Intra-abdominal hypertension and renal function:

Renal dysfunction is a common early presentation of elevated intra-abdominal pressure. Oliguria is seen at intra-abdominal pressures over 15 to 20 mm Hg and anuria is common once pressures exceed 25-30 mm Hg.

The causes of renal dysfunction are likely multifactorial: reduced cardiac output, increased renal vascular resistance, decreased glomerular filtration gradient.

Renal arterial flow is decreased for several reasons. The primary underlying reason for renal hypoperfusion is venous compression from elevated IAP. As intra-abdominal pressure rises to levels higher than central venous pressures it causes vena caval collapse and reduced blood return to the heart (preload.) The combination of reduced preload plus elevated intra-thoracic pressure (that occurs as the diaphragms are pushed cephlad) leads to reduced cardiac output with resultant increases in systemic vascular resistance and vasoconstriction of the arterial tree including the renal artery. There may also be some direct renal artery compression from the elevated IAP. Renal arterial blood flow reduction is further exacerbated by humeral factors such as increased antidiuretic hormone and increased plasma renin and aldosterone activity. Finally, elevated intra-abdominal pressures cause direct compression of the renal veins leading to reduction of venous drainage and renal congestion.

The combination of renal congestion, direct renal compression and reduced arterial blood flow to the kidneys all lead to a reduction in the renal filtration gradient (See Diagram that graphically outlines this). The filtration gradient is the hydrostatic pressure across the glomerulus that drives urine production and renal function. Filtration gradient (FG) equals glomerular filtration pressure minus proximal tubular pressure. When IAP is elevated, proximal tubular pressure is essentially the same as intra-abdominal pressure and glomerular filtration pressure is the difference between MAP and IAP. So Filtration gradient = MAP-(2 x IAP). Therefore, changes in IAP will have a more profound effect on urine formation than will changes in arterial pressure.

Sugrue, et al, demonstrated the importance of IAP as a predictor of renal impairment. These authors prospectively studied 263 ICU patients and found intra-abdominal pressure to be an independent predictor of renal impairment. In their study, 40% of patients developed IAH (IAP >18 mm Hg) and one third of these developed renal impairment (compared to one eighth of patients with lower IAP, p=0.004). They also noted a lag time between development of elevated IAH and renal impairment suggesting that the effect on renal function is gradual rather than immediate. Although not addressed in this study, multiple other studies have demonstrated immediate improvement in renal function once IAH is lowered.

Other authors have found a direct correlation between IAP and renal function. DeWaele noted immediate increase in urinary output following medical interventions that lowered intra-abdominal pressure and immediate decreases in UOP when the IAP rose. Biancofiore found a close relationship between renal failure, mortality and IAP in post-operative liver transplant patients. Recent publications in the nephrology literature validate the under-appreciation that clinicians have for IAH as a cause for renal problems and conclude that intra-abdominal hypertension should be considered (and IAP measured and monitored) in the differential diagnosis of all at risk patients with acute renal insufficiency.

In summary, IAH is a proven contributor to renal impairment in critically ill patients. It occurs gradually and responds to interventions that reduce IAP. The cause is multifactorial, but appears to be due to a combination of reduced renal blood flow, increased renal parenchymal pressure (impeding glomerular filtration) and hormonal changes induced by intra-abdominal hypertension.