Books: 'Glomeruli'

1

Bartolomei, Juan Carlos. Immunocytochemical and synaptological characterization of rat olfactory bulb glomeruli. [New Haven, Conn: s.n.], 1994.

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2

Dembner, Jeffrey Marc. The topological distrubition of olfactory receptor neuron axons in the olfactory bulb glomeruli of the rat: A confocal microscopic study with DiI staining. [New Haven, Conn: s.n.], 1996.

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3

Glomerular pathology. Edinburgh: Churchill Livingstone, 1991.

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4

Gupta, Pallav, and Ramesh K. Gupta. Pathology of Glomerular Diseases. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1430-0.

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5

Newbold, Kenneth Mark. Morphometric studies of the human glomerulus. Birmingham: University of Birmingham, 1990.

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6

International Symposium on Glomerular Basement Membrane (2nd 1983 Vienna, Austria). Glomerular basement membrane: Contributions to the 2nd International Symposium on Glomerular Basement Membrane, Vienna, September 1983. Edited by Hudson Billy G and Lubec Gert. London: Libbey, 1985.

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7

International Symposium on Glomerular Basement Membrane (2nd 1983 Vienna). Glomerular basement membrane: Contributions to the 2nd International Symposium on Glomerular Basement Membrane, Vienna, September 1983. Edited by Lubec Gert and Hudson Billy G. London: Libbey, 1985.

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8

1865-1922, Mackenzie J. J., ed. A new conception of the glomerular function. [Toronto]: University Library, pub. by the Librarian, 1994.

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9

1915-, Senoo Sachimaru, Satellite Symposium on Biopathology of Vascular Wall and Glomerular Dysfunction (1984 : Kurashiki-shi, Japan), and International Congress on Cell Biology (3rd : 1984 : Tokyo, Japan), eds. Glomerular dysfunction and biopathology of vascular wall. Tokyo: Academic Press, 1985.

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10

Membranes, International Symposium on Renal Basement. Progress in basement membrane research: Renal and related aspects in health and disease : proceedings. London: J. Libbey, 1988.

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11

1926-, Kincaid-Smith Priscilla, and Dowling J. P, eds. Atlas of glomerular disease: Morphological and clinical correlation. Balgowlah, Australia: AIDS Health Science Press, 1985.

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12

Marie-Claire, Gubler, and Sternberg Michel, eds. Progress in basement membrane research: Renal and related aspects in health and disease : proceedings of the IVth International Symposium on Renal Basement Membranes and Related Research held in Paris, 21-25 July 1987. London: Libbey, 1988.

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13

Jay, Bernstein, and Glassock Richard J, eds. Renal disease: Classification and atlas of glomerular diseases. 2nd ed. New York: Igaku-Shoin, 1995.

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14

Color atlas of kidney biopsy: Pathology of glomerular diseases. New York: Liss, 1985.

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15

Elger, Marlies, Tatsuo Sakai, and Wilhelm Kriz. The Vascular Pole of the Renal Glomerulus of Rat. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80449-6.

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16

1953-, Sakai T., and Kriz Wilhelm 1936-, eds. The vascular pole of the renal glomerulus of rat. Berlin: Springer, 1998.

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17

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

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18

Hikaru, Koide, and Hayashi T, eds. Extracellular matrix in the kidney: 6th International Symposium on Basement Membrane, Shizuoka, May 29-June 1, 1993. Basel: Karger, 1994.

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19

Yeow, Jen Nei. Identification of the glomerular factor X activator in murine lupus nephritis. Ottawa: National Library of Canada, 1999.

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20

McDermott, Gerard F. The effects of ageing on glomerular morphology and mesangial cell function. Ottawa: National Library of Canada, 1995.

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21

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

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22

Diagnostic electron microscopy: A text/atlas. New York: Igaku-Shoin, 1988.

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23

Perampalam, Subodini. Characterization and localization of glomerular factor X activator in murine lupus nephritis. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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24

Derylo, Bogdan. Role of the polyol pathway in high glucose-induced altered glomerular mesangial cell function. Ottawa: National Library of Canada, 1995.

