Renal congestion syndrome in critically ill patients: a neglected mechanism of acute kidney injury - A narrative review.

We propose the concept of "renal congestion syndrome" as a pathophysiological construct describing a potential contributor to acute kidney injury (AKI) in the intensive care unit (ICU). This concept should be considered as hypothesis-generating rather than a validated clinical entity with established diagnostic or therapeutic implications. Growing experimental and clinical evidence supports a plausible contributory role in kidney dysfunction. However, interventional evidence is currently lacking, and the clinical utility of targeting congestion remains to be established. When renal venous pressure rises, hydrostatic pressure in Bowman's space and the interstitium increases. This reduces net ultrafiltration pressure and glomerular filtration rate, even if arterial pressure is preserved. Edema within the non-distensible capsule compresses tubules and peritubular capillaries, aggravating hypoxia and tubular injury. Lymphatic drainage may initially buffer this process, but fails with sustained congestion. In the ICU, congestion is common and multifactorial: fluid overload, right heart dysfunction, high intrathoracic pressures from ventilation, or intra-abdominal hypertension. Experimental data suggest that congestion may precipitate early loss of renal autoregulation, leaving kidneys vulnerable even at apparently normal mean arterial pressures. Moreover, it often coexists with hypotension, reducing mean perfusion pressure (MPP), further lowering renal perfusion pressure, and increasing the risk of AKI. Diagnosis relies on an integrated assessment combining clinical context with haemodynamic monitoring and, when available, imaging-based evaluation of venous congestion. Central venous pressure remains the standard reference for assessing central venous hypertension; however, its specificity for renal congestion is limited. Doppler ultrasound with Venous Excess Ultrasound (VExUS) score may improve detection and risk stratification, though interpretation can be confounded by mechanical ventilation or intra-abdominal hypertension. Management is conceptually aimed at relieving congestion while preserving renal perfusion. Based on physiological rationale and limited observational data, this may involve preventing fluid accumulation and implementing individualized decongestive strategies (e.g., fluid stewardship, diuretics when appropriate, or ultrafiltration when indicated). Haemodynamic-guided deresuscitation, integrating congestion markers with real-time MPP assessment, appears promising but remains supported only by feasibility data. Renal congestion-related mechanisms are likely frequent, under-recognized, and potentially reversible contributors to AKI in the critically ill patient. Systematic assessment of congestion-related mechanisms warrants further investigation. Whether their integration into haemodynamic evaluation improves clinical outcomes remains to be determined.