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Abstract Background Persistent hyperparathyroidism is one of the main causes of hypercalcemia following kidney transplantation; differential diagnosis is required. Case Presentation We report the case of a 61-year-old kidney transplant recipient who underwent transplant in September 2016. She was admitted in March 2017 presenting with a 3-week history of asthenia, hypotension, and cough. Laboratory analysis showed acute kidney injury with hypercalcemia and elevation of inflammatory markers. She was initially treated with hydration therapy. A few days after admission she developed respiratory failure: chest computed tomography showed a ground-glass pattern. A diagnosis of Pneumocystis jirovecii was made on bronchoalveolar lavage. A subsequent graft biopsy was performed that revealed intratubular calcium deposition without signs of rejection. The patient was given trimethoprim/sulfamethoxazole, with improvement in pulmonary and renal function as well as improvement in hypercalcemia. Conclusions P jirovecii infection can trigger activation of intra-alveolar macrophages that leads to extrarenal vitamin D production with subsequent hypercalcemia. This rare event should be considered in renal transplant patients with pulmonary infection accompanied by hypercalcemia. In our case, hypercalcemia also provoked acute kidney injury. Highlights • Hyperparathyroidism is a main cause of hypercalcemia following kidney transplantation. • Hypercalcemia associated with Pneumocystis jirovecii is rare in kidney transplantation. • P jirovecii should be considered in renal transplant patients with lung infection and hypercalcemia. [ABSTRACT FROM AUTHOR]

Abstract Background Recurrence of focal segmental glomerulosclerosis (FSGS) in renal allograft recipients after first transplant occurs in the second graft in virtually all patients. There is little evidence regarding optimal treatment. Case presentation A 55-year-old man with primary FSGS and disease recurrence in both the first and the second kidney grafts is presented. In 1999, the patient developed FSGS 3 years after transplant, which was treated with plasmapheresis and cyclophosphamide. Hemodialysis was started at 8 years from the onset of relapse. In February 2014, the patient received a second kidney transplant, and after 2 weeks laboratory analysis showed nephrotic proteinuria (5.9 g/d) with increased serum creatinine. Biopsy results revealed recurrence of FSGS. At that time, he was treated with steroids and plasmapheresis with partial efficacy, achieving a serum creatinine level of 1.1 mg/dL with decreased proteinuria (1 g/d). After 4 months, creatinine worsened (1.6 mg/dL) with new evidence of proteinuria. Second biopsy results showed evidence of FSGS progression. The patient then received plasmapheresis and 2 doses of rituximab. Follow-up was characterized by progressive remission up to complete resolution. The patient is currently free from relapses after 3 years with good renal function and almost no proteinuria. Conclusions More evidence and prospective studies are needed to better understand the role of rituximab in FSGS in order to obtain an optimized therapeutic protocol for recurrence of FSGS in renal transplant recipients. Highlights • A case of recurrent focal segmental glomerulosclerosis recurrence in the first and second kidney grafts is presented. • The patient underwent plasmapheresis and received 2 doses of rituximab. • After 3 years the patient is currently relapse-free with good renal function. [ABSTRACT FROM AUTHOR]

Abstract: Objective: : The aim of the present study was to analyze if alterations of peripheral-type benzodiazepine receptor (PBR) characteristics occurred in platelet membranes of patients affected by primary fibromyalgia (FM). Design and methods: : Platelets were obtained from 30 patients with FM. Evaluation of kinetic parameters of PBR was performed using [3H] PK11195 as specific radioligand compared with 16 healthy volunteers. Results: : The results showed a significant increase of PBR binding sites value in platelet membranes from FM patients (B max was 5366±188 fmol/mg vs. controls, 4193±341 fmol/mg, mean±SEM) (**p <0.01) but not for affinity value (K d was 4.90±0.39 nM vs. controls, 4.74±0.39 nM, mean±SEM) (p >0.05). Symptom severity scores (pain and tiredness) were positively correlated with B max. Conclusions: : Our results showed an up-regulation of PBR in platelets of FM patients, and this seems to be related to the severity of fibromyalgic symptoms. [Copyright &y& Elsevier]