Renal Pathophysiology

CHAPTER 11 Acute Kidney Injury

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Patients who have greater than a 75% narrowing of one or both renal ar teries are often hypertensive, as the angiotensin II formed within the kidney during the autoregulatory response can also enter the systemic circulation and induce vasoconstriction. An ACE inhibitor will usually partially or com pletely reverse the hypertension in this setting. It will, however, also tend to impair autoregulation, thereby lowering the GFR. This effect will not signifi cantly raise the plasma creatinine concentration in patients with a unilateral lesion because filtration will be maintained in the contralateral, nonstenotic kidney. However, AKI can occur in some patients with bilateral renal artery stenosis or unilateral stenosis in a solitary kidney. It should be emphasized that, although the risk is greatest with an ACE inhibitor, any antihypertensive agent can lead to AKI if the stenoses are se vere. As shown in Figure 11.3A-C, the ability to autoregulate GFR in normal

CHAPTER 11 Acute Kidney Injury

Afferent

Efferent

P GC

A

Normal

Prostaglandin mediated vasodilation

AII-mediated vasoconstriction

B

Autoregulation

NSAIDs

RASi

C

Hemodynamic GFR

„ FIGURE 11.3 Autoregulation of GFR. Schematic representation of a single glomerulus with afferent inflow and efferent outflow depicted. P GC is glomerular capillary pressure and reflects the net driving force for filtration across the glomeru lar basement membrane. A: Normal condition. B: Reduced mean arterial pressure, and as depicted in Figure 11.2, GFR is maintained by prostaglandin-mediated af ferent vasodilation and efferent vasoconstriction. C. Reduced GFR in the setting of medications that inhibit afferent vasodilation and efferent vasoconstriction such as NSAIDs and renin-angiotensin system (RAS) inhibitors.

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