PMID- 17329915 OWN - NLM STAT- MEDLINE DCOM- 20070409 LR - 20190606 IS - 1349-7235 (Electronic) IS - 0918-2918 (Linking) VI - 46 IP - 5 DP - 2007 TI - Prognostic factors for renal amyloidosis: a clinicopathological study using cluster analysis. PG - 213-9 AB - 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 AND PATIENTS: 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. CONCLUSION: 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. FAU - Sasatomi, Yoshie AU - Sasatomi Y AD - Division of Nephrology & Rheumatology, Department of Internal Medicine, Fukuoka University School of Medicine, Fukuoka, Japan. sasatomi@fukuoka-u.ac.jp FAU - Sato, Hiroshi AU - Sato H FAU - Chiba, Yoshiro AU - Chiba Y FAU - Abe, Yasuhiro AU - Abe Y FAU - Takeda, Seiji AU - Takeda S FAU - Ogahara, Satoru AU - Ogahara S FAU - Murata, Toshiaki AU - Murata T FAU - Kaneoka, Hidetoshi AU - Kaneoka H FAU - Takebayashi, Shigeo AU - Takebayashi S FAU - Iwasaki, Hiroshi AU - Iwasaki H FAU - Saito, Takao AU - Saito T LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20070301 PL - Japan TA - Intern Med JT - Internal medicine (Tokyo, Japan) JID - 9204241 RN - 0 (Amyloid) RN - 0 (Serum Amyloid A Protein) RN - 0 (amyloid L, human) RN - AYI8EX34EU (Creatinine) SB - IM MH - Adult MH - Aged MH - Amyloid/metabolism MH - Amyloidosis/complications/*pathology/*physiopathology MH - Blood Vessels/pathology MH - Cluster Analysis MH - Creatinine/blood MH - Disease Progression MH - Female MH - Heart/physiopathology MH - Humans MH - Kidney/blood supply/metabolism/pathology MH - Kidney Diseases/complications/*pathology/*physiopathology MH - Kidney Tubules/pathology MH - Male MH - Middle Aged MH - Multivariate Analysis MH - Nephrotic Syndrome/complications/physiopathology MH - Prognosis MH - Proteinuria/complications/physiopathology MH - Serum Amyloid A Protein/metabolism MH - Severity of Illness Index MH - Survival Analysis EDAT- 2007/03/03 09:00 MHDA- 2007/04/10 09:00 CRDT- 2007/03/03 09:00 PHST- 2007/03/03 09:00 [pubmed] PHST- 2007/04/10 09:00 [medline] PHST- 2007/03/03 09:00 [entrez] AID - JST.JSTAGE/internalmedicine/46.1690 [pii] AID - 10.2169/internalmedicine.46.1690 [doi] PST - ppublish SO - Intern Med. 2007;46(5):213-9. doi: 10.2169/internalmedicine.46.1690. Epub 2007 Mar 1.