Development of systemic lupus erythematosus in an elderly male hemodialysis patient with pleuritis.

This report describes a 70-year-old man who developed systemic lupus erythematosus (SLE) during treatment with maintenance hemodialysis. At initiation of maintenance dialysis, the etiology of end-stage renal disease (ESRD) was diabetic nephropathy and no clinical symptom or laboratory data suggested SLE. Fever, pleural effusion that did not respond to ultrafiltration, and immunological findings such as low complement and elevated anti-double-strand DNA antibody level appeared 4 years after maintenance dialysis initiation. Immunosuppressive therapy with corticosteroids improved these abnormalities remarkably. This case underscores the necessity of considering SLE in the differential diagnosis of pleural effusion with male ESRD patients, even if another etiology of ESRD exists.

AP-VAS 2012 case report: a case of myeloperoxidase antineutrophil cytoplasmic antibody-positive microscopic polyangiitis with rapidly progressive glomerulonephritis and hearing loss.

A 74-year-old Japanese woman was admitted to our hospital because of fever, fatigue, and hearing loss associated with vertigo. She had a 1-year history of hearing impairment that got worse gradually and had been treated as otitis media with effusion, but without remarkable improvement. After admission, she developed renal dysfunction associated with hematuria and proteinuria. Laboratory tests showed leukocytosis and elevated C-reactive protein. Myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA) was elevated, but proteinase-3 antineutrophil cytoplasmic antibody (PR3-ANCA) was negative. Renal biopsy revealed pauci-immune focal necrotizing glomerulonephritis with crescents. She was diagnosed as having MPO-ANCA-associated polyangiitis. After treatment with 500 mg methylprednisolone applied intravenously for 3 days, followed by 40 mg prednisolone administered orally, renal function recovered completely. Her hearing also improved. Although otolaryngological symptoms are common in PR3-ANCA associated vasculitis, hearing loss is a rare manifestation of MPO-ANCA associated vasculitis (MPO-AAV). Our case suggests that AAV should be considered in the differential diagnosis of hearing loss.

Parathyroid hemorrhage occurring after administration of cinacalcet in a patient with secondary hyperparathyroidism.

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.

Paraquat-induced oxidative stress and dysfunction of the glutathione redox cycle in pulmonary microvascular endothelial cells.

Oxidative stress and changes in the antioxidant defense system that include the glutathione redox cycle in cultured pulmonary microvascular endothelial cells after exposure to paraquat at 0.1 and 0.5 mM were examined as a function of time. Cell viability was substantially lost 72 h after exposure to 0.5 mM paraquat, but not 0.1 mM paraquat. Viability loss was accompanied by increased glutathione-protein mixed disulfide formation, as well as a loss in glyceraldehyde-3-phosphate dehydrogenase activity, indicating a low defense potential. At 4 h after exposure to paraquat at both doses, however, a marked loss in NADPH was found, together with a decrease in aconitase activity. With 0.5 mM paraquat, increased NADP(+) accompanied by NADPH loss diminished constantly after 48 h without recovery of lost NADPH, suggesting destruction of pyridine nucleotides under oxidative stress. NAD(+) decreased 72 h after exposure to 0.5 mM paraquat, but NADH was not influenced. 3-Aminobenzamide did not protect the loss in NADP(+) or NAD(+) and cell viability. Although oxidized glutathione did not increase by exposure to paraquat at both doses through a 96-h exposure period, reduced glutathione increased at 48 to 72 h, with an increase in glutathione disulfide reductase activities. In contrast, a marked loss in glutathione peroxidase activity was produced 48 h after exposure to 0.5 mM paraquat, preceding cell injury. Mercaptosuccinate, an inhibitor of glutathione peroxidase, distinctly hastened viability loss by paraquat. These results indicate that the reduced ability of the glutathione redox cycle, leading to high oxidative stress, is closely associated with paraquat-induced cytotoxicity.