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25

Miller, Judith Anne. Determinants of glomerular filtration rate and renal blood flow in human insulin dependent diabetes mellitus. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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26

Ning, Xiaohua Terri. Role of chloride in the regulation of receptor-mediated divalent cation entry in glomerular mesangial cells. Ottawa: National Library of Canada, 1995.

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27

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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28

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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29

Glomerulopathies: Cell biology and immunology. Australia: Harwood Academic Press, 1996.

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30

Zaltzman, Jeffrey Steven. Timed creatinine clearance using oral cimetidine (TCC) an assessment of a novel test of glomerular filtration rate (GFR). Ottawa: National Library of Canada, 1994.

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31

Virginia. Department of Medical Assistance Services. Estimated glomerular filtration rate reporting among clinical laboratory providers: Report of the Virginia Department of Medical Assistance Services to the Governor and the General Assembly of Virginia. Richmond: Commonwealth of Virginia, 2007.

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32

Characterization of rat glomerular epithelial cells in culture: A comparison to rat glomeruli in vivo. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1993.

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33

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. The kidney in systemic disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0170.

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Many systemic diseases can affect the kidney, including autoimmune conditions, malignancies, infections, and vascular diseases. Autoimmune conditions can cause inflammation of the glomeruli or tubules, or deposition of inflammatory proteins (AA amyloidosis). Malignancy can cause infiltration of normal renal tissue, immunoglobulin deposition in the renal vessels, glomeruli or tubules, or paraneoplastic renal dysfunction as occurs in secondary focal segmental glomerulosclerosis. Infections can cause inflammation in glomeruli, in association with immune complex deposition. Vascular disease and vasculitis reduce kidney blood supply and cause renal ischaemia. This chapter provides an overview of these diseases.

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34

Niaudet, Patrick, and Alain Meyrier. Idiopathic nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0054_update_001.

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Idiopathic nephrotic syndrome is defined by the combination of massive proteinuria, hypoalbuminaemia, hyperlipidaemia, and oedema, and of non-specific histological abnormalities of the glomeruli. Light microscopy may disclose minimal change disease, diffuse mesangial proliferation, or focal segmental glomerular sclerosis (FSGS). The two main causes of idiopathic nephrotic syndrome are characterized histologically. On electron microscopy the glomerular capillaries show a fusion of visceral epithelial cell (podocyte) foot processes and with the exception of some variants no significant deposits of immunoglobulins or complement by immunofluorescence. In a majority of children only minimal changes are seen on light microscopy. These children are referred to as having ‘minimal change disease’. In adults with idiopathic nephrotic syndrome, lesions of FSGS are more frequent.

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35

On the functions of the glomeruli of the kidney: A contribution to the story of albuminuria. [S.l: s.n., 1985.

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36

On the functions of the glomeruli of the kidney: A contribution to the story of albuminuria. [S.l: s.n., 1985.

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37

O’Callaghan, Chris A. Renal function. Edited by Rutger Ploeg. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0126.

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The kidneys play a central role in homeostasis by maintaining extracellular fluid composition and volume. They do this by continuous filtration of plasma in the renal glomeruli and then subsequent modification of the filtered fluid as it passes along the nephron. The filtration process excludes large molecules, but most small molecules and ions are freely filtered. The filtrate that is produced in the glomeruli has a similar composition to plasma with respect to small molecules and ions. Most of the water and solutes are reabsorbed along the tubules and this process requires high levels of metabolic activity. In addition, a range of compounds and ions are secreted into the tubules along the nephron. Renal function is central to homeostasis and an appreciation of normal renal physiology is essential to understand the role of the kidney in a wide variety of disease processes.

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38

Duffield, Jeremy S. Disordered scarring and failure of repair. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0140.

