Correlation Of Respiratory Virus Infections And HSP Renal Injury

Objective: Allergic purpura, also known as the Heng-shu syndrome（Henoch-Schonlein purpura, HSP）, a wide range of white blood cells rupturevasculitis as the main pathological changes of systemic vasculitis. Predilectionin school-age children, boys more than girls. The etiology is not completelyclear, microbial infection, food, drug allergy is a common trigger. The lesionscan affect the skin, joints, gastrointestinal tract, kidney and other organs. Oftenwith skin purpura as initial symptoms, a small number of children withabdominal pain, joint pain, kidney damage as first manifestation.Purpuranephritis （Henoch-Schonlein purpura nephritis, HSPN） is the kidney damagecaused by allergic purpura, more appeared within6months of disease, theincidence rate of25%⁸0%, is the most common childhood secondaryglomerular disease, is also the decisive factor affecting the prognosis ofHenoch-Schonlein purpura.Normal children the urine usually contain urine protein no more than100mg per square per24hours, urinary sediment red blood cell less than3perHP. When the immune response induced by HSP leads to kidney damage, theglomerular basement membrane （GBM） filtration aperture increases, thebasement membrane rupture, the filtration membrane glycoprotein withnegative charge resulted in a decrease in plasma protein filtration withnegative charge increases obviously, the charge barrier damage, kidneypermeability increasing, this time in the clinical form of protein in the urine（24hours urine protein quantitative>150mg/d） and （or） renal hematuria（urinary sediment red blood cell count>3/HP）. Urinary microalbumin （urinemALB） test can be more sensitive reaction to early renal injury[1].MALB>20mg/L is abnormal. Respiratory viruses in children often include: adenovirus, respiratorysyncytial virus, influenza virus （a, b） and parainfluenza virus. HSP patientsserum virus IgM antibodies can be tested by indirect immunofluorescence,inorder to understand the infection status. Research has shown that, respiratoryvirus infection may be associated with the allergic purpura[2]. But there is stilla lack of reports about relationship between respiratory virus infection andrenal damage in children with Henoch-Schonlein purpura. This article aims todynamic changes of HSP virus IgM antibody test in children with respiratorytract, urinary protein, urinary sediment, to study on the relationship betweenrespiratory infection and Henoch-Schonlein purpura with renal injury.Methods:1.The research object: from2011December to2012December in pediatricHebei Medical University second hospital income Hospital of92patients withallergic purpura and initial treatment were as the research object. Diagnosis ofallergic purpura: typical skin rash, with or without gastrointestinal tract,joints, kidneys symptoms and blood platelet count not less. Diagnosis ofHenoch-Schonlein purpura nephritis: in the course of the disease on the basisof allergic purpura in6months, hematuria and （or） proteinuria.2.Research methods: The inclusion of children with four common respiratoryvirus detected before treatment, according to the test results, patients withvirus-positive is observe group （A group） and patients with virus-negative iscontrol group （B group）. Virus-positive group was treated with RibavirinInjection10～15mg/kg·d antiviral treatment for seven days. Three months later,test the respiratory virus IgM antibody again. Detection results have not yetbeen negative for the A₁group, negative for the A₂group. A total of6monthsof follow-up, both groups were observed and compared the incidence of renalinjury, and statistical analysis.3. Detection method:3.1Respiratory virus test: detection of2ml venous blood was sampled fromthe outpatient department of Pediatrics in our hospital respiratory commonpathogens of serum IgM antibody, using indirect immunofluorescence method. Method: serum and the quality control of dilution were added in the slide hole,incubated at37℃for90minutes; washed twotimes with PBS, distilled wateronce; into fluorescein conjugates, incubated at37℃for30minutes; washedtwo times with PBS, distilled water is a natural dry, add a small drop closedmedium, covered with cover glass; observed in fluorescence microscopy400times magnification.3.2Urinary protein quantitative: take24hours urine, to calculate the totalmount of urine, mixing it fully, then send3ml urine to the laboratory, usepyrogallol red colorimetric assay for the quantitative detection, collectinspection data analysis.3.3urinary sediment detection: take10ml of morning mid-portion urine, sendto the urinary sediment laboratory of nephrology department within2hours.Detection method:10ml urine centrifugation at1500r/min for5min; to keep0.2ml supernatant, sediment; rocked the centrifuge tube,blending components;with10×10lens, observe the tangible component panorama and tube type;observation of cell components and the number of10×40lens, continuousobservation of10different visual field, take the minimum and maximumvalues, recording the results.3.4Detection of microalbumin in urine: take2ml of morning mid-portionclean urine,send to the Laboratory of pediatrics department. Method: to detectsamples by dry-type quantitative immunofluorescence method. Kit andi-CHROMA Reader fluorescence analyzer are produced by South Korea’sBoditech Med Inc.4. Statistical analysis: using SPSS Statistics13.0software for data statistics,description and statistical analysis of data. Select P<0.05for statisticalsignificance.Results:1general information:Observation group of43patients,24males and19females. The male to female ratio is1.26:1, with an average age of8.33±2.86years. The control group of49patients, including27males and22females, the male to female ratio is1.23:1, with an average age of8.53± 2.77years. The two groups of gender, age comparisons were not statisticallydifferent.26months follow-up, the observe group renal injury incidence rate is53.5%,the control group renal injury incidence rate is28.5%, the difference wasstatistically significant. Description respiratory viral infections can increasethe incidence of renal damage in children with HSP.Among them, the virusremains positive group （group A₁） renal injury incidence is64.7%（11/17）,virus become negative group （group A₂） renal injury incidence is46%（12/26）,control group （group B） renal injury incidence is28.5%, there is significantdifference between three groups. That virus persistence has more influence onthe significance of renal injury.3Different virus infection rates: The influenza virus26.09%（24/92）, parainf-luenza virus11.96（11/92）, adenovirus5.43%（5/92）, respiratory syncytial virus3.26%（3/92）.4The virus continue positive kidney injury,64.7%（11/17）> the overcastgroup46%（12/26）> virus-negative group,28.6%（14/49）, the differencewas statistically significant. Description virus infection in the HSP kidneyinjury occurred. Virus persistence greater significance kidney damage.5Different viruses （adenovirus, influenza virus, respiratory syncytial virus,parainfluenza virus） kidney injury incidence:40%,54.17%,0%,72.73%,and the difference was not statistically significant. The respiratory viralinfections can lead to kidney damage occurred, but it has little to do with thetypes of the virus.Conclusion:1Allergic purpura with respiratory tract infection rate of renal injury increases,the possible mechanisms for infection virus as antigen induced antibody,antigen, antibody binding to form immune complexes, due to the deposition ofthe renal injury in the kidney. But renal injury of the HSP patient has littlerelationship with the kinds of virus. There is no evidence of a single virus ispathogenic factors of HSP renal injury. 2Children with HSP influenza virus infection is highest, that of influenzavirus plays an important role in the pathogenesis of allergic purpura, specificmechanism needs further study.3Virus infection persists as antigen to stimulate the body repeatedly, increasethe incidence of renal injury.