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Books on the topic 'Fibrosi renale'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv, eds. Renal Fibrosis: Mechanisms and Therapies. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2.

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2

Journées Gabriel Richet (1994 Le Coudray Montceaux, France). Molecular and experimental aspects of renal fibrogenesis: Journées Gabriel Richet. Edited by Sraer Jean-Daniel, Ronco Pierre, and Rondeau Eric. Blackwell Science, 1995.

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3

Hanssen, Lydia. Die pathophysiologische Bedeutung des Y-box-bindenden Proteins-1 (YB-1) in der renalen Fibrose. s.n.], 2012.

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4

Razzaque, M. S., and T. Taguchi, eds. Renal Fibrosis. S. Karger AG, 2003. http://dx.doi.org/10.1159/isbn.978-3-318-00964-4.

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5

(Editor), Mohammed S. Razzaque, and Takashi Taguchi (Editor), eds. Renal Fibrosis (Contributions to Nephrology). S. Karger Publishers (USA), 2003.

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6

Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv. Renal Fibrosis: Mechanisms and Therapies. Springer, 2019.

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7

Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv. Renal Fibrosis: Mechanisms and Therapies. Springer, 2020.

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8

Liu, Bi-Cheng, Hui-Yao Lan, and Lin-Li Lv. Renal Fibrosis: Mechanisms and Therapies. Springer, 2019.

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9

Lan, Hui Y., and David J. Nikolic-Paterson, eds. Advances in Mechanisms of Renal Fibrosis. Frontiers Media SA, 2018. http://dx.doi.org/10.3389/978-2-88945-499-0.

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10

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 a

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11

Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by h

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12

Galperin, Timur A., Kieron S. Leslie, and Antonia J. Cronin. Cutaneous manifestations of end-stage renal disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0131.

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A broad range of skin diseases occur in patients with end-stage renal disease. Some of these conditions are benign, and make little impact on patients’ lives. Others, however, have a greater impact on quality of life, may be physically disabling, and even life-threatening. Mostly, they result from a combination of factors, such as electrolyte imbalance and co-morbid disease. Uraemic pruritus is the most commonly troublesome and an approach to it is presented. Other non-specific skin manifestations of CKD include skin-colour changes, xerosis, half-and-half nails Specific manifestations include

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13

München, Universität, ed. Nierenfunktion und renale Effekte von Sekretin bei Patienten mit Cystischer Fibrose unterschiedlichen Genotyps. 1994.

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14

Schiller, Adalbert, Adrian Covic, and Liviu Segall. Chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.

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Chronic tubulointerstitial nephropathies (CTINs) are a group of renal diseases, characterized by variable interstitial inflammation and fibrosis and tubular atrophy, and a slow course towards end-stage renal disease (ESRD). The causes of CTIN are numerous, including nephrotoxic drugs and chemicals, infections, autoimmune diseases, obstructive uropathies, and metabolic disorders. Taken together, CTIN are responsible for less than 10% of all ESRD cases requiring renal replacement therapy. The clinical manifestations of CTIN typically comprise low-grade proteinuria, leucocyturia, and variably red

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15

Hughes, Jeremy. Proteinuria as a direct cause of progression. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.

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Proximal tubular cells reabsorb any filtered proteins during health via cell surface receptors such as megalin and cubulin so that very low levels of protein are present in the excreted urine. Significant proteinuria is a common finding in patients with many renal diseases. Proteinuria is a marker of glomerular damage and podocyte loss and injury in particular. The degree of proteinuria at presentation or during the course of the disease correlates with long-term outcome in many renal diseases. Proteinuria per se may be nephrotoxic and thus directly relevant to the progression of renal disease

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16

Chen, Dan-Qian, and Zhiyong Guo, eds. New Insights Into Renal Fibrosis and Therapeutic Effects of Natural Products. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-272-9.

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17

Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.

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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘

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18

London, Gerard M. Cardiovascular complications in end-stage renal disease patients. Edited by Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0268.

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Cardiovascular complications are the predominant cause of death in patients with end-stage renal disease (ESRD). The high incidence of cardiovascular complications results from pathology present before ESRD (generalized atherosclerosis, diabetes, hypertension) and an additive effect of multiple factors including haemodynamic overload and metabolic and endocrine abnormalities more or less specific to uraemia or its treatment modalities. These disorders are usually associated and can exacerbate each other. While ischaemic heart disease is a frequent cause of cardiac death, heart failure and sudd

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19

Glockner, James F., Kazuhiro Kitajima, and Akira Kawashima. Magnetic resonance imaging. Edited by Christopher G. Winearls. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0015_update_001.

