Photo Credit: Selvanegra

The following is a summary of the “2024 Update on Classification, Etiology, and Typing of Renal Amyloidosis,” published in the March 2024 issue of Nephrology by Leung et al.

Amyloidosis, a protein-folding disorder, poses significant threats to organ function and overall mortality. Human amyloidosis encompasses a spectrum of 42 proteins known to induce pathological amyloid formation. While hereditary amyloidoses are characterized by pathogenic variants leading to protein amyloidogenicity, acquired amyloidosis involves the formation of amyloid from wild-type proteins. 

Among the identified types of amyloid, including serum amyloid A (AA), transthyretin (ATTR), apolipoprotein AIV (ApoAIV), and beta-2-macroglobulin (AB2m), both acquired and mutant variants can occur. Additionally, iatrogenic amyloidosis arising from protein medications has been documented, with recent reports implicating AIL1RAP (anakinra) in renal involvement. Notably, the mechanisms underlying amyloid formation in leukocyte cell-derived chemotaxin-2 (ALECT2) still need to be discovered. 

This comprehensive review examines the various forms of amyloidosis affecting the kidneys, delving into their classification and typing intricacies to understand these complex pathological processes better.

Source: sciencedirect.com/science/article/abs/pii/S0272638624006796