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 ≥12 mmHg. Sustained IAP of ≥20 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 ≥50 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 factors account for the effects of IAH on the cardiovascular system. Firstly, IAH increases intrathoracic pressure, which is reflected by cranial displacement of the diaphragm and results in compression of the heart. Secondly, cardiac preload is reduced via a decrease in venous return. Finally, systemic afterload is increased through direct compression of vascular beds. Ultimately, increased IAP induces a decrease of cardiac output. Decreases in urine output and glomerular filtration rate were clearly observed in humans with experimentally induced IAP. Directly measured renal vein pressure increased from 5.8 mmHg to 18.3 mmHg and urine flow was reduced by half when the IAP was raised by external compression to 20 mmHg [8]. Given the low-pressure system of the postglomerular intrarenal vascular network, it is not surprising that an IAP of 20 mmHg leads to significant intrarenal venous congestion and reduction of glomerular filtration rate. AKI in heart failure—the so-called cardiorenal syndrome—and hepatorenal syndrome with ascites are other circumstances in which increased renal venous pressure may contribute to the development of AKI. Mullens et al [9] discovered that venous congestion is the most important hemodynamic factor driving the worsening of renal function in decompensated heart failure. The fact that successful volume reduction, even in small amounts, is followed by the recovery of kidney function in patients with cardiorenal syndrome is a commonly observed phenomenon. Moreover, some patients with hepatorenal syndrome exhibit diuresis and improvement of azotemia after paracentesis, despite concerns about hypovolemia. The precise role of IAH in hepatorenal syndrome should be determined in future studies.

In this issue of the journal, Chang et al [10] prospectively enrolled patients who were admitted to a medical ICU with established AKI, and IAP was measured once a day for the first 3 days. The authors used a standard transvesicular technique, and the mean IAP levels were consistent over three measurements. They discovered that IAH, defined as a sustained elevated IAP of ≥12 mmHg, was highly prevalent (up to 79%) in ICU patients with AKI. However, the presence of IAH was not associated with the severity of AKI at the baseline. Furthermore, IAH was not a predictor of AKI recovery or in-hospital mortality.

For several reasons, this article is recommended to nephrologists. Firstly, the article addresses the significance of IAH as a risk factor for, or cause of, AKI in critically ill patients. Given its high prevalence (79%), the presence of IAH in addition to other well-known nephrotoxic insults should be ascertained in patients who develop AKI, particularly in ICU settings. Nephrologists are apt to overlook the contribution of IAH to AKI in clinical practice. Secondly, this paper elucidated the association between AKI and IAH in a different manner from previous studies showing that preceding IAH predisposed critically ill patients to the development of AKI. In this study, IAH was not related to either renal or patient outcome in patients with established AKI. This suggests that IAH following AKI is secondary to volume retention. In case of established AKI, IAP would lose its prognostic power because the severity of AKI was the most potent determinant of short-term renal recovery. In contrast with previous epidemiological studies, disease severity, as represented by a Simplified Acute Physiology Score II (SAPS II), was the most potent predictor of mortality in the study. Finally, there was another noteworthy finding [10]; although the authors attributed little attention to it. Among patients with AKI, baseline kidney function was abnormal in most cases with normal IAP, whereas baseline kidney function was normal in most cases with high IAP. In other words, de novo AKI frequently involves IAH, whereas acute-on-chronic kidney disease is seldom accompanied by IAH. This distinction between AKI and acute-on-chronic kidney disease warrants further investigation.

In conclusion, Chang et al [10] demonstrated that increased IAP is highly prevalent in critically ill patients with AKI. However, they failed to show that IAH was a prognostic factor of renal or patient outcome in patients with established AKI, suggesting that IAH following AKI is a secondary phenomenon. Although it is generally accepted that increased IAP is an important risk factor for AKI in critically ill patients, IAH following AKI may have a different clinical significance.