Amyloidosis is a protein folding disease that causes organ injuries and even death. In humans, 42 proteins are now known to cause amyloidosis. Some proteins become amyloidogenic as a result of a pathogenic variant as seen in hereditary amyloidoses. In acquired forms of amyloidosis, the proteins form amyloid in their wild-type state. Four types (serum amyloid A (AA), transthyretin (ATTR), apolipoprotein AIV (ApoAIV), and beta-2-macroglobulin (AB2m)) of amyloid can occur either as acquired or as a mutant. Iatrogenic amyloid from injected protein medications have also been reported and AIL1RAP (anakinra) has been recently found to involve the kidney. Finally, the mechanism of how leukocyte cell derived chemotaxin-2 (ALECT2) forms amyloid remains unknown. This paper will review amyloids that involve the kidney and how they are typed.
Keywords: AL; ALECT2; ATTR; ApoAIV; ApoCIII; amyloidosis; kidney; mass spectrometry.
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