inflammatory drugs, and other antihypertensive medications. The urine albumin-to-creatinine (Ua/Uc) ratio and the percentage reduction were determined for each phase of therapy. Baseline clinical, biochemical, and histological features were comparable in the two groups. In the first phase, treatment with low-dose enalapril (group A) resulted in median 34.8% Ua/Uc reduction compared with 62.9% with high doses (group B) ( P<0.01). High-dose enalapril was associated with a significant reduction in Ua/Uc ratio in both groups. The combined median Ua/Uc (95% confidence interval) reduction in the low-dose phase was 33% (-10.3% to 72.4%) and in the high-dose 52% (15.4%-70.4%) ( P<0.05). The median Ua/Uc ratio at the end of 20 weeks was 1.1 and 1.8 in groups A and B, respectively ( P>0.05). Systolic and diastolic blood pressure reductions were similar in both groups. No period or carry-over effect was found. Prolonged treatment with enalapril thus resulted in a dose-related reduction in nephrotic-range proteinuria. Titration of the dose of enalapril may be a useful strategy for achieving substantial reduction of proteinuria in children with SRNS.
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http://dx.doi.org/10.1007/s00467-003-1314-y | DOI Listing |
Indian J Nephrol
August 2024
Holy Family College of Nursing, Delhi University, New Delhi, India.
Background: Nephrotic syndrome (NS) is relapsing-remitting illness affecting children and characterized by proteinuria, edema, and hypoalbuminemia. The disease involves the significant formative years of a child's life and profoundly impacts their physical and psychosocial well-being. There is a scarcity of literature exploring the quality of life (QoL) of children with NS and the factors influencing them.
View Article and Find Full Text PDFItal J Pediatr
March 2025
Department of Pediatrics, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, 221002, China.
Background: Glucocorticoid (GC) response heterogeneity has been recognized as an unfavorable prognostic factor, yet the underlying mechanism remains elusive. In this study, we endeavored to investigate the potential causes from an epigenetic perspective.
Methods: The protein expression levels of the glucocorticoid receptor (GR), acetylated GC receptor (Ac-GR), acetylated histone3 (Ac-H3), histone4 (Ac-H4), and the activity of nuclear factor-κB (NF-κB) were quantified in the peripheral blood lymphocytes of patients exhibiting diverse GC responses.
Aim: Steroid-resistant nephrotic syndrome (SRNS) in children is a common acquired cause of kidney failure. The treatment practices vary widely. With this web-based survey, we aim to report common medication and follow-up practices by pediatric nephrologists in the USA who treat children with SRNS.
View Article and Find Full Text PDFPediatr Nephrol
March 2025
Department of Pediatric Gastroenterology, Nephrology and Metabolic Diseases, Charité Universitätsmedizin, Berlin, Berlin, Germany.
Background: Steroid-resistant nephrotic syndrome (SRNS) is the second leading cause of chronic kidney disease (CKD) in childhood. It represents a heterogeneous group of diseases with variable kidney outcomes that are still challenging to predict. In this study, our main objective is to describe predictive factors of remission states and kidney survival comparing genetic and non-genetic SRNS.
View Article and Find Full Text PDFInt J Mol Sci
February 2025
Federal State Autonomous Institution "National Medical Research Center of Children's Health" of the Ministry of Health of the Russian Federation, 119991 Moscow, Russia.
Schimke immuno-osseous dysplasia (SIOD) is a hereditary autosomal-recessive multi-system disorder with early mortality. It has variable clinical presentations, mainly characterised by disproportional short stature, steroid-resistant nephrotic syndrome, spondyloepiphyseal dysplasia, and T-cell immunodeficiency. In the majority of cases, SIOD is caused by pathogenic sequence variants (PSVs) in the gene that encodes protein involved in chromatin remodelling.
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