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Thematische Bibliographien / Membrane, Basement / Bücher

Bücher zum Thema „Membrane, Basement“

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Autor: Grafiati

Veröffentlicht am 4. Juni 2021

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1

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. Herausgegeben von Lubec Gert und Hudson Billy G. London: Libbey, 1985.

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2

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. Herausgegeben von Hudson Billy G und Lubec Gert. London: Libbey, 1985.

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3

Kefalides, Nicholas A. Basement membranes: Cell and molecular biology. San Diego, CA: Elsevier/Academic Press, 2006.

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4

Kefalides, Nicholas A. Basement membranes: Cell and molecular biology. Amsterdam: Elsevier Academic Press, 2005.

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5

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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6

International Symposium on Renal Basement Membranes (4th 1987 Paris, France). 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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7

International Symposium on Basement Membranes (1985 Mishima-shi, Japan). Basement membranes: Proceedings of the International Symposium on Basement Membranes held in Mishima (Japan) on June 24-26, 1985. Amsterdam: Elsevier Science Publishers, 1985.

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8

Costigan, Michael. Basement membrane gene expression in the normal and streptozotocin diabetic rat. Manchester: Universityof Manchester, 1996.

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9

International Symposium on Basement Membranes (6th 1993 Shizuoka-shi, Japan). Extracellular matrix in the kidney: 6th International Symposium on Basement Membrane, Shizuoka, May 29-June 1, 1993. Herausgegeben von Koide Hikaru und Hayashi T. Basel: Karger, 1994.

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10

Kalaaji, Amer N. Mayo Clinic atlas of immunofluorescence in dermatology: Patterns and target antigens. Rochester, MN: Mayo Clinic Scientific Press, 2006.

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11

Kalaaji, Amer N. Mayo Clinic atlas of immunofluorescence in dermatology: Patterns and target antigens. Boca Raton, FL: Mayo Clinic Scientific Press/Taylor & Francis, 2006.

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12

Tryggvason, Karl. Inherited Basement Membrane Disorders. Chapman & Hall, 1998.

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13

Cui, Zhao, Neil Turner und Ming-hui Zhao. Antiglomerular basement membrane disease. Herausgegeben von 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.

14

Cui, Zhao, Neil Turner und Ming-hui Zhao. Antiglomerular basement membrane disease. Herausgegeben von Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0072_update_001.

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Antiglomerular basement membrane (anti-GBM) disease may present as rapidly progressive glomerulonephritis alone, or in the presence of a secondary pulmonary insult (e.g. smoking or other toxicity, or infection) in combination with lung haemorrhage. Rarely it presents as lung disease alone (with haematuria) or as subacute glomerulonephritis. The major differential diagnoses are small vessel vasculitis, which is a more common cause of pulmonary haemorrhage with rapidly progressive glomerulonephritis, and causes of simultaneous pulmonary and renal failure. For most of these, the lung lesion is not pulmonary haemorrhage. The diagnosis often most quickly, most sensitively, specifically and usefully made by renal biopsy, but immunoassays showing a high titre of anti-GBM antibodies in the setting of severe renal disease are also useful. Borderline and even normal anti-GBM titres are not so specific or reliable in some forms of the disease though.

