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Books on the topic 'Glomerular basement membrane'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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. Libbey, 1985.

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2

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. Libbey, 1985.

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3

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

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4

Lennon, Rachel, and Neil Turner. The molecular basis of glomerular basement membrane disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0320_update_001.

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The glomerular basement membrane (GBM) is a condensed network of extracellular matrix molecules which provides a scaffold and niche to support the function of the overlying glomerular cells. Within the glomerulus, the GBM separates the fenestrated endothelial cells, which line capillary walls from the epithelial cells or podocytes, which cover the outer aspect of the capillaries. In common with basement membranes throughout the body, the GBM contains core components including collagen IV, laminins, nidogens, and heparan sulphate proteoglycans. However, specific isoforms of these proteins are r

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5

Heidet, Laurence, Bertrand Knebelmann, and Marie Claire Gubler. Thin glomerular basement membrane nephropathy and other collagenopathies. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0325_update_001.

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The discovery of a thin glomerular basement membrane in a renal biopsy without any other abnormalities can be explained in a number of ways. This could be an early biopsy in a patient with Alport syndrome, or it could be an individual who is a carrier for an Alport gene. These carriers are at increased risk of significant renal disease in their lifetime and some have proteinuria as well as haematuria, so they can no longer be equated with the historic label of benign familial haematuria. Some families with a thin glomerular basement membrane and haematuria inherited in an autosomal dominant fa

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6

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0071.

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Antiglomerular basement membrane disease is characteristically the most rapidly progressive (crescentic) nephritis. It is often accompanied by lung haemorrhage, and occasionally causes lung disease alone. Its hallmark is linear deposition of immunoglobulin G along the glomerular basement membrane. There are usually few systemic symptoms apart from any related to the lung disease. Urine shows haematuria, often macroscopic in very acute disease.

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7

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0073_update_001.

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Cyclophosphamide and plasma exchange are the standard of care in rapidly progressive glomerulonephritis or lung haemorrhage caused by antiglomerular basement membrane (anti-GBM) disease, and it is unusual to encounter patients at earlier stages. Steroids are universally used in addition. There is some evidence that plasma exchange may not be a critical part of treatment at an earlier stage. There is no more than anecdotal evidence for other therapies. Slower-onset therapies such as antibodies to B cells are rarely appropriate. If untreated, patients with severe anti-GBM disease will not recove

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8

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0075.

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Alport antiglomerular basement membrane (anti-GBM) disease is a rare example of disease caused by allo-sensitization after renal transplantation, first described in 1992. Because the recipient lacks a specific glomerular basement membrane (GBM) protein, they can become sensitized to the normal molecule present in the GBM of the donor kidney. The disease is restricted to the allograft. Interestingly severe disease arises from this only arises rarely, certainly less than 1 in 20, probably closer to 1 in 50. It characteristically causes late graft loss in a first transplant with accelerated tempo

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9

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 charact

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10

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

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11

Carton, James. Renal pathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0010.

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This chapter discusses renal pathology, including acute kidney injury (AKI), chronic kidney disease (CKD), nephrotic syndrome, hereditary renal diseases, Alport’s syndrome and thin basement membrane lesion, hypertensive nephropathy, diabetic nephropathy, minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy, glomerulonephritis, IgA nephropathy, post-infectious glomerulonephritis, C3 glomerulopathy, anti-glomerular basement membrane disease, monoclonal gammopathy-associated kidney disease, acute tubular injury, acute tubulointerstitial nephritis, ref

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12

Carton, James. Renal pathology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0009.

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Chronic kidney disease 142Acute renal failure 144Hypertensive nephropathy 145Diabetic nephropathy 146Minimal change disease 147Focal segmental glomerulosclerosis 148Membranous nephropathy 149IgA nephropathy 150Acute tubular injury 151Acute drug-induced interstitial nephritis 152Anti-glomerular basement membrane disease 153Reflux nephropathy 154...

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13

Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0139.

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Experimental studies show that podocyte death first causes focal scars, but beyond approximately 40% loss is lethal to a glomerulus. Podocytes have limited ability to regenerate, although some degree of replacement may occur from stem cells located near the urinary pole of Bowman’s capsule. It is not yet known whether this plays a significant part in ameliorating damage in disease processes. In one interpretation, foot process effacement may be seen as an adaptation by the podocyte to remain attached to the glomerular basement membrane after injury, at the expense of proteinuria. Podocyte dysf

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14

Saleem, Moin A., and Corinne Antignac. Molecular basis of nephrotic syndrome. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0327_update_001.

