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Objective To improve clinicians’ understanding of post transplant lymphoproliferative disorder (PTLD) after renal transplantation,a rare case of this disease was reported and literature was reviewed.Method The clinical data and pathological changes of the allograft,immunohistochenmistry (IHC) and in situ hybridization (ISH) were analyzed.In addition,the relevant literature was reviewed.The clinicopathological features and differential diagnoses of PTLD were discussed.Result A renal mass (5.6 cm × 5.4 cm),which was suggestive of primary renal malignancy,had been detected on the patient after received renal transplantation for a year and a half.Grossly,the mass was 7cm in diameter,with fleshy texture.Microscopically,the renal parenchyma was destructed and infiltrated with massive inflammatory cells,mostly lymphoid cells and occasionally Reed-Steruberg-like cells.IHC showed CD20 and CD79a were predominantly expressed in lymphoid cells.ISH showed diffused Epstein-Barr virus encoded RNAs (EBERs) positivity.The above findings were consistent with PTLD,polymorphic B cell hyperplasia (polymorphic PTLD),with concurrent EpsteinBarr virus infection.Conclusion Lymphoid infiltration in a renal allograft needs to be differentiated from T-cell rejection,viral infection,nephropyelitis,as well as PTLD.Early detection and proper management of PTLD may help improve the graft survival rate.
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Objective To report a Chinese boy suffering from nephrotic syndrome associated with Schimke immuno-osseous dysplasia (SIOD). Methods The clnical data and pathological changes of renal biopsy were analyzed and associated literatures were reviewed. The clinicopathological features and diagnosis of SIOD were discussed. Results The first symptom of the patient was recurrent infections. Growth retardation, spondyloepiphyseal dysplasia accompanied by nephrotic syndrome and defective cellular immunity were seen as clinical features in this patient. Renal pathology showed focal segmental glomerulosclerosis. Conclusion Combining the clinical manifestation with renal pathology, the case is diagnosed as Schimke immuno-osseous dysplasia.
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Objective To investigate the role of Notch signaling in the progression of peritoneal fibrosis in a rat model induced by high glucose dialysate. Methods Male Sprague Dawley rats were subjected to daily peritoneal dialysis (PD) with a lactate-buffered solution containing 4.25% glucose. They were sacrificed at 2 and 4 weeks after PD. The parietal thickness was measured with Masson staining. The expression of TGF-β1, E-cadherin, α-SMA and collagen Ⅰ was examined by immunoblotting. The expression of Notch ligand Jagged-1 and the negative Notch signaling regulato--Numb was analyzed by both immunoblotting and RT-PCR. The expression of a Notch nuclear target gene Hcs-1 was examined by RT-PCR. Results Both HE and Masson trichrome staining revealed an increase in peritoneal thickness with a loss of mesothelial cells and a rich of collagen matrix deposition in the submesothelial zone was evident at 4 weeks after PD. Meanwhile, compared to healthy rats, the expression of TGF-β1, ct-SMA and collagen Ⅰ was significantly increased, but the expression of E-cadherin was decreased in peritoneum after PD treatment. It was difficult to detect the Jagged-1 and Hes-1 expression in normal peritoneum, but their expression was graduaUy increased after PD. In contrast, the expression level of Numb, a negative regulator of Notch signaling, was dramatically decreased after PD. Conclusions Notch signaling is activated during the process of PD-induced peritoneal fibrosis and the activation of Notch signaling is associated with the loss of negative regulation of Notch signaling via decreased expression of Numb. Inhibition of Notch signaling via overexpression of its negative regulators such as Numb may be a novel therapeutic approach for peritoneal fibrosis in PD patients.
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AIM: To investigate the role of CD134 (OX40) and NF-?B in the pathogenesis of lupus nephritis (LN). METHODS: Renal in situ CD134 and NF-?B expression were examined in 40 biopsy specimens from LN patients by immunohistochemistry and microwave-based immunohistochemistry, respectively. The relationship between expression of CD134 and NF-?B was analyzed. RESULTS: The expression of glomerular and tubular CD134 and NF-?B in LN were higher than that in normal control, especially in class Ⅳ LN, where there was intense staining of endothelial cell, distal tubules, and interstitial mononuclear cell. The CD134 expression of glomerular and tubular was closely related to NF-?B expression, respectively ( r=0.5542,P
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AIM: To investigate the effect of retinoic acid on proliferation of renal interstitial myofibroblasts in a rat model of the left unilateral ureteal obstruction (UUO). METHODS: UUO model was established by unilateral ligation of ureter in 36 SD rats. Rats were divided into 2 groups: Retinoic acid-treated group and control group, each with 18 rats. UUO rats were treated with either daily subcutaneous injection of 10 mg/kg body weight of all trans-retinoic acid or vehicle alone two days before the operation until being sacrificed. Groups of 6 rats were killed on day 3, 7 and 12 after ligation of the left ureter. The percentage of renal tubular lesion, interstitial fibrosis score, the number of interstitial myofibroblasts, the number of proliferating myofibroblasts and the expression of TGF?-1 mRNA were determined. RESULTS: There were significant accumulation and local proliferation of myofibroblasts in the interstitium of the UUO rats. On day 7 of the UUO model, the percentage of tubular lesions and interstitial fibrosis score were significantly lower in the retinoic acid-treated group than those in control group [(15.9?2.0)% vs (27.3?2.2)% and (0.47?0.12) vs (1.65?0.18), P