Host: The Japanese Society of Toxicology
With the onset and progression of chronic kidney disease (CKD), the frequency of onset of various diseases such as cardiovascular disease, osteoarthritis, infectious disease, and malignant tumor increases, which affects the prognosis and quality of life (QOL) of CKD patients. These phenomena are especially observed in dialysis patients, and uremic substances related to them have been identified and are being studied daily to lead to prevention or treatment. Among them, the pathophysiology of CKD-related diseases, especially dialysis amyloidosis, has been elucidated, and how much these uremic substances can be removed is considered to be a treatment method for improving the prognosis or QOL of CKD patients.
Among uremic substances, β2-microglobulin (β2-MG), which is a water-soluble medium-molecular-weight substance, is known to be a precursor protein for dialysis-related amyloidosis because its high blood concentration affects the prognosis of CKD patients. In addition, amyloid fibers composed of β2-MG are deposited mainly in the bone joint tissue of long-term dialysis patients, causing carpal tunnel syndrome, destructive spondyloarthropathies, etc., and as they progress further, they become cardiovascular and other organs, deposits and causes dysfunction.
In dialysis therapy, treatment methods are evolving to improve the removal of β2-MG, but residual syndrome with uremia symptoms remains a problem. It is still unclear how much of a substance with a large molecular weight that is difficult to remove by dialysis or a substance bound to albumin (Alb) should be removed. Among them, increasing the leakage of Alb does not affect the β2-MG reduction rate, but the α1-MG reduction rate increases correlatively. If the removal of α1-MG increases, the removal of TNF-α, Il-6, Il-1β, etc. with a molecular weight of around 30,000 will also increase. Aggressive Alb removal may be required to remove cytokines such as TNF-α, Il-6, and Il-1β.
[Case report]
The reported cases the experience of renal toxicity due to drug experienced clinical.
Case 1. Diffuse tubular interstitial nephritis induced by cilostazol
Case 2. Alogliptin-induced microvariant nephrotic syndrome and tubular interstitial nephritis
