title: Renal tubular injury is present in acute inflammatory bowel disease prior to the introduction of drug therapy.
abstract: BACKGROUND
  5-aminosalicylic acid (5-ASA) has been associated with renal complications in inflammatory bowel disease. Renal function is typically monitored using serum creatinine; however, significant disease may predate increases in creatinine.
  
  
  OBJECTIVE
  To identify whether markers of early renal disease (urinary albumin, alpha-1-microglobulin [alpha-1-M] and N-acetyl-beta-D-glucosaminidase [NAG], and serum cystatin C) are useful in the assessment of renal function in inflammatory bowel disease patients receiving 5-ASA.
  
  
  METHODS
  Twenty-one patients with a new diagnosis of inflammatory bowel disease were investigated. Samples were taken at diagnosis, and at 3-monthly intervals after the commencement of 5-ASA, for 1 year.
  
  
  RESULTS
  Mean creatinine clearance was 100 mL/min and did not change following treatment. Inflammatory bowel disease was not associated with albuminuria. Urinary N-acetyl-beta-D-glucosaminidase and alpha-1-microglobulin at diagnosis were increased in 10 (48%) and 11 (52%) patients, respectively: treatment was not associated with consistent changes in urinary protein excretion. There was a significant correlation between cystatin C and creatinine clearance both at diagnosis (r=-0.533, P=0.0275) and combining the initial and follow-up data (r=-0.601, P < 0.01), but not between creatinine and creatinine clearance (P > 0.05).
  
  
  CONCLUSIONS
  Tubular proteinuria is an extra-intestinal manifestation of inflammatory bowel disease irrespective of 5-ASA treatment. Tubular proteins are not useful predictors of an adverse renal response to 5-ASA. Serum cystatin C may be an improved marker of glomerular filtration rate in this setting.
authors.affiliation: Department of Gastroenterology, East Kent Hospitals NHS Trust, Kent and Canterbury Hospital, Canterbury, Kent, UK.
authors.forename: J S
authors.initials: JS
authors.lastname: Fraser
authors.forename: A F
authors.initials: AF
authors.lastname: Muller
authors.forename: D J
authors.initials: DJ
authors.lastname: Smith
authors.forename: D J
authors.initials: DJ
authors.lastname: Newman
authors.forename: E J
authors.initials: EJ
authors.lastname: Lamb
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000510:Alpha-Globulins / Q000652:urine; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000627:therapeutic use*; D015415:Biomarkers; D003404:Creatinine / Q000097:blood; D055316:Cystatin C; D015891:Cystatins / Q000652:urine; D005260:Female; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000150:complications* / Q000188:drug therapy; D007674:Kidney Diseases / Q000209:etiology*; D007684:Kidney Tubules / Q000473:pathology*; D008297:Male; D019804:Mesalamine / Q000009:adverse effects / Q000627:therapeutic use*; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D011446:Prospective Studies; D011507:Proteinuria / Q000209:etiology* / Q000652:urine
chemical_list: D000510:Alpha-Globulins; D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; C525030:CST3 protein, human; D055316:Cystatin C; D015891:Cystatins; C016001:alpha-1-microglobulin; D019804:Mesalamine; D003404:Creatinine; D000118:Acetylglucosaminidase