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Scarring is the name given to fibrous tissue accumulation in the skin, which, when it forms elsewhere, is known as fibrosis, but the terms are frequently used interchangeably. The scientific study of fibrosis or scarring was established and developed in skin wounding, as a part of the normal repair response, long before it was appreciated that pathological fibrosis or scarring occurs as a consequence of sustained or iterative injury to internal organs. Increasing experimental evidence indicates that the process of skin wounding with scarring is very similar to the process of organ injury with fibrosis detected in vital organs including the kidney. Kidney fibrosis develops in glomeruli, where it is known as glomerulosclerosis (literally hardening of glomeruli due to fibrotic tissue), or in the interstitial virtual space between tubules and peritubular capillaries, known as interstitial fibrosis. Increasingly fibrosis of the kidney and the cells that make fibrous tissue are seen as targets for therapeutic intervention in chronic diseases of the kidney.

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39

Schreuder, Michiel F. Renal hypoplasia. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0348.

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In true renal hypoplasia, normal nephrons are formed but with a deficit in total numbers. As nephron number estimation is not possible in vivo, renal size is used as a marker. A widely used definition of renal hypoplasia is kidneys with a normal appearance on ultrasound but with a size less than two standard deviations below the mean for gender, age, and body size. A distinct and severe form of renal hypoplasia is called (congenital) oligomeganephronia, which is characterized by small but normal-shaped kidneys with a marked reduction in nephron numbers (to as low as 10–20% of normal), a distinct enlargement of glomeruli, and a reduced renal function. In many cases, the small kidney also shows signs of dysplasia on ultrasound, leading to the diagnosis of renal hypodysplasia. Based on the hyperfiltration hypothesis and clinical studies, glomerular hyperfiltration can be expected, resulting in hypertension, albuminuria, and renal injury, for which long-term follow-up of all patients with renal hypoplasia is desirable.

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40

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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41

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Interstitial renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0160.

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Tubulointerstitial renal diseases affect the renal tubules and/or the supporting interstitial tissue around them. The glomeruli are typically spared in early disease. Acute interstitial nephritis is characterized by an inflammatory infiltrate (often containing eosinophils). Chronic tubulointerstitial nephritis (TIN) is characterized by extensive tubular atrophy and interstitial fibrosis. The processes are clinically distinct but a prolonged acute interstitial nephritis will develop into chronic disease. This chapter looks at the etiology of interstitial renal disease, as well as its symptoms and clinical features, demographics, complications, diagnosis, and treatment.

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42

Wenzel, Ulrich, Thorsten Wiech, and Udo Helmchen. The effect of hypertension on renal vasculature and structure. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0211.

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The concept of hypertensive nephrosclerosis was introduced by Volhard and Fahr in 1914 and has been extensively used in the literature since then, but its existence is controversial. While it is indisputable that malignant hypertension is a cause of end-stage renal disease (ESRD), there remains controversy as to whether the so-called benign nephrosclerosis can also lead to ESRD.Pressure, if it is great enough, will eventually disrupt any structure. Obviously, this is also true of blood pressure. It is therefore not surprising that an experimentally induced great increase in pressure disrupts the integrity of the blood-vessel wall. Such vascular lesions may be caused or at least influenced by several factors: humoral factors such as angiotensin II, catecholamines, mineralocorticoids, and vasopressin may increase vascular permeability, thereby damaging the vessel walls independently of, or superimposed upon, elevated blood pressure.Nephrosclerosis (literally, hardening of the kidney, Greek derivation: nephros, kidney; sclerosis, hardening) refers to diseases with predominant pathological changes occurring in the pre-glomerular vasculature and secondary changes involving the glomeruli and interstitium. Therefore, it is appropriate to describe first those vascular lesions, which, at least under defined experimental conditions, are believed to be caused solely by the presence of hypertension.

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43

Lai, Kar Neng, and Sydney C. W. Tang. Immunoglobulin A nephropathy. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0069_update_001.

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A working hypothesis is that patients with immunoglobulin A (IgA) nephropathy have inherited defects in B cells producing galactose-deficient polymeric IgA1. Additional cofactors are required to form immune complexes and their deposition in glomeruli. Molecular characterization of IgG autoantibodies that recognize abnormally underglycosylated IgA1 reveals a specific amino acid substitution in the variable region of the IgG1 heavy chain. This substitution greatly enhances IgG1 binding to the galactose-deficient IgA1. The triggering antigens may include viral or bacterial antigens, or possibly by ingested food epitopes. Antiglycan IgG1 antibodies are one of the additional risk factors, or a second/multiple hit, which predisposes to disease development.

