<unk>  as a hepatokine, a substance made and released into the circulation by liver hepatocyte cells that acts as a hormone or signaling agent to regulate the function of other cells. While the pathogenesis of<unk>  is unclear, the intact<unk>  protein may have a tendency to fold abnormally thereby forming non-soluble fibrils that are deposited in tissues. It has been suggested that individuals with the disease have an increase in<unk>  production and/or a decrease in<unk>  catabolism (i.e. breakdown) which may increase its tendency to deposit in tissues. On the other hand, there are genetic variations which appear to cause the deposition of<unk>  in tissues. Studies to date have failed to obtain evidence for<unk>  gene mutations in the disorder but most cases examined in the United States are associated with a particular homozygous single nucleotide polymorphism (i.e. SNP) in the<unk>  gene. This SNP occurs in exon 3 at codon 58 of the gene, contains a guanine rather than adenine nucleotide at this site, and consequently codes for the amino acid valine rather than isoleucine. Although not yet proven to occur in vivo, the Val58Ile variant of<unk>  may have a propensity to fold abnormally, form insoluble fibrils, and therefore deposits in tissues. The Val58Ile<unk>  variant is common in Hispanics and appears to be the cause of their high incidence of<unk> . However, not all homozygous Hispanic carriers of the variant ever exhibit<unk> . This suggests that another factor(s) besides the variant Val58Ile protein's structure is involved in its organ/tissue deposition. A second SNP which is also commonly found in Mexicans occurs at codon 172 of the<unk>  gene. This variant is homozygous for a G nucleotide at this codon position and is associated with an increased incidence of<unk> . A reason for this association has not yet been proposed. It has been found repeatedly that the mere presence of<unk>  amyloid tissue deposits does not necessarily indicate the presence of<unk>  disease. For example, autopsy studies find that up to 3.1% of Hispanics have these deposits in their kidneys but no history of signs or symptoms that could be attributed to<unk> . This finding suggests that the<unk>  and its ethnic bias reflect multiple poorly understood factors.
LECT2 amyloidosis
AA amyloidosis
AL amyloidosis
Secondary systemic amyloidosis
Anti-AQP4 disease
Sarcoglycanopathy
Hyaluronidase deficiency
Monoclonal gammopathy