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Nephrotic syndrome is broadly a disorder of the glomerular filtration barrier, but in practice the site of dysfunction in the great majority of pathologies is in the podocyte. Genetic causes of nephrotic syndrome provide the strongest proof of this. Almost all the genetic associations with nephrotic syndrome are podocyte proteins. Some basement membrane protein mutations associated with nephrotic syndrome may act through signalling to podocytes, or by causing severe disruption to their environment.

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15

Woywodt, Alexander, and Diana Chiu. The glomerulus and the concept of glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0042.

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The key features of glomerular diseases—haematuria, proteinuria, loss of glomerular filtration rate, and hypertension—were recognized in the nineteenth century, and some earlier, but Richard Bright is usually given credit for synthesizing the concepts of renal disease, and glomerulonephritis came under the heading of Bright’s disease for almost a century. Separation into different types was based on first clinical syndromes, but in the early twentieth century, pathological description was improving and with the introduction of percutaneous renal biopsies in the 1950s, in the 1960s histopatholo

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16

Berden, Jo H. M., and Jack F. M. Wetzels. Immunological investigation of the patient with renal disease. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0017.

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Laboratory techniques (electrophoresis, indirect immunofluorescence, ELISA, and immunoblotting) required for immunological investigation of the patient with renal disease are described. Renal disease-related aspects of immunoglobulins (immunoglobulin A, paraproteins, cryoglobulins), complement, antinuclear antibodies, anti-C1q antibodies, antineutrophil cytoplasmic antibodies, anti-glomerular basement membrane antibodies, antipodocyte antibodies, antiphospholipid antibodies, and antimicrobial responses (streptococci, hepatitis C, hepatitis B) are reviewed. Laboratory assays which evaluate the

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17

Turner, Neil. Crescentic (rapidly progressive) glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0070.

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Crescent formation refers to the appearance of proliferating cells in Bowman’s space in response to severe glomerular inflammation. Any aggressive ‘nephritic’ diseases that cause basement membrane breaks may provoke this. Specific serum proteins appear to be responsible for provoking crescent formation as it is largely abolished by defibrination in animal models. The cells in the crescent are initially mostly hypertrophying and proliferating parietal epithelial cells that normally line Bowman’s capsule. Foci of proliferation of these cells (extracapillary proliferation) are the first steps of

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18

Korbet, Stephen M., Melvin M. Schwartz, and Edmund J. Lewis. Fibrillary and immunotactoid glomerulopathy. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0081.

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Fibrillary or immunotactoid nephropathy is a rare deposition disease of unknown cause in which highly organized deposits containing immunoglobulin and complement are found in the glomerular basement membrane and mesangium. These deposits are not amyloid fibrils and do not stain with Congo red. They are usually polyclonal and are not associated with monoclonal paraproteins, or with cryoglobulins or systemic lupus, distinguishing them from other non-amyloid fibrillary glomerulopathies. There is debate about whether there is a useful distinction between distinct fibrillary and rarer immunotactoid

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19

Progress in basement membrane research: Renal and related aspects in health and disease : Proceedings of the IVth International Symposium on Renal Basement ... Research held in Paris, 21-25 July 1987. Libbey, 1988.

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20

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-li

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21

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/9780199592548.003.0324.

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Management of Alport syndrome has in the past been expectant and supportive. Modern hearing aids have substantially improved the function of affected individuals. However, animal data and more recently observational data from Alport registries strongly suggest a protective effect of angiotensin-converting enzyme inhibitors. There is a suggestion that early commencement of treatment may slow progression substantially. These should now be recommended for all with proteinuria, and possibly even before then for those known to harbour mutations certain to cause end-stage renal failure. A very small

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22

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0074_update_001.

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Individuals appear to be predisposed to antiglomerular basement membrane (anti-GBM) disease by carrying a predisposing human leucocyte antigen type, DRB1*1501 being identified as the highest risk factor, and there are likely to be other predisposing genes or influences on top of which a relatively rare ‘second hit’ leads to the development of autoimmunity. In anti-GBM disease this appears to have a self-perpetuating, accelerating component, that may be to do with antibodies and altered antigen presentation. Lymphocyte depletion may also predispose to the disease. A number of second hits have b

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