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Deleterious Effects of Increased Intra-Abdominal Pressure on Kidney Function

DOI: 10.1155/2014/731657

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Elevated intra-abdominal pressure (IAP) occurs in many clinical settings, including sepsis, severe acute pancreatitis, acute decompensated heart failure, hepatorenal syndrome, resuscitation with large volume, mechanical ventilation with high intrathoracic pressure, major burns, and acidosis. Although increased IAP affects several vital organs, the kidney is very susceptible to the adverse effects of elevated IAP. Kidney dysfunction is among the earliest physiological consequences of increased IAP. In the last two decades, laparoscopic surgery is rapidly replacing the open approach in many areas of surgery. Although it is superior at many aspects, laparoscopic surgery involves elevation of IAP, due to abdominal insufflation with carbonic dioxide (pneumoperitoneum). The latter has been shown to cause several deleterious effects where the most recognized one is impairment of kidney function as expressed by oliguria and reduced glomerular filtration rate (GFR) and renal blood flow (RBF). Despite much research in this field, the systemic physiologic consequences of elevated IAP of various etiologies and the mechanisms underlying its adverse effects on kidney excretory function and renal hemodynamics are not fully understood. The current review summarizes the reported adverse renal effects of increased IAP in edematous clinical settings and during laparoscopic surgery. In addition, it provides new insights into potential mechanisms underlying this phenomenon and therapeutic approaches to encounter renal complications of elevated IAP. 1. Introduction Under normal conditions the intra-abdominal pressure (IAP) is usually below 4?mmHg and even in most obese subjects it does not exceed 8?mmHg [1, 2]. Elevated IAP occurs when the abdomen becomes subject to increased pressure. Sustained or repeated elevation of IAP above 12?mmHg, called intra-abdominal hypertension (IAH), is considered an important mortality risk factor in intensive care unit (ICU). When not treated, IAH has a series of consequences, explicitly, leading to abdominal compartment syndrome (ACS), where IAP increases over 20?mmHg, causing multisystem organ failure, and finally death. Elevated IAP could take place in various clinical settings including trauma, major burns, abdominal surgery, severe heart failure, hepatorenal syndrome, and critically ill patients [2]. The latter are prone to develop elevated IAP as a result of risk factors such as (i) diminished abdominal wall compliance due to mechanical ventilation, obesity, and patient position, (ii) increased intra- and extraluminal abdominal

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