in the myocardium or brain of afflicted individuals. Thus, LECT2 amyloidosis, while classified as a form of systemic amyloidosis, is almost exclusively manifested clinically as renal amyloidosis. Diagnosis LECT amyloidosis is diagnosed by two findings: a) histological evidence of Congo red staining material deposited in the interstitial, mesangial, glomerular, and/or vascular areas of the kidney and b) the identification of these deposits as containing mainly LECT2 as identified by proteomics methodologies. Kidney biopsy shows the presence of LECT2-based amyloid predominantly in the renal cortex interstitium, glomeruli, and arterioles. Treatment There Is too little experience on the treatment of LECT2 amyloidosis (ALECT2) to establish recommendations. There is no recommended specific treatment for LECT2 amyloidosis other than support of kidney function and dialysis. It is important to accurately diagnose ALECT2-based amyloid disease in order to avoid treatment for other forms of amyloidosis. Prognosis Based on studies conducted in the United States, the prognosis for individuals with LECT2 amyloidosis is guarded, particularly because they are elderly and their kidney disease is usually well-advanced at the time of presentation. Rheumatoid arthritis Studies conducted in a mouse model of rheumatoid arthritis indicate that the LECT2 protein suppresses the inflammatory component of this disorder. In human studies, the Val58Ile variant of LECT2 protein which has been associated with the development of LECT2 amyloidosis in Hispanics has also been associated with rheumatoid arthritis. That is, individuals homozygous for the gene making the Val58Ile variant of LECT2 have a small but significant increase in both the incidence and severity of this disease based on a study conducted in Japan. An increase in the severity and joint destruction of rheumatoid arthritis in humans was confirmed in a separate study conducted in Germany. These studies suggest that LECT2 normally functions to suppress the development and/or severity of human rheumatoid arthritis and that the Val58Ile variant of LECT2 is less effective in doing so. Osteoarthritis In a model of osteoarthritis, mice made deficient in LECT2 using a gene knockout method developed more severe osteoarthritis induced by anti-type II collagen antibodies and lipopolysaccharide. The effect was reversed by administering human LECT2 to the animals. A study conducted in Japan found that the expression levels of LECT2 were significantly higher in cartilage of osteoarthritic individuals than in control patients suggesting that LECT2 may be a useful biomarker for the disease. Sepsis In mouse models of bacterial sepsis caused by of E. coli, P.