Calculi ; chemically induced ; Ceftriaxone ; adverse effects ; Child ; Humans ; Lithiasis ; chemically induced

Abnormalities, Multiple ; diagnosis ; pathology ; physiopathology ; Branchio-Oto-Renal Syndrome ; diagnosis ; pathology ; physiopathology ; therapy ; Child ; Deafness ; etiology ; physiopathology ; Diagnosis, Differential ; Ear ; abnormalities ; Female ; Humans ; Kidney ; abnormalities ; Renal Insufficiency ; etiology ; physiopathology ; therapy

Child ; Humans ; Tuberculosis, Renal

Objective To explore the causes of acute renal failure resulted from tacrolimus in the treatment of nephrotic syndrome. Method The clinical data of acute renal failure caused by tacrolimus in treatment of nephrotic syndrome in 3 children during January 2012 and December 2015 were retrospectively analyzed. Results There were 2 male and 1 female aged 3, 11,and 13 years respectively. Clinical manifestations were consistent with simple type of primary nephrotic syndrome. One child was frequently recurrent and another two were secondary steroid resistant. The renal pathology showed minimal changes. Acute renal failure occurred within 4 weeks after treatment with tacrolimus on the basis of hormone therapy in all patients who had infection within one week. Renal function recovered to normal within 2 weeks after discontinuation or reduction of tacrolimus combined with anti-infection and diuresis treatment. Two children continued with tacrolimus, but the other one was replaced with cyclosporin A. The renal function of all patients remained normal during the follow-up for 10-42 months. Conclusion In the first 4 weeks of tacrolimus therapy in children with nephrotic syndrome, infection may lead to reversible acute renal failure.

Liver ischemia reperfusion injury is a common pathophysiological process in hepatic surgery,which is the consequence of multiple mechanisms such as oxidative stress,inflammatory reaction,apoptosis,and autophagy and so on.However,the molecular mechanisms behind these processes have not been completely elucidated,the current treatment of liver I/R injury is merely supportive care,and thus new therapeutic strategies are needed.The recent studies indicate that the ischemic precondition and pharmacological precondition may protect the liver against hepatic ischemiareperfusion injury.It will be an important clinical significance of further studying its molecular mechanisms and protective strategies.

OBJECTIVE: To evaluate the curative effect and clinical significance of bone cement on coagulation functions during percutaneous vertebroplasty in patients with osteoporotic spinal compression fractures.METHODS: A total of 24 patients, comprising 18 females and 6 males, aged 69 years averagely (range 48-83 years), with 44 osteoporotic vertebral compression fractures underwent percutaneous vertebroplasty in Department of Spinal Surgery, Third Hospital of Hebei Medical University between December 2006 and December 2007. The fracture segment was within T_5-L_3 (20 thoracic vertebrae and 24 lumbar vertebrae). Under the guidance of C-arm fluoroscopy, bone marrow biopsy needle was inserted percutaneously via transpedicular way into the fractured vertebrae. Polymethylmethacrylate (PMMA, bone cement) was injected into the fractured vertebrae. The relative parameters were observed in all patients 10 minutes before, 10 minutes, 30 minutes, 1 hour, 2 hours and 3 hours after bone cement implantation, including prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen (FIB), plasma protamine paracoagulation test (3P test), and D-dipolymer (D-D). RESULTS: PT was decreased, and FIB, 3P test, D-D were increased 10 minutes after bone cement implantation in percutaneous vertebroplasty peaked at 1 hour and gradually decreased afterward; moreover, there were significant difference between bone cement preimplantation and 10 minutes, 30 minutes, 1 hour, 2 hours and 3 hours after bone cement implantation (P < 0.05), but no difference was observed in APTT and TT (P > 0.05). The influence of bone cement on the parameters was vanished in 3 hours after bone cement implantation, and all indexes were similar to pre-implantation (P > 0.05).CONCLUSION: Bone cement implantation causes temporal hypercoagulabale state in percutaneous vertebroplasty. It is important to monitor blood clotting state in 3 hours after bone cement implantation in order to avoid thrombus disease.

