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Journal articles on the topic 'Glomerulonephritis, pathology'

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Published: 4 June 2021
Last updated: 10 February 2022

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1

Kim, Yong-Jin. "Pathology of C3 Glomerulonephritis." Journal of the Korean Society of Pediatric Nephrology 17, no. 1 (2013): 1. http://dx.doi.org/10.3339/jkspn.2013.17.1.1.

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2

Kim, Yong-Jin. "Pathology of Glomerulonephritis - Specimen Preparation and Basic Pathologic Changes -." Childhood Kidney Diseases 15, no. 1 (April 30, 2011): 29–37. http://dx.doi.org/10.3339/jkspn.2011.15.1.29.

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3

Cimbaluk, David. "Pathology, classification and pathogenesis of lupus glomerulonephritis." Diagnostic Histopathology 19, no. 5 (May 2013): 151–57. http://dx.doi.org/10.1016/j.mpdhp.2013.02.001.

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4

Fogo, Agnes B., Mark A. Lusco, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Membranoproliferative Glomerulonephritis." American Journal of Kidney Diseases 66, no. 3 (September 2015): e19-e20. http://dx.doi.org/10.1053/j.ajkd.2015.07.007.

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5

Lusco, Mark A., Agnes B. Fogo, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Fibrillary Glomerulonephritis." American Journal of Kidney Diseases 66, no. 4 (October 2015): e27-e28. http://dx.doi.org/10.1053/j.ajkd.2015.08.002.

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6

Fogo, Agnes B., Mark A. Lusco, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Postinfectious Glomerulonephritis." American Journal of Kidney Diseases 66, no. 4 (October 2015): e31-e32. http://dx.doi.org/10.1053/j.ajkd.2015.08.005.

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7

Fogo, Agnes B., Mark A. Lusco, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Cryoglobulinemic Glomerulonephritis." American Journal of Kidney Diseases 67, no. 2 (February 2016): e5-e7. http://dx.doi.org/10.1053/j.ajkd.2015.12.007.

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8

Weiss, M., K. Tzavella, J. Müller-Höcker, A. Nerlich, and E. Held. "Fibrilläre Glomerulonephritis." Der Pathologe 19, no. 2 (February 23, 1998): 141–45. http://dx.doi.org/10.1007/s002920050266.

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9

Kawasaki, Yukihiko, Syuto Kanno, Atsushi Ono, Yuichi Suzuki, Shinichiro Ohara, Masatoki Sato, Kazuhide Suyama, Koichi Hashimoto, and Mitsuaki Hosoya. "Differences in clinical findings, pathology, and outcomes between C3 glomerulonephritis and membranoproliferative glomerulonephritis." Pediatric Nephrology 31, no. 7 (February 4, 2016): 1091–99. http://dx.doi.org/10.1007/s00467-015-3307-z.

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10

Kambham, Neeraja. "Crescentic Glomerulonephritis." Advances In Anatomic Pathology 19, no. 2 (March 2012): 111–24. http://dx.doi.org/10.1097/pap.0b013e318248b7a1.

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11

Kambham, Neeraja. "Postinfectious Glomerulonephritis." Advances In Anatomic Pathology 19, no. 5 (September 2012): 338–47. http://dx.doi.org/10.1097/pap.0b013e31826663d9.

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12

Harrison, D. J., D. Thomson, and M. K. MacDonald. "Membranous glomerulonephritis." Journal of Clinical Pathology 39, no. 2 (February 1, 1986): 167–71. http://dx.doi.org/10.1136/jcp.39.2.167.

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13

Seshan, Surya V., and J. Charles Jennette. "Renal Disease in Systemic Lupus Erythematosus With Emphasis on Classification of Lupus Glomerulonephritis: Advances and Implications." Archives of Pathology & Laboratory Medicine 133, no. 2 (February 1, 2009): 233–48. http://dx.doi.org/10.5858/133.2.233.

