title: Revisiting medullary tophi: a link between uric acid and progressive chronic kidney disease?
abstract: BACKGROUND
  It is well-established from autopsy studies that gouty tophi can form in the kidney, particularly in the renal medulla. Recently hyperuricemia has been identified as a risk factor for progression of chronic kidney disease (CKD). Because each collecting duct serves more than 2,000 nephrons, we postulated that obstruction or disruption of collecting ducts by medullary tophi may explain, at least in part, the association between hyperuricemia and progressive CKD. This work was done to determine the prevalence of medullary tophi in CKD patients.
  
  
  METHODS
  We queried our nephropathology database over the last 10 years for native kidney biopsies that had medullary tophi. The presence or absence of CKD and uric acid levels around the time of biopsy were determined by chart review.
  
  
  RESULTS
  Predominant medullary tissue was reported in 796 of 7,409 total biopsies, and 572 of these were from patients with established CKD. Medullary tophi were seen in 36 patients, 35 of whom had CKD, suggesting a minimum prevalence of tophi in CKD and no-CKD of 6.11 and 0.45%, respectively Medullary tophi occurred with and without hyperuricemia or a history of gout.
  
  
  CONCLUSIONS
  Medullary tophi appear to be far more likely to occur in CKD compared to no-CKD patients. This cross-sectional study cannot determine whether medullary tophi are a cause or consequence of CKD. However, given their location and bulk, it is possible that medullary tophi contribute to progression of established CKD by causing upstream nephron damage.
authors.forename: Isabelle
authors.initials: I
authors.lastname: Ayoub
authors.forename: Salem
authors.initials: S
authors.lastname: Almaani
authors.forename: Sergey
authors.initials: S
authors.lastname: Brodsky
authors.forename: Tibor
authors.initials: T
authors.lastname: Nadasdy
authors.forename: Jason
authors.initials: J
authors.lastname: Prosek
authors.forename: Lee
authors.initials: L
authors.lastname: Hebert
authors.forename: Brad
authors.initials: B
authors.lastname: Rovin
mesh_terms: D000328:Adult; D000368:Aged; D001706:Biopsy / Q000379:methods; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D033461:Hyperuricemia / Q000652:urine; D007679:Kidney Medulla / Q000737:chemistry*; D007685:Kidney Tubules, Collecting / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009399:Nephrons / Q000473:pathology; D051436:Renal Insufficiency, Chronic / Q000473:pathology*; D012189:Retrospective Studies; D012307:Risk Factors; D014527:Uric Acid / Q000032:analysis* / Q000097:blood; D055815:Young Adult
chemical_list: D014527:Uric Acid; D003404:Creatinine