Renal perfusion pressure: role and implications in critical illness

Annals of Intensive Care volume 15, Article number: 115, Published: 08 August 2025

Abstract

The pressure-flow relationship is fundamental to circulatory hemodynamics of any organ. In the kidney, renal perfusion pressure (RPP), defined as the gradient between mean arterial pressure and renal venous pressure or mean systemic filling pressure, serves as the principal driving pressure for renal blood flow (RBF). This concept recognizes that both arterial hypotension and venous congestion can reduce the pressure gradient for renal perfusion, potentially contributing to renal dysfunction or acute kidney injury (AKI). In health, whenever RPP fluctuates, the kidney autoregulates intrarenal vascular resistance to maintain stable RBF and glomerular filtration rate over a range of RPP. However, in critical illness, autoregulatory capacity may be impaired, and the degree of impairment can vary not only between patients but also within the same patient depending on the disease context or stage of illness. Therefore, during critical illness, inadequate RPP tends to overwhelm renal autoregulation capacity earlier than anticipated, leading to tissue hypoperfusion and increased risk of AKI. Relying on standard blood pressure targets to optimize RPP may not account for such inter- or intra-individual variations in autoregulation. Experimental models have shown that AKI can develop without overt macrocirculatory changes, implicating microcirculatory dysfunction as an important contributor too. Dynamic, multi-modal assessment of renal perfusion may offer a more precise approach to renal protection. Additionally, the focus of research has shifted towards providing new insights into individualized perfusion targets and refining RPP-guided strategies to prevent AKI among high-risk patients in ICU. The objective of this review is to describe the role of RPP, implications of dysregulated renal perfusion, approaches to monitoring renal perfusion, and potential therapies targeting RPP on the horizon for critically ill patients.

 

Extremely early initiation of vasopressors might not decrease short-term mortality for adults with septic shock: a systematic review and meta-analysis

Annals of Intensive Care volume 15, Article number: 18 (2025)

Published: 27 January 2025

Background

The optimal timing for initiating vasopressor therapy in patients with septic shock remains unclear. This study aimed to assess the impact of early versus late vasopressor initiation on clinical outcomes.

Methods

A systematic review and meta-analysis were conducted by searching PubMed, Embase, and Cochrane databases. Studies comparing early and late vasopressor administration in septic shock patients were included. The primary outcome was short-term mortality, and subgroup analyses were performed based on different initiation timings.

Results

Eleven studies with 6,661 patients were included. Different studies define the ‘early administration’ timeframe variously, ranging from one to seven hours. No significant difference in short-term mortality was observed between early and late administration in the combined analysis of 3,757 patients from two RCTs and three quasi-experimental studies (OR: 0.66, 95% CI: [0.36, 1.19], I²: 82%). However, lower mortality was found in subgroups with early but not extremely early initiation (one to three hours, OR: 0.70, 95% CI: [0.60, 0.82], I²: 0%), and those using septic shock diagnosis as time zero (OR: 0.64, 95% CI: [0.48, 0.85], I²: 39%).

Conclusion

Our findings found that earlier initiation of vasopressor therapy, particularly within one to three hours after the diagnosis of septic shock, may be associated with reduced short-term mortality in certain subgroups. However, due to the heterogeneity in study definitions and potential confounding factors, these results should be interpreted cautiously. Further standardized investigations are warranted to precisely determine the optimal timing for vasopressor initiation to maximize survival outcomes in patients with septic shock.