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with an ACE inhibitor, so hypotension is generally a concern only if it is accompanied by postural symptoms, worsening renal function, blurred vision, or syncope.

In patients treated with high-dose diuretics, in whom the activation of the renin- angiotensin system (induced by hypovolemia and hyponatremia) concurs to maintain blood pressure levels, the first doses of ACEI might cause symptomatic hypotension. In these patients, although hypotension should subside with repeated administration of the same doses of ACEI, it would be prudent to lessen their dependence on the renin- angiotensin system by reducing the dose of diuretics, liberalizing salt intake, or both, provided the patient does not have significant fluid retention.

In states characterized by reduced renal perfusion (such as HF), glomerular filtration is critically dependent on angiotensin-mediated vasoconstriction of the efferent arteriole52, whose dilation, induced by ACE inhibition administration, may cause functional renal insufficiency53. A significant increase in serum creatinine (e.g., greater than 0.3 mg per dl) with the use of ACE inhibitors is observed in 15% to 30% of patients with severe HF54, but in only 5% to 15% of patients with mild to moderate symptoms55.

The risks are substantially greater if patients have bilateral renal artery stenosis or are taking non-steroidal anti-inflammatory drugs56. Renal function usually improves after a reduction in the dose of concomitantly administered diuretics, and thus, these patients can generally be managed without the need to withdraw treatment with the ACE inhibitor. However, if the dose of diuretic cannot be reduced because the patient has fluid retention, the physician and patient may need to tolerate mild to moderate degrees of azotemia to maintain therapy with the ACE inhibitor.

Hyperkalemia can occur during ACE inhibition in patients with HF and may be sufficiently severe to cause cardiac conduction disturbances. In general, hyperkalemia is seen in patients whose renal function deteriorates or who are taking oral potassium supplements or potassium-sparing diuretics, especially if they have diabetes mellitus57.

Adverse Effects Related to Kinin Potentiation

52 Packer M, Lee WH, Kessler PD. Preservation of glomerular filtration rate in human heart failure by activation of the renin-angiotensin system. Circulation 1986;74:766-74.

53 Packer M, Lee WH, Medina N, Yushak M, Kessler PD. Functional renal insufficiency during long-term therapy with captopril and enalapril in severe chronic heart failure. Ann Intern Med 1987;106:346-54.

54 Ljungman S, Kjekshus J, Swedberg K. Renal function in severe congestive heart failure during treatment with enalapril (the Cooperative North Scandinavian Enalapril Survival Study [CONSENSUS] Trial). Am J Cardiol 1992;70:479-87.

55 Giles TD, Katz R, Sullivan JM, et al. Short- and long-acting angiotensin-converting enzyme inhibitors: a randomized trial of lisinopril versus captopril in the treatment of congestive heart failure. The Multicenter Lisinopril-Captopril Congestive Heart Failure Study Group. J Am Coll Cardiol 1989;13:1240-7.

56 Burnier M, Waeber B, Nussberger J, Brunner HR. Effect of angiotensin converting enzyme inhibition in renovascular hypertension. J Hypertens Suppl 1989;7:S27-S31.

57 Packer M, Lee WH, Medina N,Yushak M, Kessler PD, Gottlieb SS. Influence of diabetes mellitus on changes in left ventricular performance and renal function produced by converting enzyme inhibition in patients with severe chronic heart failure. Am J Med 1987;82:1119-26.

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