Renal parenchymal calcification secondary to systemic AA amyloidosis

A 28-year-old man presented with a history of hyper-IgD and periodic fever syndrome (HIDS), which had resulted in systemic AA amyloidosis. He had evidence of amyloid deposition in the kidney, liver and spleen. A living donor kidney transplant in 2005 failed after 6 years due to recurrent amyloid in the transplant kidney. A trial of tocilizumab, an anti-IL-6 monoclonal antibody, started in July 2012 with a marked reduction of symptoms and inflammatory markers. He received a second living donor kidney transplant in August 2012. The transplant function is good and biopsy has shown no evidence of recurrent amyloidosis. Amyloid fibrils have an affinity for calcium, and radiographically detectable calcified amyloid deposits may occur in both primary and secondary amyloidosis. Fig. 1. This plain abdominal radiograph was taken at a time of intercurrent sepsis and demonstrated florid calcification of the parenchyma of both native kidneys (arrows). Of note, neither transplanted kidney has yet calcified (open arrows).