Kashin–Beck disease (KBD) is a chronic, endemic type of osteochondropathy (disease of the bone) that is mainly distributed from northeastern to southwestern China, including 15 provinces. As of 2011, Tibet has the highest incidence rate of KBD in China. Southeast Siberia and North Korea are other affected areas. KBD usually involves children ages 5–15. To date, more than a million individuals have had KBD. The symptoms of KBD include joint pain, morning stiffness in the joints, disturbances of flexion and extension in the elbows, enlarged inter-phalangeal joints, and limited motion in many joints of the body. Death of cartilage cells in the growth plate and articular surface is the basic pathologic feature; this can result in growth retardation and secondary osteoarthrosis. Histological diagnosis of KBD is particularly difficult; clinical and radiological examinations have proved to be the best means for identifying KBD. Little is known about the early stages of KBD before the visible appearance of the disease becomes evident in the destruction of the joints.This disease has been recognized for over 150 years but its cause has not yet been completely defined. Currently, the accepted potential causes of KBD include mycotoxins present in grain, trace mineral deficiency in nutrition, and high levels of fulvic acid in drinking water. Selenium and iodine have been considered the major deficiencies associated with KBD. Mycotoxins produced by fungi can contaminate grain, which may cause KBD because mycotoxins cause the production of free radicals. T-2 is the mycotoxin implicated with KBD, produced by members of several fungal genera.
Amyloidosis is the accumulation on misfolded protein fibers in the body. This is very common condition associated with many of the chronic illness. Haemodialysis-associated amyloidosis is a form of systemic amyloidosis associated with chronic kidney failure. Even if this is common in CKD patients with chronic regular dialysis, it can be also seen in patient with CKD but have never dialysed too. Presentation
Long-term haemodialysis results in a gradual accumulation of β2 microglobulin, a serum protein, in the blood. It accumulates because it is unable to cross the dialysis filter. Affected individuals usually present after 5 years of dialysis rarely before that. The tendency of haemodialysis-associated amyloidosis is to be articular in general affecting the joints. Diagnosis
Prevention
The mainstay of management of the dialysis related amyloidosis is the prevention than the other type of treatment methods. Because most of the medical and surgical managements for this condition may not prevent the symptoms completely. Therefore we have to take adequate precautions to prevent future dialysis disequilibrium syndrome in CKD patients. There are several steps in prevention of dialysis related amyloidosis. Use of high flux dialyzers
Use of Beta 2 globulin absorber
Preserve the residual kidney functions
Early kidney transplant
In addition low copper dialysis is theorized to prevent or delay onset. Management
Management of haemodialysis associated amyloidosis is symptomatic. Although there are lot of methods to prevent and delay the complications, probably the steroids and analgesics may helpful in the management of the condition. However there are some surgical procedure to reduce the pain. See also
Hepatoerythropoietic porphyria
List of cutaneous conditions

References
External links
https://academic.oup.com/ndt/article-pdf/13/suppl_1/58/9896967/130058.pdf