Acute renal failure associated to renin angiotensin system (RAS) inhibitors its burden in a nephrology department

Sir, The introduction of renin–angiotensin system (RAS) inhibitors has been a progress in the cardiovascular therapies. Despite their beneficial actions on peripheral resistances, on heart function and on vasculopathy, we should no forget their effects on renal haemodynamics. As it is well-known, angiotensin II (AII) is an important actor in the auto-regulation of glomerular filtrationrate (GFR). AII increases efferent glomerular arteriole resistance, having an important role in the control of the glomerular capillary hydrostatic pressure [1]. Its reduction by RAS inhibition could have a renoprotective effect in case of glomerular hypertension [2], but it has a potential harmful effect on GFR when glomerular perfusion is maintained in the normal range precisely by the constrictor effect of AII on the efferent arteriole set. Such a situation takes place when real or effective hypovolaemia occurs (i.e. dehydration, heart failure or renal artery stenosis) [3]. In fact, renal failure associated to the use of RAS inhibitors has been described in up to 19% of patients with hypertensive nephroesclerosis [4], and the decrease in GFR could be irreversible if severe atheromatous disease, renal asymmetries or pre-existent renal insufficiency are concurrent [5]. Furthermore, patients suffering from acute renal failure (ARF) during treatment with RAS inhibitors are frequently attended in emergency rooms. Prompted by this ‘epidemic’ pathology, we have retrospectively analysed its prevalence during 2004 in our Nephrology Department. Forty-one patients suffering from ARF without any immunologic, septic or toxic-related cause were admitted in our centre. Associated RAS inhibitors therapy was documented in 20 of them (48.7). Their mean age was 70.8 ± 24 years (46–94); 12 males and 8 females. Nineteen had hypertension, 10 diabetes, 10 renal echographic asymmetries higher than 15 mm, six chronic heart failure, five stroke and four symptomatic peripheral vasculopathy. In addition to ACEIs or ARBs, furosemide, potassium supplements or espironolactone were associated in seven patients. Co-adjuvants to ARF were vomiting and/or diarrhoea in 14 patients, insufficient fluids supply in two patients and digestive haemorrhage in one patient. Serum creatinine before ARF was 153 ± 104 μmol/l (84–293) and at admittance, 658 ± 330 μmol/l (300–1700). Fourteen patients (70%) showed hyperkalaemia: 5.8 ± 1.5 mEq/l (3.4–8.6). Haemodyalisis was assessed in 13 cases (65%). One patient died in this setting. At discharge, mean serum creatinine level was 262 ± 23 μmol/l (98–700). In our experience, RAS inhibitors could have a pathogenic role in almost 50% of patients with haemodynamic ARF admitted to our Department. Advanced age, vascular disease, previous renal failure and renal asymmetries appear to constitute main risk factors. In this subset of patients, this therapy must be carefully balanced in terms of risk/benefit. A correct hydration must be warranted and frequent control of renal function and serum potassium levels are mandatory. Conflict of interest statement. None declared.