A 58-year-old man was referred to our institution for an evaluation of nephrotic range proteinuria. Renal biopsy showed a marked expansion of the mesangial matrix and thickening of glomerular basement membrane (GBM) in periodic acid-silver methenamine (PAM). Immunofluorescence (IF) revealed strong staining for the monoclonal kappa light chain. EM demonstrated massive subendothelial and mesangial dense deposits. As a result, light chain deposition disease (LCDD) was diagnosed. Melphalan and prednisolone (MP) therapy was started, which was continued for 10 years with minimal complications. Serial evaluations of renal histology revealed the resolution of nodular lesions and the glomeruli became nearly normal. MP therapy can therefore be an effective therapeutic option for LCDD if it is continued over the long term.
We herein report an unusual case of spontaneous parathyroid gland rupture. A man was admitted with respiratory distress in September 2010. He had been receiving hemodialysis since 1995. He was diagnosed secondary hyperparathyroidism in 2006 and began receiving cinacalcet therapy in 2009. His intact parathyroid hormone (iPTH) level decreased, and massive traumatic bleeding occurred, following which rupture of the parathyroid gland was detected during surgery. The ruptured gland showed nodular hyperplasia. Previous reports have indicated that parathyroid bleeding is associated with glandular hypertrophy. This is the first report of parathyroid apoplexy occurring after suppression of elevated parathyroid function caused by cinacalcet therapy.