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Objective:To report a rare case of renal injury secondary to Strongyloides stercoralis infection, and investigate common pathological subtypes, pathogenesis and differential diagnosis of Strongyloides stercoralis infection-associated renal injury combined with literature. Methods:The pathological features of renal biopsy were analyzed by immunofloruscence, light microscope and electronic microscope. The pathological changes of digestive tract and pathogen morphology were observed through endoscope and digestive tract biopsy. The correlation between clinical-pathological features and pathological changes of kidney and digestive tract was analized.Results:The 26-year-old male patient presented with nephrotic syndrome. The pathological changes of renal biopsy were consistent with minimal change disease with interstitial focal eosinophil infiltration. Laboratory examination showed that the patient had unexplained eosinophilia and increased IgE level. Hence the patient was treated with glucocorticoid. After 2 months of therapy, proteinuria decreased and turned to negative while the patient developed progressive headache, gastrointestinal bleeding and progressive decrease of hemoglobin. Emergency gastroscopy showed extensive congestion and erosion of the stomach and duodenum. Gastric mucosal biopsy showed a large number of slender "s" shape larvae in the mucosa. The patient also had bilateral lung infection, positive Escherichia coli in cerebrospinal fluid and purplish skin rash around the umbilicus. A serious infection of Strongyloides stercoralis was diagnosed. After antibiotics and anthelmintic treatment, gastrointestinal symptoms and headache disappeared, and no parasite was found in endoscopy. No recurrence of nephrotic syndrome was found during 2 years of follow-up. Conclusions:Strongyloides stercoralis infection might first present with nephrotic syndrome with handful hints of digestive tract combined with eosinophilia and increased IgE levels. Therefore, in epidemic areas or patients with suspicious exposure history, it is necessary to exclude Strongyloides stercoralis infection before immunosuppressive therapy to avoid fatal complications.
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Objective:To explore the application value of modified technique of ureter implantation in murine renal transplantation.Methods:Thirty left donor kidneys from BALB/c mice was transplanted into syngeneic mice. Cuff technique was applied for anastomosing kidney artery and vein. The procedure of ureter-bladder anastomoses shifted from implication-fixation-embedding to fixation-implication-embedding. Operative duration, recipient survival rate and complications were recorded.Results:Time for separating vessels, perfusion and excision of donor graft was (25±3) min, (10±6) s for warm ischemia and (25±5) min for cold ischemia. Time for separating recipient vessels was (12±5) min, (7±1) min for arterial anastomosis, (7±1) min for venous anastomosis, (13±2) min for ureter-bladder anastomosis, (5±1) min for right kidney excision and (5±1) min for abdominal closure. Operative duration was(77±3)min. Twenty-six recipients survived over 3 months. The successful operative rate was 86.7%.Conclusions:With a shorter learning curve, modified technique of ureter implantation is easier and faster so as to reduce the postoperative incidence of urinary tract complications during murine renal transplantation.
