Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis

Abstract

During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.

Incidence and Predictors of Development of Acute Renal Failure Related to Treatment of Congestive Heart Failure with ACE Inhibitors

“…We have estimated the incidence of development of ARF in NYHA class III and IV CHF patients treated with ACEI in 25%, in accordance with other recent studies [2,3,4,5,6]. The predictors of development of ARF among decompensated CHF patients treated with ACEI, already described are: advanced age, a diagnosis of NYHA class IV CHF, low ejection fraction of left ventricle, concurrent renal insufficiency, and ABP <65 mm Hg.…”

“…The ‘CONSENSUS’ (Cooperative North Scandinavian Enalapril Survival Study) [1] recommends close monitoring of serum creatinine and potassium levels after introduction of ACEI therapy and after an increase in its dosage. This study shows a 20–30% reduction of glomerular filtration rate (GFR) after introduction of enalapril that trends toward stabilization following a 20- to 30-day period; however, other studies have demonstrated a higher reduction in GFR after introduction of ACEI, especially in certain risk groups of patients [2,3,4,5,6]. …”

“…Under these circumstances, three major factors would play an important role in the development of ARF: (a) insufficient cardiac output; (b) a decrease >25 mm Hg in ABP, and (c) a ACEI-suppressing effect on autoregulation of renal perfusion, culminating in higher risk of development of ARF. Also, hypertensive and diabetic patients could be more susceptible to ARF because of preexisting microangiopathy [2, 7]. …”

“…Bridoux et al [2] studied 27 cases of acute renal failure (ARF) after introduction of ACEI for treatment of CHF and/or systemic arterial hypertension in patients without renal artery stenosis. The most relevant clinical findings were: volume depletion in 21 patients and hypotension in 12 patients.…”

Nephrosclerosis: A Term in Quest of a Disease

“…Some drugs such as clonidine [30,] di-hydropyridines [31,32] and hydralazine [33] hinder renal autoregulation. Ang II antagonists may complicate nephrosclerosis with acute kidney insufficiency in the absence of atherosclerotic renal disease [34] and it is conceivable that overcorrection of hypertension with this class of drugs that act on the glomerular efferent arteriole might in the long-term trade off glomerulomegaly and FSGS for ischemic glomerular obsolescence [35]. …”