Haemodynamic predisposition to acute kidney injury: Shadow and light!

Acute kidney injury (AKI) could well be regarded as a sentinel complication given it is relatively common and associated with a substantial risk of subsequent morbidity and mortality. On the aegis of ‘prevention is better than cure’, there has been a wide interest in evaluating haemodynamic predisposition to AKI so as to provide a favourable renoprotective haemodynamic milieu to the subset of patients presenting a significant risk of developing AKI. In this context, the last decade has witnessed a series of evaluation of the hypotension value and duration cut-offs associated with risk of AKI across diverse non-operative and operative settings. Nevertheless, a holistic comprehension of the haemodynamic predisposition to AKI has been a laggard with only few reports highlighting the potential of elevated central venous pressure, intra-abdominal hypertension and high mean airway pressures in considerably attenuating the effective renal perfusion, particularly in scenarios where kidneys are highly sensitive to any untoward elevation in the afterload. Despite the inherent autoregulatory mechanisms, the effective renal perfusion pressure (RPP) can be modulated by a number of haemodynamic factors in addition to mean arterial pressure (MAP) as the escalation of renal interstitial pressure, in particular hampers kidney perfusion which in itself is a dynamic interplay of a number of innate pressures. The present article aims to review the subject of haemodynamic predisposition to AKI centralising the focus on effective RPP (over and above the conventional ‘tunnel-vision’ for MAP) and discuss the relevant literature accumulating in this area of ever-growing clinical interest