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Objective To investigate the clinico-pathological features and renal outcomes of primary IgA nephropathy (IgAN) with glomerular IgM deposition.Methods Primary IgAN diagnosed with biopsy from January 2006 to December 2011 were recruited.Patients were divided into groups according to IgM deposition (Group A) and without IgM deposition (Group B).In addition,Group A was subdivided into two groups based on the position of IgM deposits as the mesangium (Group A1) and both mesangium and capillary wall (Group A2).Renal outcomes were defined as end stage renal disease (ESRD) and/or the doubling of baseline serum creatinine.Clinico-pathological features were retrospectively compared.Kaplan-Meier was conducted for renal outcomes,and Cox regression model was used to analyze the prognostic value of IgM deposition and the position of IgM deposition in the progression of nephropathy in IgAN patients.Results 939 patients were enrolled with 422 (44.9％) having IgM deposition (Group A).Of the 422 patients,382 patients were divided as Group A 1,whereas 40 patients were noted as Group A2.Compared to Group B,hemoglobin,serum protein,albumin and serum IgG levels in group A were significantly lower,and the cholesterol and serum IgM levels were significantly higher (all P ＜ 0.05).There was no significant difference in serum creatinine,estimated glomerular filtration rate (eGFR),urinary protein,blood pressure and uric acid between group A and B.In terms of pathological manifestations,patients in Group A exhibited more severe histological lesions including glomerular sclerosis,S1,M1 and interstitial inflammatory cell infiltration (all P＜0.05).Immunofluorescence showed that the proportion of IgG,C1q and Fg deposition in group A was significantly higher than that in group B (all P ＜ 0.05).By Kaplan-Meier,cumulative renal survival rate has no significant difference between Group A and B (Log-rank test x2=0.019,P=0.891).Univariate and muhivariable Cox regression analysis showed that IgM deposition had no significant effect on the renal progression in IgAN patients.Subgroup analysis showed that patients in Group A2 exhibited higher urine protein,creatinine and blood pressure,and lower eGFR and serum albumin,also had worse histological lesions including M1,E1 and T1-2 of Oxford classification (all P＜0.05),Immunofluorescencc showed that the proportion of IgG,C1q and Fg deposition in group A2 was significantly higher than that in group A1 (all P ＜ 0.05).By Kaplan-Meier,renal survival rates calculated from outcomes were lower in Group A2 (Log-rank test x2=1 8.207,P ＜ 0.001).In addition,IgM deposited both in the mesangium and capillary wall was a risk factor for renal progression of IgAN patients with IgM deposition by a univariate Cox hazards regression mode and multivariable-adjusted Cox models (HR=3.621,95％CI 1.924-6.814,P＜ 0.001;HR=2.309,95％CI 1.176-4.533,P=0.015respectively).Conclusions The IgAN patients with IgM deposition relatively had more severe clinicopathological changes,especially those with IgM deposited both in the mesangium and capillary wall.In this study,IgM deposition was not found to be an independent risk factor for the prognosis of kidney in IgAN patients.However,IgM deposited both in the mesangium and capillary wall was an independent risk factor for renal prognosis in IgAN patients with IgM deposition.
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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 explore the clinicopathologic characteristics of polyomavirus nephropathy (PyVN) in renal transplantation.Methods Clinicopathological data from 101 cases of PyVN from January 2006 to October 2016 in our hospital were collected and analyzed retrospectively.There were 72 males and 29 females.The mean time from operation to the diagnosis of PyVN was 16.5 months (2.2-63.9 months),with 86 cases (85.1％) occurring within 2 years.The indications for biopsy included elevated serum creatinine in 81 cases (80.2％),elevated serum creatinine with proteinuria in 13 (12.9％) cases,active BK virus(BKV) infection in 5 cases (5.0％) and proteinuria in 2 cases (2.0％).Results BK viruia was detected in 98 (97.0％) recipients with viral loads of 1.5 × 109 (0-9.0 × 1011) copies/ml,and BK viremia in 80 (79.2％) recipients with viral loads of 1.8 × 104 (0-2.1 × 107) copies/ml.5 patients lost their graft function at biopsy and the other 96 patients reserved graft function with serum creatinine of 187.0 μmol/L.After 20.1 (3.7-109.6) months of follow-up,19 (18.8％) patients lost their graft function.The average serum creatinine of the 77 patients with graft function was 165.0 μmol/L,with no statistical difference (P ＞ 0.05) compared with that of patients at diagnosis.There were 18 cases of stage A,72 cases of stage B and 11 cases of stage C with 5-year allograft cumulative survival of 92.9％,82.8％ and 55.6％,respectively.Conclusions PyVN can occur within 5 years after renal transplantation,mostly within 2 years.The typical clinical manifestations include elevated serum creatinine,BK viruia and BK viremia.The severe the histopathological lesions were correlated the worse the clinical prognosis.
