title: Prognostic factors for renal amyloidosis: a clinicopathological study using cluster analysis.
abstract: OBJECTIVE
  There is no standardized therapy for renal amyloidosis, which shows rapid progression and poor prognosis. Here, we used cluster analysis to examine the correlation between amyloid-related renal damage and prognosis, and determined the clinicopathological prognostic factors for renal amyloidosis.
  
  
  METHODS
  We analyzed 125 patients with renal amyloidosis (men/women: 43/82; mean age at renal biopsy: 58.8+/-11.1 years, +/-SD; range: 21-78 years). Cluster analysis was performed using clinical parameters, renal histological findings, type of renal amyloidosis, and follow-up data. We also analyzed survival data.
  
  
  RESULTS
  We divided 125 cases (prognosis was checked in 97 [77.6%] cases) into three groups by cluster analysis. In the cluster groups, accelerated progression correlated with serum creatinine (s-Cr) levels at renal biopsy and histological grade of renal damage by amyloid deposition (p<0.0001). The most important prognostic factors were glomerular, tubulointerstitial, and vascular lesions induced by amyloid deposition at biopsy (p<0.0001). We also found that amyloid-A (AA) type amyloidosis correlated is more significantly with amyloid-mediated vascular (P=0.0010) and tubulointerstitial lesions (p=0.0705) than with amyloid-L (AL) type amyloidosis. Proteinuria and nephrotic syndrome were more severe in AL than AA amyloidosis (p=0.0836). The 10-year individual survival rate was about 20%, and most deaths were due to cardiovascular disease and infection.
  
  
  CONCLUSIONS
  Our results indicate that the quantity of amyloid deposition in the kidney, and the extent of glomerular, tubulointerstitial, and vascular damage are significant renal prognostic factors in amyloidosis.
authors.affiliation: Division of Nephrology & Rheumatology, Department of Internal Medicine, Fukuoka University School of Medicine, Fukuoka, Japan. sasatomi@fukuoka-u.ac.jp
authors.forename: Yoshie
authors.initials: Y
authors.lastname: Sasatomi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sato
authors.forename: Yoshiro
authors.initials: Y
authors.lastname: Chiba
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Abe
authors.forename: Seiji
authors.initials: S
authors.lastname: Takeda
authors.forename: Satoru
authors.initials: S
authors.lastname: Ogahara
authors.forename: Toshiaki
authors.initials: T
authors.lastname: Murata
authors.forename: Hidetoshi
authors.initials: H
authors.lastname: Kaneoka
authors.forename: Shigeo
authors.initials: S
authors.lastname: Takebayashi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iwasaki
authors.forename: Takao
authors.initials: T
authors.lastname: Saito
mesh_terms: D000328:Adult; D000368:Aged; D000682:Amyloid / Q000378:metabolism; D000686:Amyloidosis / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D001808:Blood Vessels / Q000473:pathology; D016000:Cluster Analysis; D003404:Creatinine / Q000097:blood; D018450:Disease Progression; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000150:complications / Q000473:pathology* / Q000503:physiopathology*; D007684:Kidney Tubules / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D009404:Nephrotic Syndrome / Q000150:complications / Q000503:physiopathology; D011379:Prognosis; D011507:Proteinuria / Q000150:complications / Q000503:physiopathology; D000685:Serum Amyloid A Protein / Q000378:metabolism; D012720:Severity of Illness Index; D016019:Survival Analysis
chemical_list: D000682:Amyloid; D000685:Serum Amyloid A Protein; C518669:amyloid L, human; D003404:Creatinine