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Introducción: El síndrome de intestino irritable (SII) y la enfermedad inflamatoria intestinal (EII), son motivos de consulta frecuente. Usualmente su tratamiento se hace en primer nivel de atención, con ajuste de estilo de vida y cambios dietarios. Los tratamientos farmacológicos tienen eficacia limitada e importantes efectos secundarios, por lo que existe un interés creciente en terapias diferentes como el uso de probióticos.Métodos: Se realizó una revisión de la literatura en las bases de datos Medline y Embase buscando estudios que asociaran suplementos nutricionales, con SII o EII, haciendo énfasis en probióticos.Resultados: De un total de 1598 referencias, 43 cumplieron criterios finales de inclusión. El uso de probióticos en SII y EII sugiere ser una terapia que ayuda a mantener los periodos de remisión de enfermedad, mejorar la calidad de vida y atenuar el proceso fisiopatológico.Conclusiones: El uso de probióticos y prebióticos podría ser una alternativa de soporte nutricional en pacientes seleccionados.

Background: Acute kidney injury (AKI) is a common cause of morbidity and mortality. It mainly targets the renal tubular epithelium with pathological changes, referred to as acute tubular injury. The latter is followed by a regenerative response that is difficult to visualize on routine hematoxylin and eosin (H&E) stains. In this study, we examined the regenerative capacity of renal tubules by correlating vimentin (VIM) immunohistochemical (IHC) expression and pathological findings of AKI and renal tubular regeneration (RTR) on H&E. Methods: We reviewed 23 autopsies performed in the clinical setting of AKI and RTR. VIM expression was scored in the renal cortical tubular epithelium using a statistical cutoff ≥ 3% for high expression and < 3% for low expression. Results: Of the 23 kidney tissues examined, seven (30.4%) had low VIM expression, and 16 (69.6%) had high VIM expression. Kidney tissues with evidence of AKI and RTR had significantly higher VIM expression. Renal peritubular microenvironment features showing regenerative changes on H&E were associated with high VIM expression. In the univariate model, kidney tissues with RTR were 18-fold more likely to have high VIM expression. Conclusions: In conclusion, our findings suggest that VIM could serve as an IHC marker for RTR following AKI. However, correlation with H&E findings remains critical to excluding chronic tubular damage. Collectively, our preliminary results pave the way for future studies including a larger sample size to validate the use of VIM as a reliable biomarker for RTR.