Sepsis most often involves the kidney and is one of the most common causes of acute kidney injury. The prevalence of septic acute kidney injury has increased significantly in recent years. The gut microbiota plays an important role in sepsis. It interacts with the kidney in a complex and multifactorial process, which is not fully understood. Sepsis may lead to gut microbiota alteration, orchestrate gut mucosal injury, and cause gut barrier failure, which further alters the host immunological and metabolic homeostasis. The pattern of gut microbiota alteration also varies with sepsis progression. Changes in intestinal microecology have double-edged effects on renal function, which also affects intestinal homeostasis. This review aimed to clarify the interaction between gut microbiota and renal function during the onset and progression of sepsis. The mechanism of gut–kidney crosstalk may provide potential insights for the development of novel therapeutic strategies for sepsis.

Backgroud To explore whether monitoring of non-invasive urine oxygen tension (PuO2) for 3 consecutive days can reflect renal medulla microcirculation injury early and whether changes in PuO2 (△PuO2) have reliable early diagnostic value for sepsis-associated acute kidney injury (SA-AKI). Methods Twenty-four patients who were hospitalised for more than 48 h in our hospital and were diagnosed with sepsis were retrospectively divided into non-SA-AKI group and SA-AKI group according to the occurrence of acute kidney injury (AKI). The general and oxygen metabolism data of the two groups were compared. The results of urine analysis (PuO2, PuCO2, and urinary lactic acid) for 3 consecutive days were compared with common clinical kidney injury indices, and a changing trend was observed. Results In the PICU, a total of 24 patients with sepsis were included (14 males, 58.33%; mean age, 5 years), with 15 cases in the non-SA-AKI group and 9 cases in the SA-AKI group, with incidence of SA-AKI being 37.5%. PuO2 gradually decreased from D0 to D2 in the SA-AKI group; PuCO2 increased naturally. The variation trend of PuO2 was statistically significant in D1-D0, D2-D0, and D2-D1 (P<0.05), and the △PuO2 of D2-D0 (10.83±25.69 vs. -41.13±34.98, P=0.001). The early diagnostic value of PuO2 was significant (AUC=0.885, 95% CI: 0.704–1.000). Conclusions Three consecutive days of PuO2 monitoring can reflect early renal medullary microcirculation injury, and △PuO2 has early diagnostic value for SA-AKI.