Introduction: Cardiovascular disease (CVD) is the main cause of death among chronic kidney disease (CKD) patients. However, the cardiovascular (CV) prognostic evaluation in CKD is not established. Despite previous reports establishing troponin as a CV mortality prognosticator in CKD, there is no consensus on its applicability. Moreover, studies on high-sensitivity troponin I (hsTnI) in this context are scarce. We evaluated the association between hsTnI and CV and overall mortality among CKD patients to identify higher CV-risk patients.

Introduction: COVID-19 is a multisystem disease that can affect the renal system, resulting in worse outcomes. Objective: To analyze the prevalence of acute kidney failure (AKI) in patients with COVID-19. Method: Cross-sectional study to analyze the relationship of the disease with sex, age, comorbidities, comparing with control group. Results: Medical records of patients hospitalized for SARS-CoV-2 were analyzed, divided into without kidney injury and with kidney injury - with and without hemodialysis. About 15% developed AKI as a complication, 9.5% with hemodialysis. Length of stay and mechanical ventilation, rates of pulmonary involvement, need for ICU, urea and creatinine values were worse in patients with AKI, and mortality was higher in the group with AKI and hemodialysis (86%). The prevalence of ARI in patients with COVID-19 was higher in those over 50 years of age, in men and in those with arterial hypertension. Conclusion: Patients with AKI had worse outcomes and a greater number of complications.

Thyroid hormones (THs) are essential for brain development, and their dysregulation is associated with cognitive deficits and neurodevelopmental disorders. Down syndrome (DS), caused by trisomy 21, is frequently associated with thyroid dysfunction and impaired neurogenesis. Here, we investigated THs signaling dynamics during neural differentiation using human induced pluripotent stem cells (hiPSCs) derived from individuals with DS and controls. We analyzed the gene expression of key THs regulators—deiodinases, transporters, and receptors—and downstream target genes in hiPSCs, hiPSC-derived neural progenitor cells (NPCs), hiPSC-derived astrocytes, and hiPSC-derived neurons. DS-derived hiPSCs, hiPSC-derived NPCs, and hiPSC-derived neurons exhibited 2- to 7-fold increases in the gene expression of DIO2 and 3- to 8-fold reductions in DIO3, alongside 1- to 3-fold downregulation of THRA and THRB isoforms. hiPSC-derived astrocytes showed a 4-fold decrease in the gene expression of DIO2, a 4-fold increase in DIO3, upregulation of SLC16A10 (2-fold), and downregulation of SLC7A5 (0.5-fold) and THs receptors (0.5- to 12-fold). hiPSC-derived neurons exhibited marked downregulation of the gene expression of HOMER1 (0.5-fold), GRIN3A (14-fold), and GRIN3B (4-fold), accompanied by impaired spontaneous activity in multi-electrode array recordings. These findings reveal a robust, cell-type-specific imbalance between THs availability and signaling competence in DS hiPSC-derived neural cells, providing mechanistic insight into THs-related contributions to the function of DS hiPSC-derived neural cells and identifying potential therapeutic targets.

Resumo Introdução: Doença cardiovascular (DCV) é a principal causa de óbito entre pacientes com doença renal crônica (DRC). Entretanto, a avaliação prognóstica cardiovascular (CV) na DRC não está estabelecida. Apesar de relatos anteriores estabelecerem a troponina como prognóstico de mortalidade CV na DRC, não há consenso sobre sua aplicabilidade. Além disso, estudos sobre a troponina I de alta sensibilidade (hsTnI) nesse contexto são escassos. Avaliamos a associação entre hsTnI e mortalidade CV e geral entre pacientes com DRC para identificar pacientes com maior risco CV. Métodos: 145 pacientes com DRC estágios 3 a 5 foram submetidos a medições de hsTnI, inflamação, metabolismo do cálcio-fósforo, calcificação vascular e parâmetros ecocardiográficos. A associação entre hsTnI e mortalidade CV e geral após o acompanhamento foi estabelecida por meio de curvas de Kaplan-Meier. O valor de corte da hsTnI para predição de mortalidade CV e geral foi definido com a análise da curva ROC. A análise multivariada para mortalidade CV e geral foi realizada utilizando modelos de regressão de Cox. Resultados: O valor de corte da hsTnI para mortalidade geral e CV foi 0,057 ng/mL. Pacientes com hsTnI mais elevada apresentaram maior mortalidade CV e geral. Na análise multivariada, a hsTnI foi um marcador de mortalidade CV aumentada (razão de risco 12,8 (IC 95% 1,56-105,08); p = 0,018), independente de idade, sexo, DCV anterior, diabetes e diálise, achados ecocardiográficos e osteoprotegerina (OPG). Conclusão: A hsTnI está independentemente associado à mortalidade CV em pacientes com DRC, sugerindo que pode ser um potencial marcador para estratificação de risco CV.