Background Reactive amyloid A (AA) amyloidosis is a serious and life-threatening systemic complication of rheumatoid arthritis (RA). Several biologics therapy reportedly regress gastric amyloid deposition in amyloid A (AA) amyloidosis patients with rheumatoid arthritis (RA), but it is uncertain whether the biologics therapy can also reduce renal amyloid deposition or not, because it is difficult to repeat a histological study in these patients. In patients with vascular type disease, renal involvements are limited (1), so that we can perform a follow-up renal biopsy.
Objectives The purpose of the study is to compare the mass of amyloid deposition in kidney and gastric tract by biologics treatment in AA amyloidosis patients to whom serial histologically study were performed.
Methods The diagnosis of AA amyloidosis was determined by Congo-red stain and anti-AA antibody of gastric biopsy specimen. RA patients who diagnosed AA amyloidosis and had given informed consent were enrolled in the study. The patients were received renal biopsy, and subsequently they were treated with tocilizumab or etanercept for more than three years. Gastric and renal biopsies were performed after biologics treatment at least three years' interval. Renal biopsies were examined only in patients with AA amyloidosis of vascular type disease because renal function does not significantly deteriorate .
Results The vascular type of AA amyloid patients with RA received either etanercept or tocilizumab. The RA activity and laboratory data were significantly improved and sustained for more than 3 years during treating with the biologics. Before biologics treatment, renal biopsy specimens showed amyloid deposition around the blood vessels selectively (Fig. 1A). After biologics treatment, the regression of amyloid deposition was poor and similar to those observed in the initial study (Fig. 1B). Renal function of the patients was not also changed significantly. The results of AA deposition in kidney were also confirmed by anti-AA antibody. In the gastrointestinal tract, after treatment with etanercept or tocilizumab, amyloid mass was markedly regressed (Fig. 1D) compared to the initial study (Fig. 1C) as reported previously.
Conclusions Amyloid deposition of the kidney, in contrast to the gastric tract, regress poorly in AA amyloidosis patients with RA even by biologics therapy, suggesting that regression of amyloid deposition is differently regulated between the kidney and the gastric tract.
Two distinct clinical courses of renal involvement in rheumatoid patients with AA amyloidosis. J Rheumatol. 2006;33:1482-7.
Disclosure of Interest None declared