and indirectly via aldosterone. Second, angiotensin II preferentially constricts the efferent arteriole, thus helping to preserve glomerular capillary hydrostatic pressure and, consequently, glomerular filtration rate.

When arterial pressure or body fluid volumes are sensed as subnormal, the renin-angiotensin system is activated and plasma renin activity and angiotensin II levels increase. This may occur in the context of clinical settings such as renal artery stenosis, dietary sodium restriction or sodium depletion as during diuretic therapy, congestive heart failure, cirrhosis, and nephrotic syndrome. When activated, this reninangiotensin system plays an important role in the maintenance of glomerular pressure and filtration through preferential angiotensin ¡¡-mediated constriction of the efferent arteriole. Thus, under such conditions the kidney becomes sensitive to the effects of blockade of the renin-angiotensin system by angiotensin ¡-converting enzyme inhibitor or angiotensin ¡I receptor antagonist. The highest incidence of renal failure in patients treated with ACE inhibitors was associated with bilateral renovascular disease [27]. In patients with already compromised renal function and congestive heart failure, the incidence of serious changes in serum creatinine during ACE inhibition depends on the severity of the pretreatment heart failure and renal failure.

Volume management, dose reduction, use of relatively short-acting ACE inhibitors, diuretic holiday for some days before initiating treatment, and avoidance of concurrent use of nonsteroidal anti-inflammatory drug (hyperkalemia) are among the appropriate measures for patients at risk.

Acute interstitial nephritis associated with angiotensin ¡-converting enzyme inhibition has been described [29]. (Adapted from Opie [30]; with permission.)

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