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Abstract Context.—Systemic lupus erythematosus is an autoimmune disease with protean clinical and pathologic manifestations involving almost all organs in the body. There is a high incidence of renal involvement during the course of the disease, with varied renal pathologic lesions and diverse clinical features. A renal biopsy examined by routine light microscopy, immunofluorescence, and electron microscopy contributes toward diagnosis, prognostic information, and appropriate management. Objectives.—(1) To review the clinical and various pathologic features of renal lesions in systemic lupus erythematosus patients. (2) To introduce the International Society of Nephrology and Renal Pathology Society Classification of Lupus Glomerulonephritis. Data Sources.—A literature review, illustrations with original artwork, and tabulation of clinical and pathologic data of cases obtained from the authors' renal biopsy files examined during the last 8 years were used. Conclusions.—The International Society of Nephrology/ Renal Pathology Society–sponsored Classification of Lupus Glomerulonephritis proposes standardized definitions of the various pathologic findings, describes clinically relevant lesions, incorporates prognostic parameters, and recommends a uniform way of reporting the renal biopsy findings. Lupus glomerulonephritis is divided into 6 classes primarily based on the morphologic lesions, extent and severity of the involvement, immune complex deposition, and activity and chronicity. Special emphasis is laid on describing qualitative as well as quantitative morphologic data and to include the accompanying tubulointerstitial disease and different vascular lesions, which have prognostic and therapeutic significance. This classification is intended to facilitate a higher degree of reproducibility, resulting in better patient care and more effective future clinical and translational research. Renal biopsy findings in systemic lupus erythematosus add new and independent parameters of prognostic significance to established clinical and genetic factors.
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14

Lusco, Mark A., Agnes B. Fogo, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Glomerulonephritis With Dominant C3." American Journal of Kidney Diseases 66, no. 4 (October 2015): e25-e26. http://dx.doi.org/10.1053/j.ajkd.2015.08.004.

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15

Seymour, Anthony E. "Glomerulonephritis: approaches to classification." Pathology 17, no. 2 (1985): 225–38. http://dx.doi.org/10.3109/00313028509063759.

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16

Kowalewska, Jolanta, Kelly D. Smith, and Charles E. Alpers. "Recent advances in glomerulonephritis." Current Diagnostic Pathology 13, no. 1 (February 2007): 32–42. http://dx.doi.org/10.1016/j.cdip.2006.11.004.

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17

Evsikov, E. M., N. V. Teplova, N. G. Artamonova, G. A. Chervyakova, and V. I. Vechorko. "Nature and frequency of diagnosis of different forms of glomerulonephritis as cause of development and progression of chronic kidney disease in different world regions according to clinical and morphological studies with renal biopsy." Medical alphabet, no. 17 (August 18, 2021): 43–50. http://dx.doi.org/10.33667/2078-5631-2021-17-43-50.

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The review presents current data on the prevalence of chronic glomerulonephritis in different regions of the world according to the data of in vivo studies of histology of renal biopsy specimens. The literature data on the significance of glomerulopathies in the development of chronic kidney disease and risk factors of its progression to the terminal stages are reflected. We analyzed data on the most common types of glomerulonephritis – IgA-nephropathy, lupus nephritis on the ratio of primary and secondary forms of glomerulonephritis, their significance in the development of arterial hypertension and cardiovascular complications of this pathology.
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18

Evans, D. J. "Diffuse proliferative glomerulonephritis." Histopathology 11, no. 9 (September 1987): 991. http://dx.doi.org/10.1111/j.1365-2559.1987.tb01909.x.

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19

Pound, S. E., M. K. MacDonald, and D. Thomson. "Diffuse proliferative glomerulonephritis." Histopathology 11, no. 9 (September 1987): 991–92. http://dx.doi.org/10.1111/j.1365-2559.1987.tb01910.x.

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20

Magil, A. B., D. McFadden, and A. Rae. "Lupus glomerulonephritis with thrombotic microangiopathy." Human Pathology 17, no. 2 (February 1986): 192–94. http://dx.doi.org/10.1016/s0046-8177(86)80293-3.

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21

Smith, M. L. "The Pathology and Clinical Features of Early Recurrent Membranous Glomerulonephritis." Yearbook of Pathology and Laboratory Medicine 2013 (January 2013): 210–11. http://dx.doi.org/10.1016/j.ypat.2012.10.034.

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22

Schwartz, Melvin M., Jay Bernstein, Gary S. Hill, Keith Holley, and Elizabeth A. Phillips. "Predictive value of renal pathology in diffuse proliferative lupus glomerulonephritis." Kidney International 36, no. 5 (November 1989): 891–96. http://dx.doi.org/10.1038/ki.1989.276.

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23

Rodriguez, E. F., F. G. Cosio, S. H. Nasr, S. Sethi, M. E. Fidler, M. D. Stegall, J. P. Grande, F. C. Fervenza, and L. D. Cornell. "The Pathology and Clinical Features of Early Recurrent Membranous Glomerulonephritis." American Journal of Transplantation 12, no. 4 (January 10, 2012): 1029–38. http://dx.doi.org/10.1111/j.1600-6143.2011.03903.x.

