title: Metabolic basis for low urine pH in type 2 diabetes.
abstract: OBJECTIVE
  Type 2 diabetes is associated with excessively low urine pH, which increases the risk for uric acid nephrolithiasis. This study was conducted to assess the metabolic basis responsible for the excessive urinary acidity of individuals with type 2 diabetes.
  
  
  METHODS
  Nine non-stone-forming patients who had type 2 diabetes and low urine pH and 16 age- and body mass index-matched non-stone-forming volunteers without type 2 diabetes were maintained on a constant metabolic diet for 7 days, and 24-hour urine was collected on the last 2 days of the diet.
  
  
  RESULTS
  Urine dietary markers (potassium, sulfate, phosphorus, and urea nitrogen) were not different between the two groups. Patients with type 2 diabetes exhibited a significantly lower 24-hour urine pH (5.45+/-0.27 versus 5.90+/-0.42; P<0.01) and higher net acid excretion (NAE; 57+/-12 versus 38+/-18 mEq/d; P<0.01) compared with control subjects. The proportion of NAE excreted as ammonium (NH4+/NAE) was significantly lower in patients with type 2 diabetes than in control subjects (0.70+/-0.12 versus 0.94+/-0.36; P<0.01); however, the greater NAE in patients with type 2 diabetes was not accounted for by the differences in unmeasured urinary anions.
  
  
  CONCLUSIONS
  The overly acidic urine in patients with type 2 diabetes persists after controlling for dietary factors, body size, and age. The lower pH is due to a combination of greater NAE and lower use of ammonia buffers in patients with diabetes, which predisposes them to uric acid urolithiasis.
authors.affiliation: Charles and Jane Pak Center for Mineral Metabolism and Clinical Research and Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-8885, USA. naim.maalouf@utsouthwestern.edu
authors.forename: Naim M
authors.initials: NM
authors.lastname: Maalouf
authors.forename: Mary Ann
authors.initials: MA
authors.lastname: Cameron
authors.forename: Orson W
authors.initials: OW
authors.lastname: Moe
authors.forename: Khashayar
authors.initials: K
authors.lastname: Sakhaee
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D015415:Biomarkers / Q000652:urine; D015992:Body Mass Index; D002021:Buffers; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000178:diet therapy / Q000188:drug therapy / Q000652:urine*; D003928:Diabetic Nephropathies / Q000209:etiology* / Q000652:urine; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D053040:Nephrolithiasis / Q000209:etiology* / Q000652:urine; D010758:Phosphorus / Q000652:urine; D011188:Potassium / Q000652:urine; D000644:Quaternary Ammonium Compounds / Q000652:urine; D013431:Sulfates / Q000652:urine; D013781:Texas; D014508:Urea / Q000652:urine; D014527:Uric Acid / Q000652:urine
chemical_list: D015415:Biomarkers; D002021:Buffers; D000644:Quaternary Ammonium Compounds; D013431:Sulfates; D014527:Uric Acid; D010758:Phosphorus; D014508:Urea; D011188:Potassium