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Libri sul tema "Kidney glomerulus Diseases"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 21 febbraio 2023

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1

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

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2

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

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3

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

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4

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

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5

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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6

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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7

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

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8

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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9

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

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10

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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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

Hall, Andrew, and Shamima Rahman. Mitochondrial diseases and the kidney. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0340.

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Abstract (sommario):

Mitochondrial disease can affect any organ in the body including the kidney. As increasing numbers of patients with mitochondrial disease are either surviving beyond childhood or being diagnosed in adulthood, it is important for all nephrologists to have some understanding of the common renal complications that can occur in these individuals. Mitochondrial proteins are encoded by either mitochondrial or nuclear DNA (mtDNA and nDNA, respectively); therefore, disease causing mutations may be inherited maternally (mtDNA) or autosomally (nDNA), or can arise spontaneously. The commonest renal pheno

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13

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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14

Renal Glomerular Diseases: Atlas of Electron Microscopy with Histopathological Bases and Immunofluorescence Findings. American Society Clinical Pathology, 2002.

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15

M, Dodd S., ed. Tubulointerstitial and cystic disease of the kidney. [Berlin: Springer-Verlag, 1995.

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16

Dodd, Susan M. Tubulointerstitial Cystics Kidney (Chemistry of Plant Protection). Springer-Verlag Telos, 1995.

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17

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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18

Winyard, Paul. Human kidney development. Edited by Adrian Woolf. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0343.

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Abstract (sommario):

The kidneys perform diverse functions including excretion of nitrogenous waste products, homeostasis of water, electrolytes and acid–base balance, and hormone secretion. The simplest functional unit within the kidneys is the nephron, which consists of specialized segments from glomerulus, through proximal tubule, loop of Henle, and distal tubule. Human nephrogenesis starts with two stages of transient kidneys, termed the pronephros and mesonephros, and ends with development of a permanent organ from the metanephros on each side. The latter consists of just a few hundred cells when it is formed

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19

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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Abstract (sommario):

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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20

Fervenza, Fernando C. Evaluation of Kidney Function, Glomerular Disease, and Tubulointerstitial Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0472.

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Abstract (sommario):

Several measures are used to evaluate kidney function: serum creatinine, urinalysis, renal clearance, and renal imaging. Creatinine is an end product of muscle catabolism and is commonly used as a filtration marker. Dysmorphic erythrocytes in the urinary sediment indicate bleeding in the upper urinary tract. A urine pH less than 5.5 excludes type 1 renal tubular acidosis. A pH greater than 7 suggests infection. Acidic urine is indicative of a high-protein diet, acidosis, and potassium depletion. Alkaline urine is associated with a vegetarian diet, alkalosis and urease-producing bacteria. Clear

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21

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

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22

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

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23

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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Abstract (sommario):

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 va

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24

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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Abstract (sommario):

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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25

Dickersin, Richard G. Diagnostic Electron Microscopy: A Text/Atlas. Springer, 2013.

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26

Diagnostic Electron Microscopy: A Text/Atlas. 2nd ed. Springer, 2000.

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27

Dickersin, Richard G. Diagnostic Electron Microscopy: A Text/Atlas. Springer London, Limited, 2006.

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28

Wiles, Kate, Kate Bramham, and Catherine Nelson-Piercy. Kidney disease. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0044.

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Abstract (sommario):

This chapter describes the physiological adaptations to pregnancy in women with and without renal disease, reports pregnancy outcomes in women with both acute kidney injury and chronic kidney disease, and discusses a management strategy for antenatal and peripartum care. Acute kidney injury (AKI) is difficult to define in pregnancy because of the physiological increase in glomerular filtration. A normal creatinine can mask renal injury in pregnancy. This chapter considers important causes of AKI in pregnancy including pre-eclampsia, HELLP syndrome, thrombotic microangiopathy, acute fatty liver

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29

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Chronic kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0163.

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Abstract (sommario):

Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, where the abnormalities have been present for >3 months and have implications for health. It is characterized by a reduced estimated glomerular filtration rate (eGFR) or other renal abnormalities. CKD is staged according to the eGFR or the degree of albuminuria. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for CKD is either an eGFR that is <60 ml/min 1.73 m−2 and has been present for >3 months, or one or more markers of kidney damage, when these have been present for >3 month

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30

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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31

ROTTER, W. Rotter Color Atlas of Kidney Biopsy - Pathology of Glomerular Diseases. John Wiley & Sons Inc, 1985.

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32

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Screening for kidney disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0353.

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Abstract (sommario):

Renal disease is common and, with routine reporting of estimated glomerular filtration rates, impairment of renal function is increasingly being recognized. As renal impairment is usually asymptomatic until very advanced, chronic kidney disease (CKD) guidelines have been developed to improve the identification and screening of at-risk populations. Target groups include patients with vascular risk factors (e.g. diabetes mellitus and hypertension); patients with certain multisystem diseases which can cause renal impairment; patients with urological conditions; patients on nephrotoxic medication;

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33

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Inherited renal diseases. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0169.

