Progression of renal amyloidosis is associated with severe proteinuria or n
ephrotic syndrome, and various mechanisms have been postulated to explain t
hese complications. We studied the acceleration of proteinuria and reduced
renal function by cluster analysis using clinical parameters, renal histolo
gical findings, type of renal amyloidosis and follow-up data. We divided 97
cases into three groups of renal amyloidosis. Accelerated progression corr
elated with serum creatinine (s-Cr) levels at renal biopsy and histological
grade of renal damage by amyloid deposition (p < 0.0001). The most influen
tial prognostic factors (s-Cr level <greater than or equal to>2.0 mg/dl) we
re tubulointerstitial and vascular damage induced by amyloid deposition at
biopsy (odds ratio 96.9 and 69.2, respectively). In addition, we found amyl
oidosis type amyloid associated (AA) correlated with more amyloid-mediated
vascular and tubulointerstitial damage than amyloidosis type amyloid light
chain (AL) (p < 0.001, p < 0.01, respectively). Proteinuria and nephrotic s
yndrome were more severe in cases of amyloidosis AL than in amyloidosis AA
(p = 0.076). In conclusion, less tubulointerstitial and vascular damage was
caused by amyloid deposition; this was slowly progressive. Amyloid AA was
detected in tubulointerstitial tissue and vessels more frequently than amyl
oid AL. Heavy proteinuria and/or nephrosis were not indicators of rapid pro
gression. Copyright (C) 2001 S. Karger AG, Basel.