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Abstract: FR-PO660

What Is the Potential for RAAS Blockade Optimisation for Patients with Diabetic Kidney Disease in the Era of Potassium Binders?

Session Information

Category: Diabetes

  • 502 Diabetes Mellitus and Obesity: Clinical


  • Chong, Stephanie, Royal London Hospital, London, United Kingdom
  • Pates, Katharine, Royal London Hospital, London, United Kingdom
  • Mccafferty, Kieran, Royal London Hospital, London, United Kingdom

Diabetes is the leading cause of renal failure in both worldwide and in the UK . For 2 decades RAAS blockade has been the cornerstone of management of diabetic kidney disease. Recent registry data suggest that RAAS dose maximisation is key to reduce population health care costs and improve outcomes. However, the use of RAAS blockade is often limited by hypotension or hyperkalaemia.
Potassium binders may provide a novel strategy to safely enable dose maximisation of RAAS therapy, but it is unknown how many patients are not treated or sub-maximally treated due to fears of hyperkalaemia.


We performed a retrospective study, analysing our electronic patient record to establish how many patients were sub-maximally treated with RAAS therapy and the reasons for failure of dose maximisation. We included all adult patients with type 2 diabetes, in our tertiary renal unit which covers a population of 2.5 million ethnically diverse patients across North and East London.
We excluded any patients due to commence dialysis imminently or already on renal replacement therapy and patients with secondary glomerular lesion or other clear cause of CKD.


We identified 415 diabetic patients meeting the inclusion/exclusion criteria. We found that only 72% were on ACE or ARB therapy. Of these, only 50.3% were on maximum dose therapy. This means that only 37% of patients of the total cohort were on maximal RAAS therapy. The main limiting factors were hyperkalaemia (Potassium > 5.0mmol/L) in 30.8%, hypotension (BP < 120/70 and not on other blood pressure lowering agents) in 15.4%, both in 2.3% and dose was not maximised for no specified reason despite inadequate BP control and acceptable potassium levels in 51.3% of patients. Additional reasons found to explain the lack of dose maximisation in this group of patients, were historical hyperkalaemia, fear of new hyperkalaemia, progressive CKD or AKI.


Our study demonstrated the huge unmet potential for safe dose maximisation of RAAS therapy using potassium binders in a cohort of patients with diabetic kidney disease. We estimate that if these findings were extrapolated across the 3 million patients with diabetic kidney disease across the UK then almost 1 million patients may benefit from potassium binder enabled dose maximisation.