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    Tuberculosis infection in children with proteinuria/nephrotic syndrome
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    ENWEndNote BIBJabRef, Mendeley RISPapers, Reference Manager, RefWorks, Zotero AMA Szymanik-Grzelak H, Kuźma-Mroczkowska E, Skrzypczyk P, Bielecka T, Kotula I, Pańczyk-Tomaszewska M. Tuberculosis infection in children with proteinuria/nephrotic syndrome. Central European Journal of Immunology. 2017;42(3):318-323. doi:10.5114/ceji.2017.70977. APA Szymanik-Grzelak, H., Kuźma-Mroczkowska, E., Skrzypczyk, P., Bielecka, T., Kotula, I., & Pańczyk-Tomaszewska, M. (2017). Tuberculosis infection in children with proteinuria/nephrotic syndrome. Central European Journal of Immunology, 42(3), 318-323. https://doi.org/10.5114/ceji.2017.70977 Chicago Szymanik-Grzelak, Hanna, Elżbieta Kuźma-Mroczkowska, Piotr Skrzypczyk, Teresa Bielecka, Iwona Kotula, and Małgorzata Pańczyk-Tomaszewska. 2017. "Tuberculosis infection in children with proteinuria/nephrotic syndrome". Central European Journal of Immunology 42 (3): 318-323. doi:10.5114/ceji.2017.70977. Harvard Szymanik-Grzelak, H., Kuźma-Mroczkowska, E., Skrzypczyk, P., Bielecka, T., Kotula, I., and Pańczyk-Tomaszewska, M. (2017). Tuberculosis infection in children with proteinuria/nephrotic syndrome. Central European Journal of Immunology, 42(3), pp.318-323. https://doi.org/10.5114/ceji.2017.70977 MLA Szymanik-Grzelak, Hanna et al. "Tuberculosis infection in children with proteinuria/nephrotic syndrome." Central European Journal of Immunology, vol. 42, no. 3, 2017, pp. 318-323. doi:10.5114/ceji.2017.70977. Vancouver Szymanik-Grzelak H, Kuźma-Mroczkowska E, Skrzypczyk P, Bielecka T, Kotula I, Pańczyk-Tomaszewska M. Tuberculosis infection in children with proteinuria/nephrotic syndrome. Central European Journal of Immunology. 2017;42(3):318-323. doi:10.5114/ceji.2017.70977.
    In 37 patients of nephrotic syndrome, serum protein levels, protein fractions and urinary levels of proteins and their fractions were determined. The findings of serum levels of proteins and their fractions were compared with an equal number of age and sex matched controls. Twenty three patients showed selective and 14 non-selective proteinuria. Most of the patients with selective proteinuria showed good response to steroids therapy while those with non-selective proteinuria did not respond.
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    Objective. The recovery time from abnormal levels of proteinuria with standard treatment in longitudinal studies of patients with systemic lupus erythematosus has not been well described. We aimed (1) to determine the recovery time from proteinuria in patients with lupus nephritis (LN) receiving standard treatment, and (2) to determine whether the initial level of proteinuria predicts time to improvement. Methods. We studied all patients with LN recorded in the database from 1970 until 2011. Proteinuria was defined as ≥ 0.5 g/24 h. Patients were grouped as follows: group 1 having 0.5–0.9 g/day, group 2 having 1–1.9 g/day, and group 3 having ≥ 2 g/day. Recovery from proteinuria was defined as proteinuria < 0.5 g/24 h. Time to recovery from proteinuria was studied with the Kaplan-Meier curves. Factors associated with proteinuria recovery were evaluated using proportional hazard models. Results. Among the 212 patients studied, 52% recovered from proteinuria within 2 years and an additional 22% recovered within 5 years, for a total of 74%. The level of proteinuria at baseline visit predicted the time to improvement. Patients with a higher level of proteinuria at baseline needed a longer time to normalize their proteinuria. Male sex, hypocomplementemia, high level of proteinuria at diagnosis of LN, and disease duration > 5 years at onset of LN each independently predicted late recovery of proteinuria and had an effect on the percentage of patients who recovered. Conclusion. The tempo of recovery from proteinuria in LN is slow and the level of proteinuria at baseline visit predicts the time to complete recovery.
