Secondary Amyloidosis Associated with Castleman's Disease.

An autopsy case of multicentric Castleman’s disease associated with interstitial nephritis and secondary AA amyloidosis

“…The overproduction of SAA due to IL-6 stimulation of hepatocytes can lead some patients to develop AA amyloidosis. Including the present patient, 45 cases of systemic amyloidosis associated with CD have been reported [13][14][15][16][17][18][19][27][28][29][30][31][32][33][34][35]. The main features of patients with amyloidosis secondary to CD are shown in Table 1.…”

“…Biopsies have rarely been available [6]. The most common etiology of renal failure due to CD reported is amyloidosis [7][8][9][10][11][12][13][14][15][16][17][18][19], followed by mesangial proliferative glomerulonephritis [20], and little has been reported on interstitial nephritis [21][22][23][24]. In this report, we present an autopsy case with MCD who developed interstitial nephritis, anemia, thrombocytopenia, and secondary amyloidosis leading to a fatal brain hemorrhage.…”

Membranoproliferative Glomerulonephritis in Castleman's Disease: A Systematic Review of the Literature and 2 Case Reports

“…It is more frequently found in systemic manifestations, often due to the endocrinopathy presenting in POEMS syndrome (peripheral neuropathy, organomegaly, endocrinopathy, monoclonal protein, skin changes). Even Tanaka et al, in their case report, considered that hypothyroidism could be due to amyloid deposition since their patient had no thyroid autoantibodies and no particular findings on echo or CT (12). In the present case 1, we considered that hypothyroidism with positive thyroid autoantibodies, is an immune-mediated association with CD, although the definite specific relationship is yet unknown.…”

Multicentric Castleman's disease associated with renal amyloidosis and pure red cell aplasia

“…It was revealed that large amounts of IL-6 are produced in the germinal centers of CD . Therefore, secondary amyloidosis in CD can be caused by overproduction of SAA due to IL-6 from the hyperplastic lymphoid tissue [10]. In the present case, we did not measure the serum SAA level, but the level of IL-6 was elevated.…”