title: [Prerenal kidney failure in type 1 diabetes mellitus].
abstract: METHODS
  A 22-year-old man was admitted in a severely reduced condition. Type 1 diabetes mellitus had been diagnosed when he was 13 years old, hypothyroidism was treated with L-thyroxine for 2 years. For the past 3 years he suffered from repetitive hypoglycemia, combined with vertigo, weakness and low blood pressure.
  
  
  METHODS
  He presented with hypotension and hyperpigmentation of the skin. Pathological laboratory results were: serum creatinine 2.5 mg/dl; urea 145 mg/dl; sodium 124 mmol/l; potassium 8.3 mmol/l, HbA (1c) 9.1%. The ECG showed large T waves. Additionally, plasma aldosterone was decreased (<10 ng/l), plasma renin was increased (2404 ng/l), basal serum cortisol was decreased (16.1 microg/l). No increase of plasma cortisol after i. v. stimulation with ACTH (1-24) occurred. Plasma ACTH was increased to 630 pg/ml. Test for adrenal autoantibodies were positive.
  
  
  METHODS
  Primary adrenal insufficiency with prerenal renal failure. Autoimmune polyglandular syndrome (APS) type II with Addison's disease, diabetes mellitus type 1 and hypothyroidism (Schmidt-Carpenter-Syndrome) were diagnosed.
  
  
  METHODS
  Initially, the patient was treated with sodium chloride 0.9% i. v. and oral sodium 5 g 4 times/day. In addition, he was given hydrocortisone 100 mg i. v., and then switched to 40 mg per day (20-10-10 mg), fludrocortisone 0.05 mg/ day and L-thyroxine 75 microg/ day orally the clinical condition improved dramatically within 24 hours. Intensified conventional insulin therapy was continued.
  
  
  CONCLUSIONS
  In patients with type 1 diabetes, especially in combination with associated organ-specific autoimmune diseases, autoimmune polyglandular syndrome should be considered and adequately treated with those hormones that are reduced.
authors.affiliation: Deutsche Diabetes Klinik, Deutsches Diabetes-Forschungsinstitut, Leibniz-Institut an der Heinrich Heine Universität Düsseldorf. schloot@ddfi.uni-duesseldorf.de
authors.forename: N C
authors.initials: NC
authors.lastname: Schloot
authors.forename: A
authors.initials: A
authors.lastname: Hübinger
authors.forename: W A
authors.initials: WA
authors.lastname: Scherbaum
mesh_terms: D000224:Addison Disease / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D003922:Diabetes Mellitus, Type 1 / Q000150:complications*; D003937:Diagnosis, Differential; D005438:Fludrocortisone / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000627:therapeutic use; D017495:Hyperpigmentation; D007022:Hypotension; D007037:Hypothyroidism / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy; D008297:Male; D016884:Polyendocrinopathies, Autoimmune / Q000097:blood / Q000150:complications / Q000175:diagnosis* / Q000188:drug therapy; D012965:Sodium Chloride / Q000627:therapeutic use; D013577:Syndrome; D013974:Thyroxine / Q000627:therapeutic use
chemical_list: D000893:Anti-Inflammatory Agents; D012965:Sodium Chloride; D013974:Thyroxine; D005438:Fludrocortisone; D006854:Hydrocortisone