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.
Panwar et al. (2025) studied this question.