LECT2 amyloidosis 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 LECT2 amyloidosis. This finding suggests that the LECT2 amyloidosis and its ethnic bias reflect multiple poorly understood factors. Pathophysiology While the pathogenesis of LECT2 amyloidosis is unclear, the intact LECT2 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 LECT2 production and/or a decrease in LECT2 catabolism (i.e. breakdown) which leads to its tissue deposition. However, there appears to be clear genetic variations that lead LECT2 tissue deposition. While studies to date have failed to obtain evidence for LECT2 gene mutations in the disorder, most cases examined in the United States are associated with a particular homozygous single nucleotide polymorphism (i.e. SNP) in the LECT2 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. It is suggested although not yet proven that this Val58Ile variant of LECT2 has a propensity to fold abnormally and therefore deposits in tissues. The Val58Ile LECT2 variant is common in Hispanics and appears to be the cause of their high incidence of LECT2 amyloidosis. Nonetheless, not all homozygous carriers of the variant ever exhibit LECT2 amyloidosis. A second SNP commonly found in Mexicans occurs at codon 172 of the LECT2 gene. This variant is homozygous for a G nucleotide at this codon position and has been associated with an increased incidence of LECT2 amyloidosis. A reason for this association has not yet been proposed. Presentation LECT2 amyloidosis presents with renal disease that in general is slowly progressive and at the time of presentation is of varying severity ranging from early findings of proteinuria or small elevations in blood urea nitrogen and/or creatinine to findings of end stage renal disease. At presentation, many individuals are elderly and suffer serious kidney dysfunction. They may have histological evidence of LECT2 amyloid deposition in the liver, lung, spleen, kidney, and adrenal glands of rarely show any symptoms or signs attributable to dysfunction in these organs. Unlike many other forms of systemic amyloidosis, LECT2 deposition has not been reported to be deposited