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    Proteinuria, developing after renal transplantation may influence allograft and patient outcomes. This study aimed to investigate the effect of proteinuria on patient and allograft survival. Among 514 patients, 56 (11%) patients with good allograft function and proteinuria were evaluated retrospectively. Patients with proteinuria were classified as group P (20 patients with permanent proteinuria, Male/Female: 16/4) and group T (36 patients with temporary proteinuria, M/F: 29/7) according to the type of proteinuria. Also, considering the amount of proteinuria, patients were classified as group M (32 patients with massive proteinuria, M/F: 29/3) and group NM (24 patients with non‐massive proteinuria, M/F: 16/8). The mean time interval between transplantation and appearance of proteinuria was 23.7 months (range 0–121 months) and no difference was found between groups. Two‐ and 5‐yr allograft survival rates were found to be 85 and 80% in group M, and 95 and 82% in group NM, respectively (p=0.24). In terms of type of proteinuria, 2‐ and 5‐yr allograft survival rates were found to be 70 and 58% in group P and 92 and 87% in group T, respectively. The difference between groups P and T was found to be statistically significant (p=0.02). Most (85%) of the patients with permanent proteinuria also had massive proteinuria. In conclusion, we found a significant relation between type and severity of proteinuria. The type of post‐transplant proteinuria had a stronger effect on allograft outcome than the severity of proteinuria.
    Objective To investigate the relationship between serum IgG and proteinuria in children with nephrotic syndrome.Methods Biostatistics was used to study the relationship between the serum level of IgG and the quantitative changes of urine protein in 46 pediatric patients with simple primary nephrotic syndrome which had not been treated with steroid therapy.Results No linear regression,nor correlation was found between the serum IgG and the quantity of urine protein(P0.05).Conclusion Although lowered IgG level may be seen in some nephrotic children,the present investigation revealed no linear regression or correlation betweem serum IgG and proteinuria,suggesting that heavy proteinuria may not be the main cause of the lowering of serum IgG in children with nephrotic syndrome.
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    Methods for detection of proteinuria and its causes are reviewed. Recommendations are given concerning the diagnostic procedures after detection of pathological proteinuria. The nephrotic syndrome is discussed mainly under the aspect of predictability of the histo-pathological form of the glomerular lesions from clinical and biochemical parameters.
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    Objective: To investigate the trends and the characteristics of proteinuria in 376 patients with subtertian malaria. Methods: The complete clinical information of 376 patients with subtertian malaria was collected and the data concerning proteinuria were analysed and compared statistically. Results: 28.19% of the patients had +- proteinuria; 23.67% percent had + proteinuria; 8.24% had ++ proteinuria; 1.60% had +++ proteinuria. Proteinuria usually occurred on the 2nd day after the onset of subtertian malaria. Proteinuria would decrease or vanish in most patients within a week after the disease had been controlled. Proteinuria occurred more commonly in patients with high fever of more than 39 ℃. Conclusion: Subtertian malaria usually causes functional proteinuria and the prognosis is usually good. Individual differences, fever grade, deposition of immune complexes and prompt cure are associated with positive proteinuria.
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    In the light of the theory stated in Canon of Internal Medicine and other related theories expounded by specialists of past ages, this article proposes that proteinuria has an analogy with the refined nutritious substance leaking from the spleen and kidney in traditional Chinese medicine. The pathological change, zheng-differentiation and treatment of proteinuria in nephrotic syndrome are also discussed. Through years of his clinical experience, the author recommends some kinds of herbal medicines effective for treating proteinuria. This article, therefore, provides not only a theoretical basis, but also clinical experience for the treatment of proteinuria in nephrotic syndrome.
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    The mechanism of proteinuria in nephrotic syndrome is unknown. The plasma behaviour of platelet-activating factor (ng/ml) in nephrotic and normal people has been evaluated.A total of 21 patients with nephrotic proteinuria due to glomerular pathology and 20 subjects as normal control people have been studied. Plasma PAF level is evaluated by ((125)I) RIA Kit (Du Pont NEN).Patients with glomerular proteinuria appeared to have a significant increase (p<0.05) plasma PAF bioactivity: 116.28+/-49.6 ng/ml versus 41.4+/-14.9 ng/ml of normal subjects.The study shows that PAF may be involved in the mechanism of genesis of human glomerular proteinuria.
    Platelet-activating factor
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    Proteinuria was estimated using modified biuret method in 100 consecutive essential hypertensives of both sexes with mean age of 40 +/- 0.9 (18-50 yr) attending hypertension clinic. Proteinuria (mg/1.73 M2/24 h) in 60 mild hypertensives ranged from 45.4 to 493.0 with 9 (15%) patients having abnormal proteinuria (greater than 250 mg). In 26 moderate hypertensives proteinuria ranged from 96-1010; 7 (27%) had abnormal proteinuria. The proteinuria in 14 severe accelerated, malignant hypertensives ranged from 146.5-6132.6 with 10 (71%) having abnormal proteinuria. Duration of hypertension had no correlation with the amount of proteinuria. The amount of proteinuria was much higher (P less than 0.001) in patients with renal insufficiency (1322.5 +/- 586.4) and in patients with grades III and IV hypertensive retinopathy. LVH on ECG also correlated positively with proteinuria. The group with abnormal proteinuria had more patients with LVH (42.3% vs 12.2%), severe hypertensive retinopathy (30.8% vs 4.1%) and renal insufficiency (34.6% vs 0%) as compared to patients without elevated proteinuria.
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