Renal Pathophysiology

316

RENAL PATHOPHYSIOLOGY: THE ESSENTIALS

systemic hemodynamics. Reinfusion of the patient’s ascites into the internal jugular vein via a peritoneovenous shunt can expand the plasma volume and, in many cases, improve renal function. Renal Artery Stenosis and Angiotensin-Converting Enzyme Inhibitors Narrowing of the renal artery (renal artery stenosis) is associated with a reduction in arterial pressure distal to the obstruction. Despite this fall in pressure perfusing the glomeruli, the GFR can initially be maintained by autoregulation (the mechanism of which is discussed in Chapter 1). This phenomenon, depicted in Figure 11.2, shows that the GFR is maintained in normal dogs as the renal artery pressure is lowered from 125 to 85 mm Hg. The ability to autoregulate eventually fails, and the GFR begins to decline as the renal artery pressure falls to 70 mm Hg. Angiotensin II plays an important role in the autoregulation of GFR by preferentially constricting the efferent glomerular arteriole, thereby main taining the intraglomerular pressure. If, however, the effect of angiotensin II is blocked by an angiotensin II antagonist or its production is diminished by the administration of an ACE inhibitor, then the reduction in GFR begins at a higher pressure and is more pronounced (Fig. 11.2).

110

100

Control

90

A antagonist

80

GFR (percent control)

70

60

125

70

85

105

Renal artery pressure (mm Hg)

„ FIGURE 11.2. Effect of reducing renal artery pressure (from a baseline value of ~125 mm Hg) on glomerular filtration rate (GFR) in normal dogs ( green squares ) and dogs pretreated with an angiotensin II antagonist ( blue circles ). Autoregula tion of GFR was maintained in normal dogs until the renal artery pressure fell to 70 mm Hg. Antagonizing the effect of angiotensin II led to an earlier and more marked fall in GFR, indicating an important role for angiotensin II (AII) in the autoregulation of GFR. (Modified from Epstein M, Berk DP, Hollenberg NK, et al. Renal failure in the patient with cirrhosis. The role of active vasoconstriction. Am J Med. 1970;49[2]:175-185.)

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