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24

Lusco, Mark A., Agnes B. Fogo, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Subacute Bacterial Endocarditis–Associated Glomerulonephritis." American Journal of Kidney Diseases 68, no. 2 (August 2016): e11-e12. http://dx.doi.org/10.1053/j.ajkd.2016.06.001.

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25

Fogo, Agnes B., Mark A. Lusco, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Pauci-immune Necrotizing Crescentic Glomerulonephritis." American Journal of Kidney Diseases 68, no. 5 (November 2016): e31-e32. http://dx.doi.org/10.1053/j.ajkd.2016.09.002.

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26

Drut, Ricardo, and Rosa Mónica Drut. "Mesangiolytic Poststreptococcal Glomerulonephritis." Pediatric Pathology 12, no. 1 (January 1992): 113–17. http://dx.doi.org/10.3109/15513819209023287.

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27

Jebakumar, Deborah, and Kathleen A. Jones. "Educational Case: Lupus Nephritis as an Example of Immune Complex–Mediated Glomerulonephritis." Academic Pathology 7 (January 1, 2020): 237428952090949. http://dx.doi.org/10.1177/2374289520909496.

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The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 .1
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28

Usha, Sunil Kumar, RG Singh, Sagar Tapas, Jai Prakash, and RS Garbyal. "Mesangioproliferative glomerulonephritis: An important glomerulonephritis in nephrotic syndrome of young adult." Indian Journal of Pathology and Microbiology 51, no. 3 (2008): 337. http://dx.doi.org/10.4103/0377-4929.42506.

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29

Jebakumar, Deborah, and Kathleen A. Jones. "Educational Case: Antiglomerular Basement Membrane Disease as an Example of Antibody-Mediated Glomerulonephritis." Academic Pathology 7 (January 1, 2020): 237428952091118. http://dx.doi.org/10.1177/2374289520911185.

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The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 .1
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30

Karzakova, L. M., S. I. Kudryashov, M. V. Shestipalova, and E. V. Leontyeva. "DETERMINING OF CYTOKINE LEVELS IN THE URINE IN CLINICAL PRACTICE." Russian Clinical Laboratory Diagnostics 64, no. 5 (October 7, 2019): 287–93. http://dx.doi.org/10.18821/0869-2084-2019-64-5-287-293.

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The paper presents data on the study of the content of cytokines (IL-1β, RAIL-1β, IL-2, IL-4, IL-10, IL-17A, TNF-, IFN-γ) in the morning urine using enzyme immunoassay in healthy individuals (n = 20) and in patients with acute glomerulonephritis (n = 93). The determination of cytokine levels in patients was carried out in the debut of the disease and 12 months after the onset of the disease. The obtained indicators of cytokine content in the urine are presented as absolute values in pg/ml and creatinine-normalized values calculated by the formula: cytokine level (pg/ml) / urine creatinine (µmol/ml). The study was made of changes in the content of cytokines in the urine of patients with glomerulonephritis with respect to a group of healthy individuals, as well as the dynamics of the content of cytokines in the urine during the 12-month observation period. The results of the study showed that the absolute values of cytokines in urine can distort the true picture of the cytokine profile of urine in renal pathology. Normalized values of the predominant number of pro- and anti-inflammatory cytokines (IL-1β, IL-2, IL-8, IL-10, IL-17A and TNF-α) in patients with glomerulonephritis were significantly higher than the corresponding indicators of healthy individuals. The normalized values of cytokines were shown to be as more sensitive indicators than absolute values in the course of analyzing differences in the cytokine profile in patients with glomerulonephritis, depending on chronic and acute course of the disease. These indicators influenced the outcome of glomerulonephritis, assessed, as a rule, 12 months after the onset of the disease. Thus, the low levels of IL-1β, IL-8 and IL-17А detected in the debut of the disease in combination with the high level of RAIL-1β determined the chronization of glomerulonephritis. So, the creatinine-normalized cytokine levels in the urine expand the possibilities of using the evaluation of the cytokine profile of urine to establish changes in the cytokine content in the urine in renal pathology and predict the chronization of glomerulonephritis.
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31

Beneck, D., M. A. Greco, and H. D. Feiner. "Glomerulonephritis in congenital cytomegalic inclusion disease." Human Pathology 17, no. 10 (October 1986): 1054–59. http://dx.doi.org/10.1016/s0046-8177(86)80090-9.

