For example, clarithromycin may lead to decreased zidovudine concentrations. Mechanism of action
Clarithromycin prevents bacteria from multiplying by acting as a protein synthesis inhibitor. It binds to 23S rRNA, a component of the 50S subunit of the bacterial ribosome, thus inhibiting the translation of peptides. Pharmacokinetics
Unlike erythromycin, clarithromycin is acid-stable, so can be taken orally without having to be protected from gastric acids. It is readily absorbed, and diffuses into most tissues and phagocytes. Due to the high concentration in phagocytes, clarithromycin is actively transported to the site of infection. During active phagocytosis, large concentrations of clarithromycin are released; its concentration in the tissues can be over 10 times higher than in plasma. Highest concentrations are found in liver, lung tissue, and stool. Metabolism
Clarithromycin has a fairly rapid first-pass metabolism in the liver. Its major metabolites include an inactive metabolite, N-desmethylclarithromycin, and an active metabolite, 14-(R)-hydroxyclarithromycin. Compared to clarithromycin, 14-(R)-hydroxyclarithromycin is less potent against mycobacterial tuberculosis and the Mycobacterium avium complex. Clarithromycin (20%-40%) and its active metabolite (10%-15%) are excreted in urine. Of all the drugs in its class, clarithromycin has the best bioavailability at 50%, which makes it amenable to oral administration. Its elimination half-life is about 3 to 4 hours with 250 mg administered every 12 h, but increased to 5 to 7 h with 500 mg administered every 8 to 12 h.  With any of these dosing regimens, the steady-state concentration of this metabolite is generally attained within 3 to 4 days.
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