title: Fludrocortisone therapy for persistent hyperkalaemia.
abstract: Type 4 renal tubular acidosis causes hyperkalaemia, for which diabetes and medications commonly used in this patient group are aetiological factors. Here we describe the novel use of fludrocortisone in this difficult condition.
  
  
  
  A 55-year-old woman with complex co-morbidities, including Type 2 diabetes (HbA1c37 mmol/mol 5.5%), was admitted with renal failure. Bloods on admission: eGFR 25 ml/min, creatinine 184 ?mol/L, urea 35.9 mmol/L, sodium 128 mmol/L, potassium 5.6 mmol/L, bicarbonate 15 mmol/L, and albumin 30 g/L. Her admission was prolonged, complicated by hospital-acquired sepsis (lower respiratory tract, urinary tract, and infected leg ulcers), poor venous access and severe depression. She had recurrent hyperkalaemia and deteriorating renal function, from presumed Type 4 renal tubular acidosis and excessive fluid losses from leg ulcers. Her renal function recurrently deteriorated, despite conventional treatment methods. After 69 days, she was commenced on fludrocortisone 50 mcg/day. Her renal function and serum potassium stabilized and she was discharged with potassium 4.3 mmol/L, eGFR 42 ml/min, and bicarbonate 23 mmol/L. She has remained stable on this treatment, without requiring further hospital admission for over 6 months, with eGFR 40 ml/min, and potassium 5.5 mmol/L, and albumin 26 g/L.
  
  
  
  This woman was presumed to have Type 4 renal tubular acidosis and recurrent hyperkalaemia due to renal insufficiency, in the context of underlying diabetes and chronic kidney disease, which was poorly responsive to conventional management. There is limited evidence for using fludrocortisone in this setting. Our case suggests that fludrocortisone might offer a novel therapeutic strategy when conventional management is not working.
authors.affiliation: Department of Diabetes and Endocrinology, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: S J H
authors.identifier: 0000-0002-9111-0242
authors.initials: SJH
authors.lastname: Dobbin
authors.affiliation: Department of Diabetes and Endocrinology, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: J R
authors.initials: JR
authors.lastname: Petrie
authors.affiliation: Department of Diabetes and Endocrinology, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: M E J
authors.initials: MEJ
authors.lastname: Lean
authors.affiliation: Department of Diabetes and Endocrinology, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: G A
authors.initials: GA
authors.lastname: McKay
mesh_terms: D000141:Acidosis, Renal Tubular / Q000188:drug therapy* / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D015897:Comorbidity; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D005260:Female; D005438:Fludrocortisone / Q000627:therapeutic use*; D006801:Humans; D006947:Hyperkalemia / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D007668:Kidney / Q000187:drug effects* / Q000276:immunology / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000453:epidemiology / Q000276:immunology / Q000503:physiopathology; D008875:Middle Aged; D055502:Secondary Prevention; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D005438:Fludrocortisone