Prognostic factors for renal amyloidosis: a clinicopathological study using cluster analysis.
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.
Sasatomi
Yoshie
Y
Division of Nephrology & Rheumatology, Department of Internal Medicine, Fukuoka University School of Medicine, Fukuoka, Japan. sasatomi@fukuoka-u.ac.jp
Sato
Hiroshi
H
Chiba
Yoshiro
Y
Abe
Yasuhiro
Y
Takeda
Seiji
S
Ogahara
Satoru
S
Murata
Toshiaki
T
Kaneoka
Hidetoshi
H
Takebayashi
Shigeo
S
Iwasaki
Hiroshi
H
Saito
Takao
T
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
D000682:Amyloid; D000685:Serum Amyloid A Protein; C518669:amyloid L, human; D003404:Creatinine