Objective To explore the diagnosis of pediatric clinical hematuria disease. Methods The clinical data of one pediatric patient with IgA nephropathy combined with multiple bladder hemangioma were summarized and analyzed. Results For more than 6 years, 9-year-old female presented with repeated intermittent gross hematuria and persistent microscopic hematuria with the blood clot in urine after several respiratory tract infections. Routine urine test showed protein+++, RBC in full ifeld of vision/HP, and 0 . 54-1 . 02 g of 24 h urine protein quantitation. Early damage index of kidney is mainly based on microalbumin. The ultrasound showed no abnormal abdomen and urinary tract. Also there was no abnormality in enhanced urinary tract CT scan. Renal arteriography showed no ifstula or arteriovenous malformation. Pathological diagnosis of renal biopsy was focal proliferative IgA nephropathy. Cystoscopy examination suggested multiple hemangioma of bladder. Conclusion Bladder hemangioma is a rare condition in childhood. For children presented gross hematuria with blood clots, when the imaging ifnds no abnormalities or other diseases and the treatment of IgA nephropathy is unsatisfatry after diagnosis, the cystoscopy should be performed to exclude the possibility of bladder hemangioma.

Objective To explore the diagnosis and treatment of Dent’s disease.MethodsThe clinical characteristics, treatment process and disease-causing gene mutation were retrospectively analyzed in 6 pediatric patients with Dent’s disease misdiagnosed of nephritic syndrome from January 2014 to August 2015.ResultsIn these 6 male patients aged 4.5-9.8 years old, the main clinical manifestations were nephropathy-level of proteinuria and transient low serum albumin (26-30 g/L) without obvious edema or high serum cholesterol. In 4 patients who had renal biopsy, 2 cases showed mesangial proliferative glomerulonephritis and other 2 cases showed focal segmental glomerulosclerosis. All of 6 patients were treated with at least one immunosuppressive agent after resistance to full dose of hormone and no changes in proteinuria were observed. After admission, the indexes of early renal damage and urinary protein electrophoresis pointed to low-molecular proteinuria. The ratio of alpha 1 micro albumin (α1-MG) / micro albumin (MA) (the early renal damage index) was?>?1, there was hypercalciuria, and renal function was normal. The B ultrasonography showed renal calciifcation in 2 patients. The ifndings in all the patients were in accord with the clinical diagnosis of Dent’s disease. Further genetic analysis conifrmed the presence ofCLCN5 gene mutation in these 6 patients.ConclusionAs a type of rare inherited renal tubular disorder, Dent’s disease is easily misdiagnosed, to which pediatricians need to pay attention. The early renal damage index, α1-MG/MA?>?1, can be regarded as one of the diagnostic criteria of renal tubular proteinuria.

Objective To explore the impact of the variable number of tandem repeats of monoamine oxidase A gene (MAOA-uVNTR) on the intensity of brain activation during the recognition of facial expression in patients with depression and healthy controls.Methods 28 cases of depression,as well as 33 healthy controls who were matched in gender, age and years of education were divided into different genotypes with the methods of polymerase chain reaction (PCR) amplification and 1.5% agarose gel electrophoresis separation.61 cases were scanned to compare the intensity of brain activation in the recognition of happy, sad and neutral facial expression.Results In healthy controls,cases with high-activity genotype showed increased activation in left cuneus,left inferior frontal gyrus, right medial frontal gyrus and left inferior parietal lobule in comparision with carriers of low-activity genotype.In the depressed, compared with patients with low-activity genotype, cases with high-activity genotype decreased activation in bilateral putamen, left postcentral gyrus, left fusiform gyrus, right superior temporal gyrus and right thalamus.Conclusion Healthy controls with high-activity genotype shows the trend of priority for the identification of negative emotion,this genotype may be one of the risk factors for normal people suffering from depression.Patients with high-activity genotype is associated with the inhibitory of positive emotional state, this may attribute partly to the emotional symptoms in such kind of patients more serious.

