title: The impact of stopping inhibitors of the renin-angiotensin system in patients with advanced chronic kidney disease.
abstract: BACKGROUND
  Inhibition of the renin-angiotensin-aldosterone system (RAAS) has shown to slow chronic kidney disease (CKD) progression. This is most notable at the earlier stages of diabetic and proteinuric nephropathies. Objective. Here, we observed the impact of discontinuation of angiotensin converting enzyme inhibitors (ACEi)/angiotensin receptors blockers (ARB) in patients with advanced kidney disease.
  
  
  METHODS
  52 patients (21 females and 31 males) with advanced CKD (stages 4 and 5), who attended our low clearance clinic (LCC) in preparation for renal replacement therapy (RRT). Mean age was 73.3 ± 1.8 years with an estimated glomerular filtration rate (eGFR) of 16.38 ± 1 ml/min/1.73 m(2). Baseline urine protein:creatinine ratio (PCR) was 77 ± 20 mg/mmol. 46% suffered from diabetes mellitus. Patients were followed for at least 12 months before and after ACEi/ARB were stopped.
  
  
  RESULTS
  12 months after discontinuation of ACEi/ARB eGFR increased significantly to 26.6 ± 2.2 ml/min/ 1.73 m(2) (p = 0.0001). 61.5% of patients had more than a 25% increase in eGFR, whilst 36.5% had an increase exceeding 50%. There was a significant decline in the eGFR slope -0.39 ± 0.07 in the 12 months preceding discontinuation. The negative slope was reversed +0.48 ± 0.1 (p = 0.0001). Mean arterial blood pressure (MAP) increased from 90 ± 1.8 mmHg to 94 ± 1.3 mmHg (p = 0.02), however ≥50% of patients remained within target. Overall proteinuria was not affected (PCR before = 77 ± 20 and after = 121.6 ± 33.6 mg/mmol).
  
  
  CONCLUSIONS
  Discontinuation of ACEi/ARB has undoubtedly delayed the onset of RRT in the majority of those studied. This observation may justify a rethink of our approach to the inhibition of the RAAS in patients with advanced CKD who are nearing the start of RRT.
authors.affiliation: Sheffield Kidney Institute, Northern General Hospital, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK.
authors.forename: Aimun K
authors.initials: AK
authors.lastname: Ahmed
authors.forename: Neetha S
authors.initials: NS
authors.lastname: Kamath
authors.forename: Mohsen
authors.initials: M
authors.lastname: El Kossi
authors.forename: A Meguid
authors.initials: AM
authors.lastname: El Nahas
mesh_terms: D000368:Aged; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D001794:Blood Pressure / Q000502:physiology; D002908:Chronic Disease; D000075202:Contraindications; D018450:Disease Progression; D005260:Female; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007674:Kidney Diseases / Q000503:physiopathology* / Q000517:prevention & control* / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy; D008297:Male; D011507:Proteinuria / Q000503:physiopathology; D017582:Renal Replacement Therapy; D012084:Renin-Angiotensin System / Q000502:physiology*; D012189:Retrospective Studies; D028761:Withholding Treatment
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors