Understanding fluid dynamics and renal perfusion in acute kidney injury management

Acute kidney injury (AKI) is associated with an increased risk of morbidity, mortality, and healthcare expenditure, posing a major challenge in clinical practice, and affecting about 50% of patients in the intensive care unit (ICU), particularly the elderly and those with pre-existing chronic comorbidities. In health, intra-renal blood flow is maintained and auto-regulated within a wide range of renal perfusion pressures (60-100 mmHg), mediated predominantly through changes in pre-glomerular vascular tone of the afferent arteriole in response to changes of the intratubular NaCl concentration, i.e. tubuloglomerular feedback. Several neurohormonal processes contribute to regulation of the renal microcirculation, including the sympathetic nervous system, vasodilators such as nitric oxide and prostaglandin E2, and vasoconstrictors such as endothelin, angiotensin II and adenosine. The most common risk factors for AKI include volume depletion, haemodynamic instability, inflammation, nephrotoxic exposure and mitochondrial dysfunction. Fluid management is an essential component of AKI prevention and management. While traditional approaches emphasize fluid resuscitation to ensure renal perfusion, recent evidence urges caution against excessive fluid administration, given AKI patients' susceptibility to volume overload. This review examines the main characteristics of AKI in ICU patients and provides guidance on fluid management, use of biomarkers, and pharmacological strategies.