Renal involvement in Systemic Lupus Erythematous (SLE) patients is one of the leading causes of morbidity and a significant contributor to mortality. It’s estimated that nearly 50% of SLE individuals develop kidney disease in the first year of the diagnosis. Class IV lupus nephritis (LN-IV) is the class of lupus nephritis most common in Colombian patients with SLE. Altered miRNAs expression levels have been reported in human autoimmune diseases including lupus. Variations in the expression pattern of peripheral blood circulating miRNAs specific for this class of lupus nephritis could be correlated with the pathophysiological status of this group of individuals. The aim of this study was to evaluate the relative abundance of circulating microRNAs in peripheral blood from Colombian patients with LN-IV. Circulating miRNAs in plasma of patients with diagnosis of LN-IV were compared with individuals without renal involvement (LNN group) and healthy individuals (CTL group). Total RNA was extracted from 10 ml of venous blood and subsequently sequenced using Illumina. The sequences were processed and these were analyzed using miRBase and Ensembl databases. Differential gene expression analysis was carried out with edgeR and functional analysis were done with DIANA-miRPath. Analysis was carried out using as variables of selection fold change (≥2 o ≤-2) and false discovery rate (0.05). We identified 24 circulating microRNAs with differential abundance between LN-IV and CTL groups, fourteen of these microRNAs are described for the first time to lupus nephritis (hsa-miR-589-3p, hsa-miR-1260b, hsa-miR-4511, hsa-miR-485-5p, hsa-miR-584-5p, hsa-miR-543, hsa-miR-153-3p, hsa-miR-6087, hsa-miR-3942-5p, hsa-miR-7977, hsa-miR-323b-3p, hsa-miR-4732-3p and hsa-miR-6741-3p). These changes in the abundance of miRNAs could be interpreted as alterations in the miRNAs-mRNA regulatory network in the pathogenesis of LN, preceding the clinical onset of the disease. The findings thus contribute to understanding the disease process and are likely to pave the way towards identifying disease biomarkers for early diagnosis of LN.
Introducción: el síndrome respiratorio agudo severo inducido por coronavirus-2 (SARS-CoV-2) se caracteriza por la instalación de una afectación pulmonar. Sin embargo, existen reportes de afectación renal concomitante, con manifestaciones clínicas como hematuria, proteinuria y daño renal agudo.
Objetivo: presentamos dos casos clínicos de síndrome nefrótico asociado a enfermedad por coronavirus (COVID-19).
Presentación del caso: un paciente presentó evidencia histológica de cambios mínimos y fusión de pedicelos de podocitos en muestras histológicas evaluadas por microscopía electrónica.
Discusión: la proteinuria en COVID-19 puede ser secundaria a lesiones glomerulares y tubulares agudas, con un origen multifactorial: factores hemodinámicos, tormentas de citocinas, infecciones secundarias, nefrotoxicidad inducida por fármacos e infección viral directa de las células del túbulo proximal y podocitos. Esta última podría deberse a una infección directa por el virus debido al mayor tropismo renal de este.
Conclusión: el presente informe presenta dos casos de síndrome nefrótico secundario a podocitopatía en pacientes con infección aguda por COVID-19.
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