Risk factors associated with renal crescentic formation in pediatric Henoch-Schönlein purpura nephritis: a retrospective cohort study.

BACKGROUND: The long-term prognosis of Henoch-Schönlein purpura (HSP) depends on the severity of renal involvement, and crescent formation is considered an important risk factor for poor prognosis of Henoch-Schönlein purpura nephritis (HSPN). The objective of this study was to evaluate factors affecting crescent formation in children with HSPN. METHODS: Demographic factors, clinical characteristics, and laboratory data of children with HSPN with or without crescents were retrospectively analyzed. Univariate and multivariate logistic regression analyses were used to determine the risk factors of crescent formation in HSPN. RESULTS: A total of 191 children with HSPN were enrolled in the study. There were 107 (56%) males and 84 (44%) females, with a median age of 7 years (range: 2 years-15 years). International Study of Kidney Disease in Children (ISKDC) grading was used to divide subjects into two groups: those without glomerular crescent formation (ISKDC grades I-II, n = 146 cases) and those with glomerular crescent formation (ISKDC grades III-V, n = 45 cases). Logistic regression analysis showed that higher urinary white blood cell (WBC) count (OR = 3.300; 95% CI, 1.119-9.739; P = 0.0306) and higher urinary microalbumin/creatinine ratio (ACR) (OR = 25.053; 95% CI, 1.354-463.708; P = 0.0305) were independent risk factors for the formation of crescents in HSPN. The area under the receiver operating characteristic curve of urinary WBC and ACR were 0.753 and 0.698 respectively, with the Hosmer and Lemeshow goodness-of-fit test (P = 0.0669, P > 0.05). CONCLUSION: These results suggest that higher urinary WBC count and ACR should be strictly monitored for children with HSPN. Adequate clinical intervention for these risk factors may limit or prevent renal crescent formation.

Assessment of irreducible aspects in developmental hip dysplasia by magnetic resonance imaging.

BACKGROUND: The developmental dysplasia of the hip (DDH) can cause a wide range of pathological changes, and often requires surgical treatment. Preoperative evaluation is very important for DDH. We aimed to assess the diagnostic capability of magnetic resonance imaging (MRI) for irreducible aspects preventing hip reduction in DDH. METHODS: A total of 39 pediatric patients who received DDH evaluation in pediatric orthopedics from January 2015 to December 2019 were included. The samples included 4 cases of bilateral DDH and 35 cases of unilateral DDH, a total of 43 hip joint samples. All patients underwent surgical treatment, pathological examination and MRI of hip joint. RESULTS: With pathological results or intraoperative findings as the gold standard, the sensitivity and specificity of MRI were 90.3% and 83.3% for the affected labrum, 92% and 83.3% for thickening of the round ligament, 90.0% and 91.3% for atrophy of the iliopsoas muscle, and 100% and 100% for fibrofatty pulvinar tissue and joint effusion, respectively. CONCLUTIONS: The MRI showed an extraordinary capability of detecting these irreducible factors and helped surgeon choose the appropriate treatment strategies.

Integrative microRNA and mRNA expression profiling in acute aristolochic acid nephropathy in mice.

In acute aristolochic acid nephropathy (AAN), aristolochic acid (AA) induces renal injury and tubulointerstitial fibrosis. However, the roles of microRNAs (miRNAs/miRs) and mRNAs involved in AAN are not clearly understood. The aim of the present study was to examine AA­induced genome­wide differentially expressed (DE) miRNAs and DE mRNAs using deep sequencing in mouse kidneys, and to analyze their regulatory networks. In the present self­controlled study, mice were treated with 5 mg/kg/day AA for 5 days, following unilateral nephrectomy. AA­induced renal injury and tubulointerstitial fibrosis were detected using hematoxylin and eosin staining and Masson's trichrome staining in the mouse kidneys. A total of 82 DE miRNAs and 4,605 DE mRNAs were identified between the AA­treated group and the self­control group. Of these DE miRNAs and mRNAs, some were validated using reverse transcription­quantitative PCR. Expression levels of the profibrotic miR­21, miR­433 and miR­132 families were significantly increased, whereas expression levels of the anti­fibrotic miR­122­5p and let­7a­1­3p were significantly decreased. Functions and signaling pathways associated with the DE miRNAs and mRNAs were analyzed using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG). A total of 767 DE pairs (in opposing directions) of miRNAs and their mRNA targets were identified. Among these, regulatory networks of miRNAs and mRNAs were analyzed using KEGG to identify enriched signaling pathways and extracellular matrix­associated pathways. In conclusion, the present study identified genome­wide DE miRNAs and mRNAs in the kidneys of AA­treated mice, as well as their regulatory pairs and signaling networks. The present results may improve the understanding of the role of DE miRNAs and their mRNA targets in the pathophysiology of acute AAN.