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32

Daneshvar, Dariush, Jeanne Tomlinson, and Ross Boadle. "Membranoproliferative glomerulonephritis type III, strife variant." Pathology 44 (2012): S74. http://dx.doi.org/10.1016/s0031-3025(16)32798-2.

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33

Mac-Moune Lai, F., K. N. Lai, K. W. Chan, T. C. Au, K. L. Tong, and J. Vallance-Owen. "Pattern of glomerulonephritis in Hong Kong." Pathology 19, no. 3 (1987): 247–52. http://dx.doi.org/10.3109/00313028709066558.

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34

Chan, Kwok W. "Pattern of glomerulonephritis in Hong Kong." Pathology 20, no. 3 (1988): 307–8. http://dx.doi.org/10.3109/00313028809059515.

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35

PATEY, N., P. LESAVRE, L. HALBWACHS-MECARELLI, and L. H. NOËL. "ADHESION MOLECULES IN HUMAN CRESCENTIC GLOMERULONEPHRITIS." Journal of Pathology 179, no. 4 (August 1996): 414–20. http://dx.doi.org/10.1002/(sici)1096-9896(199608)179:4<414::aid-path601>3.0.co;2-j.

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36

Sethi, Sanjeev, Oyedele A. Adeyi, and Helmut G. Rennke. "A Case of Fibrillary Glomerulonephritis With Linear Immunoglobulin G Staining of the Glomerular Capillary Walls." Archives of Pathology & Laboratory Medicine 125, no. 4 (April 1, 2001): 534–36. http://dx.doi.org/10.5858/2001-125-0534-acofgw.

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Abstract We report a case of crescentic glomerulonephritis that presented with extensive crescent formation and fibrinoid necrosis in the glomeruli. Immunofluorescence staining was strongly positive for linear and pseudolinear staining of the capillary walls for immunoglobulin G (IgG) in the absence of significant mesangial staining. Histologic examination and immunofluorescence staining suggested a diagnosis of anti–glomerular basement membrane disease. However, electron microscopy showed the presence of numerous fibrillary deposits in the subepithelial areas of the glomerular capillary walls, supporting the diagnosis of fibrillary glomerulonephritis. Test results for circulating anti–glomerular basement membrane antibodies were negative. We report this interesting case to illustrate the point that fibrillary glomerulonephritis should be considered in the differential diagnosis of crescentic glomerulonephritis with linear and pseudolinear IgG deposits within the capillary walls. In such cases, electron microscopy is critical in differentiating the cause of crescentic glomerulonephritis.
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37

Gaut, Joseph P., and Helen Liapis. "IgA dominant post-infectious glomerulonephritis: pathology and insights into disease mechanisms." Diagnostic Histopathology 19, no. 5 (May 2013): 175–81. http://dx.doi.org/10.1016/j.mpdhp.2013.02.005.

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38

Gaut, Joseph P., Susanna Mueller, and Helen Liapis. "IgA dominant post-infectious glomerulonephritis update: pathology spectrum and disease mechanisms." Diagnostic Histopathology 23, no. 3 (March 2017): 126–32. http://dx.doi.org/10.1016/j.mpdhp.2017.03.010.

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39

Lewis, Edmund J., Jimmy L. Roberts, John Lachin, Shu-Ping Lan, Patricia Cleary, Melvin M. Schwartz, Jay Bernstein, et al. "Role of pathology indices in the management of severe lupus glomerulonephritis." Kidney International 42, no. 3 (September 1992): 743–48. http://dx.doi.org/10.1038/ki.1992.342.

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40

Peng, Tao, Tingting Xie, Lei Liu, Junhui Zhen, and Xiangdong Yang. "Analysis of clinical features and pathology of serum HBsAg positive glomerulonephritis." Journal of Medical Virology 90, no. 3 (November 8, 2017): 612–15. http://dx.doi.org/10.1002/jmv.24959.

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41

Lusco, Mark A., Agnes B. Fogo, Behzad Najafian, and Charles E. Alpers. "AJKD Atlas of Renal Pathology: Proliferative Glomerulonephritis With Monoclonal Immunoglobulin Deposits." American Journal of Kidney Diseases 67, no. 3 (March 2016): e13-e15. http://dx.doi.org/10.1053/j.ajkd.2016.01.003.

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42

Liapis, Helen, and George C. Tsokos. "Pathology and immunology of lupus glomerulonephritis: can we bridge the two?" International Urology and Nephrology 39, no. 1 (January 12, 2007): 223–31. http://dx.doi.org/10.1007/s11255-006-9170-x.

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43

Peyton, Nicole, and Prerna Rastogi. "Educational Case: Necrotizing and Crescentic Glomerulonephritis With Anti-Glomerular Basement Membrane Antibodies (Anti-Gbm)." Academic Pathology 7 (January 1, 2020): 237428952097516. http://dx.doi.org/10.1177/2374289520975166.

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The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040 .1
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44

Grøndahl, Camilla, Søren Rittig, Johan Vestergaard Povlsen, and Kostantinos Kamperis. "Protracted Clinical Course of Postinfectious Glomerulonephritis in a Previously Healthy Child." Case Reports in Nephrology and Dialysis 6, no. 1 (April 14, 2016): 70–75. http://dx.doi.org/10.1159/000445678.

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Acute postinfectious glomerulonephritis (PIGN) affects children typically after upper respiratory tract or skin infections with streptococci but can complicate the course of other infections. In children, it is generally a self-limiting disease with excellent prognosis. This paper reports a previously healthy 4-year-old boy who experienced a protracted course of PIGN with persisting episodes of gross haematuria, proteinuria, decreased complement C3c levels but normal P-creatinine levels. Due to the protracted course and the nephrotic-range proteinuria, a renal biopsy was performed 6 months after the initial presentation and the overall pathology was consistent with acute endocapillary glomerulonephritis.
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45

Ohashi, Atsuki, Jiro Kumagai, Kiyotaka Nagahama, and Hajime Fujisawa. "Case of immunotactoid glomerulopathy showing high responsiveness to steroids therapy despite severe pathological features." BMJ Case Reports 12, no. 7 (July 2019): e229751. http://dx.doi.org/10.1136/bcr-2019-229751.

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A 72-year-old woman presented with nephrotic proteinuria and moderate haematuria. Renal pathology was compatible with immunotactoid glomerulopathy (ITG), for which there is no consensus for appropriate therapy. We, therefore, postponed immunosuppressive therapy. After 4 years, the patient’s renal function started to decline and renal pathology was re-evaluated, revealing a pathological change from mesangial proliferative glomerulonephritis to endocapillary proliferative glomerulonephritis. Treatment with oral prednisolone (30 mg/day) was initiated. Within 5 weeks, complete remission of proteinuria was obtained (proteinuria 6.02 g/gCr to 0.12 g/gCr), and the patient’s renal function stabilised. Generally, responsiveness to immunosuppressive therapy is poor in patients with ITG, and the present case represented a very rare clinical course. Some previous cases have indicated susceptibility to the therapy, regardless of the severity of renal damage. As a possible distinct entity that determines susceptibility to immunosuppressive therapy, we suggest the presence of a latent lymphoproliferative disease with no significant haematological symptoms.
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46

Oda, Takashi, Osamu Hotta, Yoshio Taguma, Hiroshi Kitamura, Katuhiko Sudo, Ikuo Horigome, Shigemi Chiba, Nobuyuki Yoshizawa, and Hiroshi Nagura. "Involvement of neutrophil elastase in crescentic glomerulonephritis." Human Pathology 28, no. 6 (June 1997): 720–28. http://dx.doi.org/10.1016/s0046-8177(97)90182-9.

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47

Longano, Anthony. "Concurrent anti-GBM disease and IgA glomerulonephritis." Pathology 51, no. 3 (April 2019): 336–38. http://dx.doi.org/10.1016/j.pathol.2018.09.065.

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48

Mahajan, Hema, Anita Achan, Ross Boadle, and Thomas Ng. "Fibrillary-immunotactoid glomerulonephritis: report of two cases." Pathology 41 (January 2009): 63–64. http://dx.doi.org/10.1097/01268031-200941001-00142.

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49

Perl, Steven, James L. Yong, Julie Fletcher, Jim Mackie, and Grahame Elder. "Progression from Goodpasture’s disease to membranous glomerulonephritis." Pathology 27, no. 3 (1995): 233–36. http://dx.doi.org/10.1080/00313029500169043.

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50

Xiao, Hong, Dominic Ciavatta, David L. Aylor, Peiqi Hu, Fernando Pardo-Manuel de Villena, Ronald J. Falk, and J. Charles Jennette. "Genetically Determined Severity of Anti-Myeloperoxidase Glomerulonephritis." American Journal of Pathology 182, no. 4 (April 2013): 1219–26. http://dx.doi.org/10.1016/j.ajpath.2012.12.006.

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