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Magnetic resonance imaging (MRI) provides excellent anatomic detail and soft tissue contrast for the evaluation of patients with renal disease. MRI needs longer scan time than computed tomography (CT); however, no radiation is involved. Gadolinium-based contrast agents (GBCAs) are used to help provide additional image contrast during MRI. MRI is indicated for characterization of renal mass, staging of malignant renal neoplasms, and determination of vena cava involvement by the renal tumour. Magnetic resonance (MR) angiography is widely accepted as a non-invasive imaging work-up of renal artery

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20

Henderson, Lorna K., Brian J. Nankivell, and Jeremy R. Chapman. Chronic allograft dysfunction. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0286.

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Despite improvements in short-term renal allograft survival, long-term survival has not appreciably changed. Excepting death with a functioning graft, most late graft loss results from chronic allograft dysfunction. Immune and non-immune-mediated injuries contribute to graft dysfunction over time, ultimately leading to a non-specific and irreversible histological end-point of fibrosis, tubular atrophy, and glomerulosclerosis. Screening and early identification of pathology is crucial to allow timely intervention in order to prevent permanent nephron damage and graft loss. This chapter outlines

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21

Sayer, John A., and Roslyn J. Simms. Nephronophthisis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0317_update_001.

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Nephronophthisis (NPHP) is a clinically heterogeneous autosomal recessive cystic kidney disease and the leading genetic cause of end-stage renal failure in children and young adults. Whilst enlarged dysplastic cystic kidneys are associated with infantile NPHP, more typically renal ultrasound reveals normal kidney size and corticomedullary cysts in a child with polyuria and secondary enuresis. Extrarenal manifestations occur in 10–15% including retinal degeneration, cerebellar vermis hypoplasia and liver fibrosis, requiring referral to other specialists. Mutations in 18 genes have been identifi

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22

Nahas, A. M. El. Renal Scarring - A Multi-Organ Approach to Fibrosis (Experimental Nephsology, 1995 , Vol 3, No 2-3). S. Karger AG (Switzerland), 1995.

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23

Kang, Duk-Hee, and Mehmet Kanbay. Urate nephropathy. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0092.

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Gout is a disorder of purine metabolism, characterized by hyperuricaemia and urate crystal deposition within and around the joints. The recognition of increased comorbidity burden in patients with gout rendered it as a systemic disorder rather than simply a musculoskeletal condition. Gout nephropathy (also known as chronic uric acid nephropathy or urate nephropathy) is a form of chronic tubulointerstitial nephritis, induced by deposition of monosodium urate crystals in the distal collecting ducts and the medullary interstitium, associated with a secondary inflammatory reaction. Other renal his

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24

Denton, Christopher P., and Pia Moinzadeh. Systemic sclerosis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0121.

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The term 'scleroderma' describes a group of conditions in which the development of thickened, fibrotic skin is a cardinal feature. This includes localized forms of scleroderma (e.g. morphoea) and also systemic forms of the disease that are more correctly termed systemic sclerosis. Systemic sclerosis (SSc) is a multiorgan, autoimmune disease that has a high clinical burden and mortality, due to affecting the skin as well as internal organs. As with other related diseases there is a female predominance and marked clinical diversity. The pathogenesis of SSc is not fully elucidated; it includes en

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25

Tsai, Ching-Wei, Sanjeev Noel, and Hamid Rabb. Pathophysiology of Acute Kidney Injury, Repair, and Regeneration. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0030.

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Acute kidney injury (AKI), regardless of its aetiology, can elicit persistent or permanent kidney tissue changes that are associated with progression to end-stage renal disease and a greater risk of chronic kidney disease (CKD). In other cases, AKI may result in complete repair and restoration of normal kidney function. The pathophysiological mechanisms of renal injury and repair include vascular, tubular, and inflammatory factors. The initial injury phase is characterized by rarefaction of peritubular vessels and engagement of the immune response via Toll-like receptor binding, activation of

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26

Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.

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Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal in

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27

Izzedine, Hassan, and Victor Gueutin. Drug-induced chronic tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0087.

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The chronic form of drug-induced tubulointerstitial nephritis (CTIN) is an insidious disease and most probably represents the common final response pattern of the kidney to a variety of agents (including analgesics, lithium, antineoplastic chemotherapeutic agents, like cisplatin and nitrosoureas, and immunosuppressive drugs, such as ciclosporin and tacrolimus). Drug-induced CTIN is usually asymptomatic, presenting with slowly progressive renal impairment. Because of its insidious nature, CTIN is often diagnosed incidentally on routine laboratory screening or evaluation of CKD. The diagnosis of

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28

Segall, Liviu, and Adrian Covic. Immune-mediated tubulointerstitial nephritis. Edited by 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 chr

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29

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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30

Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thromb

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31

Lee, Olivia T., Jennifer N. Wu, Frederick J. Meyers, and Christopher P. Evans. Genitourinary aspects of palliative care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0084.

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Genitourinary tract diseases in the palliative care setting most commonly involve urinary tract obstruction, intractable bleeding, fistulae, and bladder-associated pain. Sources of obstruction in the lower urinary tract include benign prostatic hyperplasia, invasive prostate or bladder cancer, urethral stricture, or bladder neck contracture. Upper tract obstruction includes intraluminal or extraluminal blockage of the renal collecting system and ureters, such as transitional cell carcinoma, fibroepithelial polyps, stricture, stones, pelvic or retroperitoneal malignancy, fibrosis, or prior radi

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32

Astroza, Gastón M., Michael E. Lipkin, and Glenn M. Preminger. Intracorporeal techniques of stone fragmentation. Edited by John Reynard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0018.

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The use of intracorporeal lithotripsy for the management of larger ureteral and intrarenal calculi has dramatically improved. Although the choice of intracorporeal fragmentation is frequently based on the location and composition of the stone to be treated, the experience of the clinician and availability of equipment often dictates this decision. Several different modalities of intracorporeal lithotripsy are currently available. Ultrasonic lithotripsy is mainly used for the fragmentation of large renal calculi during percutaneous nephrolithotripsy procedures. Ultrasound is used rarely via an

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33

Lopez, Berenice, and Patrick J. Twomey. Biochemical investigation of rheumatic diseases. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0062.

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It is important for rheumatologists to have an understanding of biochemical tests including an awareness of their limitations. The biological variability of an analyte both within and between individuals, the limitations of the measurement technology, the sensitivity of laboratory internal quality control and external quality assurance procedures, as well as interlaboratory variations in practices including sample collection procedures, may all impact on the interpretation of a result. Biochemical tests are often requested to monitor organ-specific dysfunction arising as an adverse consequence

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34

Zoccali, Carmine, Davide Bolignano, and Francesca Mallamaci. Left ventricular hypertrophy in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0107_update_001.

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Alterations in left ventricular (LV) mass and geometry and LV dysfunction increase in prevalence from stage 2 to stage 5 in CKD. Nuclear magnetic resonance is the most accurate and precise technique for measuring LV mass and function in patients with heart disease. Quantitative echocardiography is still the most frequently used means of evaluating abnormalities in LV mass and function in CKD. Anatomically, myocardial hypertrophy can be classified as concentric or eccentric. In concentric hypertrophy, the muscular component of the LV (LV wall) predominates over the cavity component (LV volume).

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35

Radović, Milan, and Adalbert Schiller. Balkan endemic nephropathy. Edited by Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.

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Balkan endemic nephropathy (BEN) is a chronic, slowly progressive tubulointerstitial nephritis, with familial clustering, occurring in several endemic rural regions in countries of the Balkan Peninsula. BEN is characterized by anaemia, tubular proteinuria, renal shrinkage, and slowly declining glomerular filtration rate (GFR). Up to one-third of patients may also develop upper urothelial tumours. The aetiology of BEN is unclear; chronic exposure to aristolochic acid and a polygenic predisposition are the most likely contributing factors. The major pathological characteristics of BEN are symmet

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36

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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37

Hajhosseiny, Reza, Kaivan Khavandi, and David J. Goldsmith. Sudden cardiac death in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0108.

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Epidemiological data demonstrate the unique vulnerability of chronic kidney disease (CKD) subjects to cardiovascular disease, the most catastrophic being sudden cardiac death (SCD). In patients with declining kidney function there is a continuum of cardiovascular risk. In those individuals who survive to reach end-stage renal disease (ESRD), the risk of suffering a cardiac event is extremely high. Some of this risk is explained by the common risk factors and traditional cardiovascular events, namely atherosclerotic plaque fissure and rupture, but there is now evidence of a distinct ‘later CKD’

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