Impact of enalapril on renal function in patients with severe chronic kidney disease

Sir, Although ACE-inhibitors are nowadays considered drugs of choice in treating hypertension in patients with chronic kidney disease (CKD) 1, the possible occurrences of acute renal failure and hyperkalemia, already described in elderly and diabetic populations 2,3, limit their use in patients with severe CKD. Hou FF et al. 4 have recently published a paper which led me to evaluate the impact of ACE inhibition on measured creatinine clearance (CrCl) in hypertensives with stages III–IV CKD who were referred to our Hypertension Unit, between 1 January 2004 and 31 December 2005. The analysis was focused on hypertensives with CrCl values ranging between 15 and 60 ml/min/1.73 m2, with or without proteinuria. Patients with renal artery stenosis or those already taking antihypertensives were not considered. In our practice, in nephropathic hypertensives, after assessing ICED score 5, main lab and instrumental parameters, furosemide (25 mg p.o. daily titrated up to 50 mg) + enalapril (10 mg p.o. daily titrated up to 20 mg) are started as a first approach in order to attain the blood pressure (BP) goal (<130/70 mmHg). Other antihypertensives are added in resistant patients. This letter reports data regarding a 8.4 ± 2.0 months (mean ± SD) follow-up in 25 caucasian patients (44% males, 15% diabetics, 64% on stage III CKD) who met the inclusion criteria. At the time of first visit, they were 60.7 ± 12.9 years old. All of them reached the BP goal, taking furosemide + enalapril at full titrations. In the entire cohort, enalapril did not influence renal function (baseline: 33.1 ± 5.1 ml/min/1.73 m2; after enalapril: 31.8 ± 6.0 ml/min/1.73 m2; paired Student's t-test: P = 0.43), even after adjusting the analysis by the stage of CKD and the ICED score. Proteinuria (g/day) significantly dropped during the follow-up (baseline: 2.6 ± 1.1; after enalapril: 1.9 ± 0.8; P = 0.03). Hyperkalaemia occurred in two patients with stage III CKD (8% of the cohort), but they recovered suddenly after withdrawing the therapy. Even keeping in mind all the differences in terms of design, follow-up, medications, outcomes and populations between this analysis and Hou's study 4, it is possible to conclude that, in my experience also, ACE-inhibition, independently from the severity of renal involvement and the global clinical picture, can control hypertension in patients with severe CKD with no effects on renal function. However, the possible occurrence of hyperkalaemia suggests a regular checking for serum potassium in this clinical setting. In conclusion, this analysis confirms that patients with severe CKD may also safely experience the renoprotective effects of ACE-inhibition. Conflict of interest statement. None declared.