# Current Status and Future Prospects of Research on Sepsis-Related Acute Kidney Injury

## TL;DR

This review summarizes recent advances in understanding and treating sepsis-related acute kidney injury, highlighting gaps and future research needs.

## Contribution

The paper provides a comprehensive synthesis of recent evidence on SA-AKI, emphasizing pathogenic mechanisms and therapeutic targets.

## Key findings

- Advances in understanding clinical risk factors and pathophysiology of SA-AKI have improved prevention and management.
- Current gaps include the complex interplay of mechanisms and signaling pathways in SA-AKI pathogenesis.
- The review identifies emerging therapeutic targets and emphasizes hierarchical relationships in disease progression.

## Abstract

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The kidney is among the organs most susceptible to sepsis-induced injury, and acute kidney injury frequently develops in this context, thereby markedly increasing mortality in affected patients. With continued advances in research, a more comprehensive understanding has been achieved regarding the clinical risk factors, pathophysiological mechanisms, therapeutic responses, and renal recovery processes associated with sepsis-associated acute kidney injury (SA-AKI). These advances have strengthened the capacity for prevention, early detection, and effective management of SA-AKI. Despite this progress, substantial gaps remain in the overall understanding of SA-AKI pathogenesis, including the complex interplay among pathophysiological mechanisms and the extensive cross-regulation of multiple signaling pathways. Consequently, SA-AKI remains a major clinical challenge and imposes a substantial global healthcare burden. There is therefore an urgent need for further research to elucidate the underlying mechanisms of SA-AKI and to identify more effective therapeutic strategies. Unlike previous reviews that primarily focused on individual mechanisms or isolated therapeutic targets, the present review synthesizes the most recent evidence on SA-AKI. Particular emphasis is placed on its pathogenic processes, associated molecular mechanisms and signaling pathways, and emerging therapeutic targets. Special attention is given to the hierarchical relationships among distinct mechanisms during disease progression and their implications for clinical translation. This review aims to inform clinical practice and to identify future research directions, thereby providing valuable insights for both researchers and clinicians in this field.