15

Cui, Zhao, Neil Turner und Ming-hui Zhao. Antiglomerular basement membrane disease. Herausgegeben von 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 recover renal function and are at risk of pulmonary haemorrhage. Evidence for the pathogenicity of circulating anti-GBM antibodies provides rationale for removal of circulating antibodies as rapidly as possible, whilst simultaneously inhibiting their synthesis. This was behind the introduction of the combination of plasma exchange with immunosuppressive therapy in mid 1970s, which revolutionized outcomes. Plasmapheresis aims to remove circulating pathogenic antibodies against GBM and possibly other mediators; cyclophosphamide prevents further synthesis of autoantibodies; and steroids act as anti-inflammatory agents to attenuate the glomerular inflammatory response initiated by anti-GBM antibodies. It is clear from experimental models and occasional observations in man that the anti-cell mediated effects of current therapies are important too. Outcomes vary, but in general patient survival is now good, while renal survival remains poor, in many series less than 50% at 1 year. Treatment is toxic and after an early peak in deaths due to pulmonary haemorrhage, secondary infections are the next threat. It may therefore be best not to immunosuppress patients with a very poor renal prognosis who appear to be at low risk of pulmonary haemorrhage. Treatment can usually be curtailed after 3 months without recurrence. ANCA and anti-GBM antibodies occur together in some patients. This is typically an older group which often has features of vasculitis, and the anti-GBM response may often be secondary. Longer treatment as for small vessel vasculitis is usually indicated.

16

Cui, Zhao, Neil Turner und Ming-hui Zhao. Antiglomerular basement membrane disease. Herausgegeben von 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 been identified and they seem to share a theme of damage to the glomerulus. There may be a prolonged (months to years) and usually subclinical phase in anti-GBM disease in which usually relatively low level antibody titres are associated with variable haematuria, sometimes minor pulmonary haemorrhage, but often no symptoms. Damage to the lung seems to determine whether there is a pulmonary component to the disease. Without pulmonary damage caused typically by smoking, inhalation of other fumes, and potentially infection or oxygen toxicity, the disease remains an isolated kidney disease. Antibodies appear to be an important component of the disease, but cell-mediated immunity is also critical to the clinical picture. In animal models, cell-mediated immunity triggered by the GBM antigen can cause severe renal damage in the absence of pathogenic antibody. The development of specific antibody also requires T-cell sensitization and help, and suppressing the response is likely to require suppressing both antibody and cell-mediated immunity. Antibodies recognize one major and some other epitopes, which are now well described. T-cell epitopes are becoming better understood. Evidence from animal models also suggests that the damage in anti-GBM disease is dependent on complement, macrophages, and neutrophils.

17

Laminins: Structure, Biological Activity and Role in Disease. Nova Science Pub Inc, 2013.

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18

Cui, Zhao, Neil Turner und Ming-hui Zhao. Alport post-transplant antiglomerular basement membrane disease. Herausgegeben von 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 in later allografts, and in its most extreme form recurs within days. However, inexplicably some subsequent transplants do not provoke aggressive recurrence. Treatment of the most aggressive disease is difficult and in most cases has been ultimately unsuccessful. Lower levels of immune response, marked by linear binding of immunoglobulin-G to GBM without glomerular disease, are not uncommon in Alport patients after transplantation and should not lead to altered treatment. Immunoassays for anti-GBM antibodies can be misleading as in most cases the target of antibodies is the α‎‎‎5 chain of type IV collagen, rather than the α‎‎‎3 chain which is the target in spontaneous anti-GBM disease. Overall the outcome of transplantation in Alport syndrome is better than average. This complication is more likely in patients with partial or total gene deletion rather than point mutations, but no other predictive features have been identified.

19

Molecular and Cellular Aspects of Basement Membrane. Elsevier, 1993. http://dx.doi.org/10.1016/c2012-0-01643-2.

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20

Molecular and cellular aspects of basement membranes. San Diego: Academic Press, 1993.

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21

Heidet, Laurence, Bertrand Knebelmann und Marie Claire Gubler. Thin glomerular basement membrane nephropathy and other collagenopathies. Herausgegeben von 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 fashion do not appear to have linkage to COL4 genes. Others have variable renal disease that has sometimes given rise to a label of mild but autosomal dominant Alport syndrome. This territory might also attract the label basement membrane 345 collagenopathy. Other uncommon conditions affecting the glomerular basement membrane include nail patella syndrome.

22

Salmivirta, Katriina. Basement Membrane Components and Their Receptors in Organogenesis. Uppsala Universitet, 1999.