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Objective To summarize the pathological characteristics of polyomavirus-associated nephropathy combined with acute rejection after renal transplantation.Methods The pathological data of 172 patients diagnosed as having polyomavirus nephropathy in our hospital from 2007 to 2018 were reviewed.Results One hundred and seventy-two patients were diagnosed as having polyomavirus nephropathy without acute rejection for the first time.In 75 (43.6％,75/172) patients who received repeat biopsy,10 (5.8％,10/172) patients developed acute rejection with an average interval of 4.8 ± 3.3 months.Common pathological features included:renal tubular epithelial cells virus inclusions reduced or even disappeared or only hyperchromatic nuclei revealed,SV40-T antigen (70％,7/10) staining negative or decreased significantly (30％,3/10),and varying degrees of interstitial inflammation,tubulitis,interstitial fibrosis and tubular atrophy.Four patients developed acute T cell-mediated rejection (Banff ⅡA),revealing aggravating tubulitis and interstitial inflammation in the area of negative SV40-T antigen (70％,7/10) staining,as well as mild endarteritis.Three patients developed acute antibody-mediated rejection,revealing glomerulitis and peritubular capillaritis and positive panel reactive antibody.Only 1 patient revealed C4d deposition of peritubular capillaries.Two patients developed mixed rejection,revealing tubulitis,interstitial inflammation,glomerulitis,peritubular capillaritis,mild endarteritis and C4d deposition of peritubular capillaries.One patient developed suspicious T cell-mediated rejection (Banff IB),revealing aggravating tubulitis and interstitial inflammation in the non-fibrotic areas but without intimal arteritis.Besides,the positive SV40-T antigen (70％,7/10) staining area was reduced significantly.Conclusion The pathological characteristics of polyomavirus nephropathy combined with acute rejection include endarteritis,glomerulitis,peritubular capillaritis and C4d deposition of peritubular capillaries.It is difficult to distinguish polyomavirus nephropathy from Banff I T cell-mediated rejection.Clinical information and repeat biopsy results are helpful for differential diagnosis.
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Objective To interpret the clinicopathological features and the key factors for diagnosis of polyomavirus-associated nephropathy (PVAN).Methods Clinicopathological data of 13casesof polyomavirus-associatednephropathyduring2008-2011inour hospitalwere retrospectively analyzed.Three cases received repeat biopsy.The clinicopathological features were analyzed according to thelight microscopicsceneandSV40-Timmunochemicalexpression.Results Recipients had a peak incidence of PVAN in 12 to 18 months period after renal transplantation,accompanied by elevated serum creatinine.Due to the progression of the disease,3patterns of histological findings could be identified.The early lesion was confined to the collected ducts,with slightly inflammatory infiltration in medullary interstitium,viral inclusions were not necessarily seen.The only findings could be enlarged nuclear and irregular arrangement of the tubular epithelial cells.At the developing stage,prominent tubulointerstitial nephritis was detected,and the involved tubules extended to other segments of renal tubule,even the parietal epithelial cells of Bowman's capsule could be compromised.The epithelial cells shed off,leading the tubular basement membrane exposed.Typical intra-nuclear inclusions as well as variable nuclear changes were found.At the end stage,the allograft showed notable chronic tubulointersititial change,with diffuse tubular atrophy and interstitial fibrosis.Although in this period,typical viral inclusions were rare, stillIHCshowedpositiveexpression of SV40-T. After immunosuppressantreductionor exchange,2 cases developed renal failure,4 cases showed sustained increment in serum creatinine,while 7 cases had a stabilized serum creatinine level.Conclusions Polyomavirus-associated nephropathy can display uneven pathological changes,as well as the morphology of the infected epithelial cells.Segments of the involved tubule are associated with the course of disease.Reduction of immunosuppressant at the early stage has a favorable effect.A prompt renal biopsy should be done in renal transplant recipient if who shows increased serum creatinine,and a routine polyomavirus immunohistochemical staining should be applied as well.
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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.