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Review
. 2001 Nov;49(5):729-37.
doi: 10.1136/gut.49.5.729.

The hepatorenal syndrome

L Dagher  1 , K Moore
Affiliations
Review

The hepatorenal syndrome

L Dagher et al. Gut. 2001 Nov.
No abstract available

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Figures

Figure 1
Figure 1
Administration of indomethacin, a non-steroidal anti-inflammatory drug (NSAID), to patients with cirrhosis AND ascites, caused a significant reduction in renal plasma flow (not shown) and glomerular filtration rate, as assessed by creatinine clearance (adapted from Boyer and colleagues79).
Figure 2
Figure 2
Measurement of renal blood flow (RBF) by 133-xenon washout shows that RBF is decreased in cirrhosis and further decreased in patients with hepatorenal syndrome (HRS). However, as is evident in the shaded area, there is a considerable overlap in RBF values between normal, cirrhotic, and HRS patients (adapted from Ring-Larsen H. Renal blood flow in relation to systemic and portal haemodynamics and liver function. Scand J Clin Lab Invest 1977;37:635-42).
Figure 3
Figure 3
The glomeruli within the kidney are dynamic structures, invaginated with mesangial cells which express actin. These contractile cells control the surface area of glomeruli available for filtration. The cells contract in response to certain agonists such as endothelin 1 (ET-1), thromboxane A2 (TXA2), arginine vasopressin (AVP), or leukotriene D4 (LTD4 ). Vasodilatory prostaglandins such prostaglandin E2 (PGE2 ) can cause relaxation of mesangial cells.
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