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23

Lennon, Rachel, und Neil Turner. The molecular basis of glomerular basement membrane disorders. Herausgegeben von 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 required to maintain the integrity of the glomerular filtration barrier.Across the spectrum of glomerular disease there is alteration in glomerular extracellular matrix (ECM) and a number of histological patterns are recognized. The GBM can be thickened, expanded, split, and irregular; the mesangial matrix may be expanded and glomerulosclerosis represents a widespread accumulation of ECM proteins associated with loss of glomerular function. Whilst histological patterns may follow a sequence or provide diagnostic clues, there remains limited understanding about the mechanisms of ECM regulation and how this tight control is lost in glomerular disease. Monogenic disorders of the GBM including Alport and Pierson syndromes have highlighted the importance of both collagen IV and laminin isoforms and these observations provide important insights into mechanisms of glomerular disease.

24

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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25

Kefalides, Nicholas, und Jacques Borel. Basement Membranes: Cell and Molecular Biology, Volume 56 (Current Topics in Membranes). Academic Press, 2005.

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26

Kefalides, Nicholas, und Jacques Borel. Basement Membranes: Cell and Molecular Biology, Volume 56 (Current Topics in Membranes). Academic Press, 2005.

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27

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, reflux nephropathy, and obstructive nephropathy.

28

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...

29

Miner, Jeffrey H. Basement Membranes. Elsevier Science & Technology, 2015.

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30

Shibata. Basement Membranes:. Elsevier Science & Technology, 1985.

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31

Basement Membranes. Elsevier, 2015. http://dx.doi.org/10.1016/s1063-5823(15)x0003-2.

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32

Miner, Jeffrey H. Basement Membranes. Elsevier Science & Technology Books, 2015.

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33

Davies, Emily. Bullous disorders. Herausgegeben von Patrick Davey und David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0252.

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This chapter focuses on immunobullous diseases. The immunobullous disorders are a group of diseases in which pathogenic autoantibodies bind to target antigens either in desmosomes (intra-epidermal intracellular adhesion junctions) or in part of the basement membrane zone, resulting in loss of adhesion, and blister formation. This chapter will focus on pemphigus vulgaris, pemphigus foliaceus, bullous pemphigoid, linear IgA disease, chronic bullous disease of childhood, and dermatitis herpetiformis; it will also mention mucous membrane pemphigoid, pemphigoid gestationis, and epidermolysis bullosa acquisita.

34

Koide, H. Extracellular Matrix in the Kidney: 6th International Symposium on Basement Membrane, Shizuoka, May 29-June 1, 1993 (Contributions to Nephrology). S Karger Pub, 1994.

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35

Saleem, Moin A., und Corinne Antignac. Molecular basis of nephrotic syndrome. Herausgegeben von 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.

36

Heidet, Laurence, und Marie Claire Gubler. Nail patella syndrome. Herausgegeben von Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0326_update_001.

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Nail patella syndrome can be recognized by its characteristic nail dystrophy and symmetrical skeletal abnormalities. Proteinuric renal disease is a variable part of the syndrome, usually mild but causing end-stage renal failure in up to 10%. An association with glaucoma has been recognized and this should be screened for. Underlying gene mutations are in a LIM homeodomain-containing transcription factor LMX1B, which seems to influence production of basement membrane proteins and other podocyte gene products.

37

Basement Membranes in Neoplasia. Gustav Fischer Verlag GmbH & Co KG, 1992.

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38

Porter, Ruth, und Julie Whelan. Basement Membranes and Cell Movement. Wiley & Sons, Incorporated, John, 2009.

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39

Porter, R., und CIBA Foundation Symposium Staff. Basement Membranes and Cell Movement. Wiley & Sons, Limited, John, 2008.

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40

Goodyer, Paul. Kidney/ear syndromes. Herausgegeben von Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0170.

