title: Minimal renal dysfunction in inflammatory bowel disease is related to disease activity but not to 5-ASA use.
abstract: BACKGROUND
  Conflicting data exist about proteinuria in inflammatory bowel diseases. It is still unclear whether the occurrence of proteinuria in inflammatory bowel disease patients is an extra-intestinal manifestation of disease or the result of adverse effects to medication, especially to aminosalicylates (ASA).
  
  
  METHODS
  A total of 95 patients (51 with Crohn's disease and 44 with ulcerative colitis) were enrolled in the study. Disease activity was assessed by Crohn's Disease Activity Index (CDAI) or the Truelove index, respectively. Urine was collected over 24 h and protein excretion of specific marker proteins for tubular (alpha 1-microglobulin-alpha 1-MG) and glomerular (albumin-Alb, Immunoglobulin G-IgG) dysfunction was measured using a highly sensitive immunoluminometric assay.
  
  
  RESULTS
  Out of 51 Crohn's disease patients, 20 showed elevated urinary alpha 1-MG. The amount of alpha 1-MGuria was strongly correlated to the CDAI (r=0.6, P < 0.001). Only four Crohn's disease patients showed slightly elevated values for glomerular proteins in urine. Similar results were obtained for ulcerative colitis: whereas only two ulcerative colitis patients showed albuminuria, tubular proteinuria was detected in 28 out of 44 ulcerative colitis patients. Proteinuria was strongly dependent on disease activity (P < 0.01) but was not related to ASA treatment.
  
  
  CONCLUSIONS
  Proteinuria of tubular marker proteins occurs in the majority of inflammatory bowel disease patients and is related to disease activity rather than to ASA treatment. Tubular proteinuria seems to reflect a renal extra-intestinal manifestation of inflammatory bowel disease and may serve as a new relevant marker of disease activity.
authors.affiliation: Department of Internal Medicine I, Division of Gastroenterology, Medical University of Luebeck, Germany. klaus.herrlinger@medinf.mu-luebeck.de
authors.forename: K R
authors.initials: KR
authors.lastname: Herrlinger
authors.forename: M K
authors.initials: MK
authors.lastname: Noftz
authors.forename: K
authors.initials: K
authors.lastname: Fellermann
authors.forename: K
authors.initials: K
authors.lastname: Schmidt
authors.forename: J
authors.initials: J
authors.lastname: Steinhoff
authors.forename: E F
authors.initials: EF
authors.lastname: Stange
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000636:Aminosalicylic Acids / Q000009:adverse effects* / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D015415:Biomarkers / Q000032:analysis; D003093:Colitis, Ulcerative / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D003424:Crohn Disease / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology*; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011507:Proteinuria / Q000453:epidemiology / Q000209:etiology*
chemical_list: D000636:Aminosalicylic Acids; D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers