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Books on the topic 'Glomerulonephriti'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

IgA nephropathy: From molecules to men. Basel: Karger, 1999.

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2

R, Clarkson A., and Woodroffe A. J, eds. IgA nephropathy: Pathogenesis and treatment. Basel: Karger, 1995.

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3

Catto, Graeme R. D., ed. Glomerulonephritis. Dordrecht: Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2225-9.

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4

Trachtman, Howard, Jonathan J. Hogan, Leal Herlitz, and Edgar V. Lerma, eds. Glomerulonephritis. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-27334-1.

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5

D, Catto Graeme R., ed. Glomerulonephritis. Dordrecht: Kluwer Academic Publishers, 1990.

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6

D, Pusey C., and Rees A. J, eds. Rapidly progressive glomerulonephritis. Oxford: Oxford University Press, 1998.

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7

Ponticelli, Claudio, Luigi Minetti, and Giuseppo D’Amico, eds. Antiglobulins, cryoglobulins and glomerulonephritis. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4289-9.

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8

Pusey, C. D., ed. The Treatment of Glomerulonephritis. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-0-585-37972-2.

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9

A, Sessa, ed. Glomerulonephritis in the elderly. Basel: Karger, 1993.

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10

D, Pusey C., ed. The treatment of glomerulonephritis. Dordrecht: Kluwer Academic, 1999.

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11

C, Ponticelli, and Glassock Richard J, eds. Treatment of primary glomerulonephritis. 2nd ed. Oxford: Oxford University Press, 2009.

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12

C, Ponticelli, and Glassock Richard J, eds. Treatment of primary glomerulonephritis. Oxford: Oxford University Press, 1997.

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13

R, Clarkson A., ed. IgA nephropathy. Boston: Nijhoff, 1987.

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14

International Symposium on IgA Nephropathy (11th 2006 Tokyo, Japan). IgA nephropathy today. Edited by Tomino Yasuhiko 1949-. Basel: Karger, 2007.

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15

Dixhoorn, Mieneke G. A. van. IgA in experimental kidney disease. [Leiden: University of Leiden, 1998.

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16

New insights into glomerulonephritis: Pathogenesis and treatment. Basel: Karger, 2013.

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17

Reid, Hugo Francis Murchison. Post streptococcal glomerulonephritis in Trinidad, West Indies. Birmingham: University of Birmingham, 1988.

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18

A, Rakiti͡anskai͡a I., and Shutko A. N, eds. Pochki i sistema immuniteta. Leningrad: "Nauka," Leningradskoe otd-nie, 1989.

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19

Fijter, Johan Willem de. The mucosal immune response in primary IgA nephropathy. [Leiden: University of Leiden, 1998.

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20

Masuda, Yu. Symposium on the relations between IgA nephropathy and tonsils: Held in Okayama, Japan, April 13, 2003 : organization of the symposium and its selected papers / chairman, Yu Masuda ; edited by Yu Masuda, ... [et al.]. Stockholm, Sweden: Taylor & Francis Health Sciences, 2004.

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21

Claudio, Ponticelli, Minetti L, and D'Amico G. 1929-, eds. Antiglobulins, cryoglobulins, and glomerulonephritis: Second International Milano Meeting of Nephrology, 30 September-1 October 1985. Dordrecht: M. Nijhoff, 1986.

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22

1947-, Ballardie Francis W., ed. Autoimmunity in nephritis. Chur: Harwood Academic Publishers, 1992.

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23

Sorger, Karin. Postinfectious glomerulonephritis: Subtypes, clinico-pathological correlations, and follow-up studies. Stuttgart: Fischer, 1986.

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24

La muerte no perdona, pero--. La Paz: Editorial Los Amigos del Libro, 1985.

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25

Meyrier, A. Optimal use of Sandimmun in nephrotic syndrome. Berlin: Springer, 1992.

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26

Prabhakar, Sharma S. An update on glomerulopathies: Clinical and treatment aspects. Rijeka, Croatia: InTech, 2011.

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27

Glomerular pathology. Edinburgh: Churchill Livingstone, 1991.

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28

Prabhakar, Sharma S. An update on glomerulopathies: Etiology and pathogenesis. Rijeka, Croatia: InTech, 2011.

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29

Kussmaul, Adolf. On a previously undescribed peculiar arterial disease (Periarteritis nodosa), accompanied by Bright's disease and rapidly progressive general muscle weakness. Rochester, MN: Mayo Foundation, 1996.

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30

B, Wilson Curtis, ed. Immunopathology of renal disease. New York: Churchill Livingstone, 1988.

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31

Qiuhai, Qian, and Ni Qing, eds. Man xing shen xiao qiu shen yan. Beijing Shi: Zhongguo yi yao ke ji chu ban she, 2003.

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32

Valaitis, Jonas. Renal glomerular diseases: Atlas of electron microscopy with histopathological bases and immunofluorescence findings : presention of 110 cases of patients undergoing kidney biopsies. Chicago: ACSP Press, 2002.

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33

Marie-Christine, Béné, Faure Gilbert, and Kessler M, eds. IgA nephropathy: The 25th year : international symposium, Nancy, August 31-September 2, 1992. Basel: Karger, 1993.

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34

Iga Nephropathy: The 25th Year (Contributions to Nephrology). S. Karger Publishers (USA), 1993.

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35

Lerma, Edgar V., Howard Trachtman, Leal C. Herlitz, and Jonathan J. Hogan. Glomerulonephritis. Springer, 2019.

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36

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Glomerulonephritis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0159.

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Abstract:

Glomerulonephritis (GN) is inflammation of the glomerulus. It can be caused by many different underlying conditions and can present in a range of ways. The key features, however, are evidence of renal dysfunction (clinical and investigative) with associated glomerular disease—the latter is often initially suspected from urine dipstick examination (Chapter 157), and may then be confirmed by a renal biopsy. This chapter looks at the etiology of GN, as well as its symptoms, clinical features, demographics, complications, diagnosis, and treatment.

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37

Grundmann, E., and J. Churg. Glomerulonephritis. Springer London, Limited, 2012.

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38

Lerma, Edgar V., Howard Trachtman, Leal C. Herlitz, and Jonathan J. Hogan. Glomerulonephritis. Springer, 2019.

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39

Grundmann, E., and J. Churg. Glomerulonephritis. Springer, 2012.

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40

Graeme R.D. Catto MD. Glomerulonephritis. Springer Netherlands, 2011.

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41

Catto, G. R. Glomerulonephritis. Springer London, Limited, 2012.

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42

Lerma, Edgar V., Howard Trachtman, Jonathan J. Hogan, and Leal Herlitz. Glomerulonephritis. Springer International Publishing AG, 2019.

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43

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0060_update_001.

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Membranous glomerulonephritis (MGN) is the most common cause of adult-onset nephrotic syndrome, and a common glomerular cause of end-stage renal failure. It is caused by antibodies to podocyte surface molecules, usually autoantibodies. In most patients with primary membranous nephropathy the target is the phospholipase A2 receptor. It is hoped that robust assays for this antibody will help to guide therapy but it has not been possible to test this adequately yet. Primary MGN accounts for about 70% of cases with regional variations. MGN is more common in men than women (approximately 2:1) and its peak incidence is in middle adult life. Secondary membranous nephropathy occurs in lupus and some other immune or autoimmune disorders, in hepatitis B infection, after exposure to some drugs or toxins, and in some cancers.

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44

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0061_update_001.

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Membranous glomerulonephritis (MGN) usually presents as nephrotic syndrome, which may be severe. It is primarily a disease of adults, men more than women, with a peak incidence in the fourth and fifth decades. It is hoped that proven tests for the characteristic anti-PLA2R antibodies of primary MGN may become established, but the diagnosis currently rests on renal biopsy showing characteristic subepithelial granular immune deposits. These usually contain immunoglobulin G4 and complement. Other patterns may suggest secondary causes of MGN. Secondary membranous nephropathy occurs in lupus and some other immune or autoimmune disorders, in hepatitis B infection, after exposure to some drugs or toxins, and in some cancers. Secondary causes are more common at extremes of age, and are often made obvious by the history or clinical picture. How hard to look for malignancy is controversial, but malignancy is much more likely in patients over 60 years, and may be apparent at presentation.

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45

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0062_update_001.

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A common rule of thumb in primary membranous glomerulonephritis (MGN) is that one-third of patients improve spontaneously, one-third progress, and one-third continue to have substantial proteinuria. The rate of spontaneous recovery may be near the truth, but MGN is usually an indolent condition and few studies have run long enough to give accurate outcomes for the remainder. However MGN is an important cause of end-stage renal failure. Treatment regimens that include cyclophosphamide or chlorambucil can improve the outcome of patients at greatest risk of deterioration, but their toxicity has limited their use in randomized studies to the highest risk patients. Steroids alone, and ciclosporin, do not improve long-term outcomes in these studies. Whether anti-B-cell antibodies offer additional benefits requires randomized studies. After confirming the diagnosis of primary MGN it is recommended to maximize supportive therapy and monitor for at least 6 months to give a clear picture of the long-term risk. For patients at lowest risk, supportive management and monitoring alone is recommended. Patients at medium risk (nephrotic range proteinuria but normal and stable glomerular filtration rate), or high risk (very heavy proteinuria, greater than 8 g/day or deterioration of glomerular filtration rate) may justify specific treatment directed at the immune response. For the medium-risk group it is not certain that it is required; for some in the high-risk group it may come too late. Overall outcomes in the high-risk group remain quite poor even with aggressive treatment.

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46

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.

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47

Cattran, Daniel C., and Heather N. Reich. Secondary membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0063.

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Primary (autoimmune) disease accounts for at least 70% of membranous glomerulonephritis (MGN). The main causes of secondary MGN are lupus, hepatitis B, drugs, and malignancy. Other autoimmune or inflammatory diseases, and some infections, are associated with it less commonly.

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48

Rodriguez-Iturbe, Bernardo, and Mark Haas. Post-infectious glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0076.

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Post-infectious glomerulonephritis (GN) defines an inflammatory lesion involving exclusively or predominantly the glomeruli that is a consequence of an infectious disease. There are numerous bacterial, viral, and fungal infections associated with GN. This chapter acts as an overview of the following chapters that discuss only post-streptococcal GN, immunoglobulin A-dominant GN associated with staphylococcal infections, GN associated with bacterial endocarditis, with infected ventriculoatrial shunts (‘shunt nephritis’), and GN associated with deep-seated infections (osteomyelitis, visceral abscesses, pleural suppuration, pneumonia).

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49

Rodríguez-Iturbe, Bernardo, and Mark Haas. Post-streptococcal glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0077_update_001.

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Post-streptococcal glomerulonephritis is a complication of Streptococcal infections that is responsible for classic acute nephritic syndrome, mostly seen in children. This is an acute nephritis associated with prominent fluid retention and oedema, hypertension and haematuria. Serum complement levels are diagnostically helpful as C3 levels are characteristically very low. However, many cases are much less severe and may pass unrecognized, only being identified by screening for dipstick haematuria. In children recovery is the rule but in adults, often with comorbid conditions, the prognosis is significantly worse. Management centres on loop diuretics plus treatment of the infection if still present, and additional hypotensive agents if required. Severe cases may require dialysis. High-dose corticosteroids have often been given in severe crescentic disease but there is no evidence that they are effective. In children, recovery of renal function is often excellent, though long-term studies now suggest that it may represent a risk factor for the development of chronic kidney disease. When it occurs in developed societies it is often in older patients with comorbid conditions and atypical presentations. Resolution may be less complete than in children.

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50

Pusey, Charles. Treatment of Glomerulonephritis. Springer London, Limited, 2007.

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