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Malformations of the external ear may signal renal disease, but it is actually the disorders of the inner ear which reflect molecular pathways that are also crucial for kidney development. In a number of monogenic renal diseases, renal dysplasia is associated with deafness. Disorders of the kidney and inner ear are also linked in complex syndromes such as the human ciliopathies. In some cases, the loss of specific genes affects shared transport physiology, basement membrane assembly, or energy metabolism.The kidney and cochlea have a common susceptibility to toxins that are selectively concentrated by comparable uptake mechanisms in the two tissues.This chapter provides an overview of the many ways in which pathologies of the two organs are linked.

41

Heidet, Laurence, Bertrand Knebelmann und Marie Claire Gubler. Alport syndrome. Herausgegeben von Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0321.

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Alport syndrome is an inherited renal disorder characterized by early haematuria, progressing to proteinuria, sensorineural hearing loss, and progressive renal failure typically in the third or fourth decade but with wide variation. It is responsible for about 1% of end-stage renal failure. Over 80% of cases are X-linked and young men are most affected, but heterozygous carriers of the abnormal gene are also at significantly increased risk of end-stage renal failure in their lifetime. Those affected by the autosomal recessive variant are phenotypically very similar. It is caused by mutations in tissue-specific isoforms of basement membrane (type IV) collagen encoded by COL4A5 (X chromosome), COL4A3, and COL4A4 (chromosome 2).

42

Berden, Jo H. M., und Jack F. M. Wetzels. Immunological investigation of the patient with renal disease. Herausgegeben von 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 immune response, in particular the identification of (auto)-antibodies are valuable tools in establishing a diagnosis and/or monitoring of the activity of the disease. Guidelines are given for immunological studies in patients with specific renal syndromes including nephrotic syndrome, rapidly progressive glomerulonephritis, systemic lupus erythematosus, and thrombotic microangiopathy.

43

Elger, Marlies, und Wilhelm Kriz. The renal glomerulus. Herausgegeben von 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.

44

Basement Membranes: Cell and Molecular Biology. Elsevier, 2005. http://dx.doi.org/10.1016/s1063-5823(05)x1032-8.

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45

Pleyer. OCULODERMAL DISEASES. Taylor & Francis, 1997.

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46

Segall, Liviu, und Adrian Covic. Immune-mediated tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.

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Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.

47

Price, Robert G. Renal Basement Membranes in Health and Disease. Academic Press, 1987.

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48

Powell, Jenny. Normal skin function. Herausgegeben von Patrick Davey und David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0243.

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In simplest terms, our skin is a layer that separates and protects us from the external environment. This assumes the skin is a passive covering to keep the insides safe and the outside out, and overlooks its enormous complexity. The skin is our largest organ and is constantly regenerating, but how efficiently it does so depends on a number of factors, some known, others unknown. It is an efficient mechanical barrier (designed for wear and repair), and a complex immunological membrane. It has a generous vascular, lymphatic, and nervous supply, all covering a considerable area. It has specialist structural and functional properties relating to specific areas, but also specialist cells within the layers of the skin. Most importantly, skin is the organ of display, an important part of social and sexual behaviour, immediately accessible to all, and often regarded as a barometer of the general state of health. Permanent scars inflicted on the skin may be a cause of great distress to the patient. Skin consists of a superficial layer, ‘the epidermis’ (concerned with producing protective keratin and a pigment called melanin), which adheres closely to the deeper layer, ‘the dermis’ (which provides the strength of the skin and houses the appendages), via the basement membrane. Loose connective tissue and fat underlie the dermis.

49

Turner, Neil. Mechanisms of glomerular injury. Herausgegeben von 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.

50

Kriz, Wilhelm. Podocyte loss as a common pathway to chronic kidney disease. Herausgegeben von 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 dysfunction is closely associated with proteinuria, which in turn is strongly associated with progressive loss of glomerular filtration rate. Continuing podocyte damage and loss could therefore account for progressive renal disease. In this hypothesis, drugs that protect against progression of renal disease may have their primary protective effects on podocytes themselves, rather than or as well as on haemodynamic factors or on fibrotic processes.