Increased intra-abdominal pressure in acute kidney injury: a cause or an effect?

The detrimental effects of increased intra-abdominal pressure (IAP) on kidneys and other intra-abdominal organs have been known for a long time, particularly in postoperative conditions [1]. In recent decades, the significance of intra-abdominal hypertension (IAH) has been increasingly recognized because it is much more prevalent than expected and is associated with increased morbidity and mortality in critically ill patients [2]. Studies of mixed populations in medical and surgical intensive care units (ICUs) demonstrated a prevalence of IAH of up to 64% [3]. The prevalence is higher in patients with septic shock, especially those who received massive volume resuscitation [3]. The development of IAH is associated with a worse clinical outcome. A large multicenter epidemiological study found that new-onset IAH is associated with a 1.85-fold increased risk of mortality in ICU patients [4]. Moreover, studies that focused on the association between IAH and acute kidney injury (AKI) demonstrated that IAH was a good predictor of AKI in unselected ICU patients who survived from shock and in patients who underwent liver transplantation [5]. IAP in critically ill patients is normally 5–7 mmHg and increases in situations of increased abdominal contents or decreased abdominal wall compliance. IAH is defined as a sustained or repeated elevation of IAP of Z12 mmHg. Sustained IAP of Z20 mmHg associated with new organ dysfunction constitutes abdominal compartment syndrome [2]. Abdominal perfusion pressure (APP) is a relatively novel parameter that reflects the circulatory compromise and IAH together. APP is calculated as the difference between the mean arterial pressure and the IAP. Some studies have suggested that APP may be superior to IAP in predicting patient outcome. The maintenance of an APP of Z50 mmHg seems to provide proper intra-abdominal circulation [6]. The most popular technique for IAP measurement is transvesicular measurement, i.e., the transduction of urinary bladder pressure through an indwelling urinary catheter. The pressure in this closed system can be measured either using a pressure transducer in the ICU or by measuring the height of the fluid in the tubing in a non-ICU environment. Common practice for the screening of patients at risk of IAH is the serial monitoring of IAP every 4–6 hours [7]. An increased IAP level can negatively affect kidney function indirectly (systemic effects) or directly (renal effects). Several