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44

Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Alport syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0323.

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The diagnosis of Alport syndrome is suspected from the clinical features and confirmed by identifying the almost pathognomonic ultrastructural changes to the basement membrane in a family member with early disease (so that glomeruli are not too sclerosed), or in modern times by identifying a causative mutation in one or more of the three implicated COL4 genes. Genetic testing is becoming simpler and cheaper, but is still out of the reach of many. Eighty-five per cent of cases are caused by COL4A5 mutations and 10–15% by autosomal recessive disease. A significant proportion of morbidity in X-linked disease occurs in female ‘carriers’ heterozygous for the disease. Changes by light microscopy are non-specific, and can be misleading unless accompanied by electron microscopy. Immunohistology can be helpful but may not be definitive as some causative mutations are not associated with absence of protein product. As COL4A5 is expressed in skin, skin studies are theoretically useful, but they are technically challenging and only a definite negative result is helpful. It is important to distinguish other disorders causing renal disease with deafness, and other causes of glomerular haematuria. Two rare syndromes are caused by extended deletions beyond the COL4A5 gene: X-linked Alport syndrome with diffuse oesophageal leiomyomatosis in which smooth muscle leoimyomas is transmitted in a dominant fashion, and X-linked Alport syndrome with mental retardation.

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45

Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.

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46

Pisharody, Ramadas. Primary Glomerular Diseases. Elsevier - Health Sciences Division, 2011.

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47

Sharpstone, P., and J. A. Trafford. Renal Glomerular Diseases. Springer Netherlands, 2012.

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48

Sharpstone, P., and J. A. Trafford. Renal Glomerular Diseases. Springer, 2012.

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49

Turner, Neil. Mechanisms of progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0136.

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Three major hypotheses attempt to explain progressive kidney disease following diverse diseases and injuries. To varying degrees they can explain the observed risk factors for progression and the ability of interventions to lower risk. The hyperfiltration hypothesis argues that progression is due to stress on residual nephrons leading to injury and damage to remaining glomeruli. The toxicity of proteinuria hypothesis proposes that serum proteins or bound substances are toxic to tubular or tubulointerstitial cells. This sets up cycles of damage which lead to tubulointerstitial scarring. The podocyte loss hypothesis contends that proteinuria is simply a biomarker for damaged or dying podocytes, and that it is further podocyte loss that leads to progressive glomerulosclerosis. Renoprotective strategies might have direct effects on podocytes. Importantly these different hypotheses suggest different therapeutic approaches to protecting the function of damaged kidneys. Differences between repair mechanisms may explain why some injuries lead to recovery and others to progressive disease, and may suggest new targets for protective therapy.

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50

Turner, Neil. Mechanisms of glomerular injury. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0045.

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Proteinuric diseases, historically termed ‘nephrosis’, are characterized by subtle abnormalities in podocytes or by abnormal glomerular matrix, including the scarring laid down by inflammatory diseases. Angiotensin blockers, corticosteroids, calcineurin inhibitors, and a wide range of other drugs known or believed to be effective in different renal diseases, appear to have direct effects on podocytes that reduce proteinuria that may be important to their effectiveness. Several of these have previously been assumed to work via haemodynamic, immune or other modes. Haematuric diseases are characterized by inflammatory disruption of the glomerular basement membrane (GBM) (‘nephritis’), or less commonly by fragile GBM without inflammation. The majority of haematuric conditions are slowly or rapidly destructive diseases associated with infiltration of inflammatory cells, and proliferation of endogenous cells of the glomerulus, probably in attempts at repair. With time, many haematuric diseases are associated with the development of proteinuria, possibly as a consequence of scarring and its effects on podocyte function.

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Books on the topic 'Glomeruli'

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