Objective To study the expression and enzyme activity of thioredoxin reductase 1 (TrxR1) in liver and peripheral blood of human and rats exposed to airborne arsenic through coal-burning as well as its role in liver injury of coal-burning-borne arsenic poisoning.Methods This study was divided into 2 parts.Part 1 was a population study:133 local residents exposed to airborne arsenic through coal-burning were selected as arsenic exposure groups including a non-patient group (25 cases),no obvious hepatopathy group (38 cases),mild (43 cases) and moderate to severe hepatopathy groups (27 cases) from areas affected by endemic arsenism in Guizhou Province.Thirty-four healthy residents from arsenic not affected areas were selected as controls.Peripheral blood samples were collected from all these people.The expression of TrxR1 mRNA was determined by real-time fluorescence quantitative PCR (qPCR),and enzyme activity of TrxR was tested by visible spectrophotometry.Part 2 was an animal experiment study:Thirty Wistar rats,weighing about 80-100 g,were divided into control group,drinking-waterborne arsenic poisoning group and coal-burning-borne arsenic poisoning group (including low,medium and high arsenic contaminated grain groups) by means of a table of random number according to body mass,6 rats in each group.The control group was fed with normal diet for 3 months; drinking-water-borne arsenic poisoning group and coal-burning-borne arsenic poisoning group were fed with 10 mg/kg As2O3 solution and different concentrations(25,50,100 mg/kg) of arsenic-containing feed,respectively,for 3 months.The expression of TrxR1 mRNA was determined by qPCR; protein expression level of TrxR1 in liver tissue was detected by immunohistochemistry,and enzyme activity of TrxR in serum and liver tissue was tested by visible spectrophotometry.Results The mRNA expressions of TrxR1 in peripheral blood were 1.599 8 (1.128 9-2.156 8),1.469 3 (1.146 1-1.976 3),1.203 6 (0.463 1-1.816 2) and 0.912 3(0.631 8-1.535 0),respectively,among non-patient group,no obvious hepatopathy group,mild and moderate to severe hepatopathy groups.Compared to the control group[1.649 7(1.161 1-2.380 2)],the differences were significant statistically in mild and moderate to severe hepatopathy groups (all P ＜ 0.05).The enzyme activity of TrxR in peripheral blood was (3.12 ± 0.76),(2.81 ± 0.84),(2.52 ± 0.73),(2.42 ± 0.76)U/ml,respectively,in those corresponding groups.Compared to the control group [(3.02 ± 0.70)U/ml],the differences were significant statistically in mild and moderate to severe hepatopathy groups (all P ＜ 0.05).The mRNA expressions of TrxR1 in peripheral blood were 1.05 ± 0.14,1.18 ± 0.18,1.04 ± 0.10 and 0.97 ± 0.13,respectively,among drinking-water-borne arsenic poisoning group,low,medium and high arsenic contaminated grain groups; all of which were lower than that in the control group (1.23 ± 0.15,all P ＜ 0.05) except that of the low arsenic contaminated grain group.The mRNA expressions of TrxR1 in liver tissue were 0.78± 0.10,0.83 ± 0.10,0.79 ± 0.09 and 0.77 ± 0.11,respectively; all of which were lower than that in the control group (0.94 ± 0.12,all P ＜ 0.05).The protein expression of TrxR1 in liver tissue was 310.33 ± 38.81,312.50 ± 23.36,305.67 ± 20.57 and 298.17 ± 23.52,respectively,among the arsenic poisoning groups; all of which were lower than that in the control group (348.50 ± 32.35,all P ＜ 0.05).The enzyme activity of TrxR in serum was (4.22 ± 0.73),(4.86 ± 0.63),(4.04 ± 0.57),(3.73 ± 0.64)U/ml,respectively; all of which were lower than that in the control group [(9.52 ± 1.08)U/ml,all P ＜ 0.05].The enzyme activity of TrxR in liver tissue was (14.82 ± 1.67),(18.76 ± 2.76),(14.90 ± 2.17),(11.55 ± 1.74) U/mg,respectively; all of which were lower than that in the control group [(23.71 ± 3.05)U/mg,all P ＜ 0.05].Conclusion Arsenic aggravates liver injury of coal-burning arsenic poisoning through down-regulating the expressions of TrxR1 mRNA and protein and reducing its enzyme activity as well.