Clinical and histological characteristics of renal AA amyloidosis: a retrospective study of 68 cases with a special interest to amyloid-associated inflammatory response

The Changing Pattern of Renal Amyloidosis in Indian Subcontinent: Two Decades of Experience from a Single Center

“…18 In our study, all the patients had edema of varying degrees, but the incidence of subnephroticrange proteinuria and renal insufficiency was significantly increased (p < 0.05) in recent years (2000s). This may be explained by more dense amyloid deposit in tubulointerstitial and vascular compartment compared to glomerular deposits as reported by Jérôme Verine et al 17 However, the reason for why such change in pattern of amyloid deposits occurred needs further study in a large cohort. In earlier study from our center, 8% of patients with amyloidosis were reported to have subnephrotic-range proteinuria.…”

“…3 However, higher incidence of hypertension (20-30%) was reported from others studies. 15,17 Helmut Hopfer et al, in their case series between 1960 and 2007, reported that 17.2% were hypertensives, and histologically amyloid deposit was found primarily in the vascular compartment of kidney. 18 Etiologies of amyloidosis in Western countries have changed markedly during the last three decades.…”

“…11,16 However, there has been no change in the sex predilection in other regions. 17,18 Clinical manifestations of renal amyloidosis correlate with the amyloid distribution in different renal compartments. However, the reason for the preferential localization to one or the other compartment is not well established.…”

“…5 However, Jérôme Verine et al, in a study in France during 1990-2005, observed renal insufficiency in 75% of patients. 17 The incidence of renal dysfunction in different studies during 1990s ranges from 16% to 53%.…”

Tocilizumab-induced remission of nephrotic syndrome accompanied by secondary amyloidosis and glomerulonephritis in a patient with rheumatoid arthritis

“…We speculated that presence of amyloid deposition aggravates crescent formation by unknown mechanisms. However, several lines of evidence have highlighted the co-existence of AA amyloid deposition and crescent formation in various underlying diseases for renal amyloidosis other than RA, indicating that crescent formation may be secondary to amyloid deposition independent of RA [24,25]. Therefore, further studies are needed to clarify whether the marked reduction of proteinuria observed after tocilizumab treatment can be attributable to the amelioration of AA amyloidosis or of non-AA amyloid-related glomerulonephritis.…”