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The causes of inherited renal diseases can be divided into cystic, glomerular, tubular, and systemic diseases. By far, the most common of these in clinical practice is adult polycystic kidney disease (APKD). This chapter reviews APKD, other inherited cystic renal diseases, inherited glomerular and tubular diseases, and inherited systemic diseases with renal involvement.

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34

Yaqoob, Muhammad M. Acidosis in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0148.

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Abstract (sommario):

Metabolic acidosis becomes increasingly common as chronic kidney disease progresses. It is associated with a number of complications, including bone disease, altered protein synthesis and degradation, skeletal muscle wasting, and lately progressive glomerular filtration rate loss. Experimental and clinical studies suggest a role for alkali therapy to lessen these complications. Recent controlled studies support this notion, and suggest that correction of metabolic acidosis in patients with chronic kidney disease slows the rate of decline of renal function and the development of end-stage renal

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35

Erickson, Stephen B., Hatem Amer, and Timothy S. Larson. Urolithiasis, Kidney Transplantation, and Pregnancy and Kidney Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0475.

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Abstract (sommario):

It was previously assumed that all kidney stones crystallized as urine passed through the renal tubules and were retained by means of crystal-tubular cell interactions. Recently uroscopy with papillary biopsies has shown 2 different pathways for stone formation, both mediated by calcium phosphate crystals. Kidney transplant has become the preferred treatment for patients with end-stage renal disease. Those benefiting from transplant included patients who would be deemed "high risk," such as those with diabetes mellitus and those older than 70 years. Anatomical changes associated with pregnancy

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36

Ho, Kwok M. Kidney and acid–base physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0005.

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Abstract (sommario):

Anatomically the kidney consists of the cortex, medulla, and renal pelvis. The kidneys have approximately 2 million nephrons and receive 20% of the resting cardiac output making the kidneys the richest blood flow per gram of tissue in the body. A high blood and plasma flow to the kidneys is essential for the generation of a large amount of glomerular filtrate, up to 125 ml min−1, to regulate the fluid and electrolyte balance of the body. The kidneys also have many other important physiological functions, including excretion of metabolic wastes or toxins, regulation of blood volume and pressure

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37

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

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Abstract (sommario):

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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38

Little, Mark, and Alan Salama. The kidney. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0025.

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Kidney dysfunction is common in patients with rheumatological disease, be it secondary to renal (usually glomerular) involvement by a multisystem rheumatological disorder, renal impairment due to nephrotoxic medication use, or incidentally noted during a rheumatological work-up. It is therefore important for the rheumatologist to know how to assess kidney function biochemically and radiologically, to appreciate when an organ-threatening process is present, and to understand the basic steps to take in the event of acute kidney injury. This chapter reviews assessment of kidney function with resp

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39

Little, Mark, and Alan Salama. The kidney. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0025_update_002.

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Abstract (sommario):

Kidney dysfunction is common in patients with rheumatological disease, be it secondary to renal (usually glomerular) involvement by a multisystem rheumatological disorder, renal impairment due to nephrotoxic medication use, or incidentally noted during a rheumatological work-up. It is therefore important for the rheumatologist to know how to assess kidney function biochemically and radiologically, to appreciate when an organ-threatening process is present, and to understand the basic steps to take in the event of acute kidney injury. This chapter reviews assessment of kidney function with resp

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40

Bramham, Kate, and Catherine Nelson-Piercy. Specific renal conditions in pregnancy. Edited by Norbert Lameire and Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0298.

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Abstract (sommario):

Pre-pregnancy glomerular filtration rate, proteinuria, and blood pressure are usually more important in determining the risk of pregnancy in patients with chronic kidney disease, but some diseases may be exacerbated in pregnancy, or appear more liable to complications. This chapter considers immunoglobulin A nephropathy, systemic lupus erythematosus (which may also be associated with some manifestations in the infant), diabetic nephropathy, polycystic kidney disease, reflux nephropathy, single kidney, urological disorders, and angiomyolipomata. Distinguishing underlying renal disease exacerbat

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41

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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Abstract (sommario):

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 pod

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42

Hwang, Young-Hwan, and York Pei. Autosomal dominant polycystic kidney disease management. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0309_update_001.

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Abstract (sommario):

Management of patients with autosomal dominant polycystic kidney disease (ADPKD) currently comprises non-specific measures including promotion of healthy lifestyle, optimization of blood pressure control, and modification of cardiovascular risk factors. A high water intake of 3–4 L per day in patients with glomerular filtration rate greater than 30 mL/min/1.73 m2 may decrease the risk of kidney stones, but its potential benefit in reducing renal cyst growth is presently unproven. Maintenance of a target blood pressure of 130/80 mmHg is recommended by expert clinical guidelines though this is u

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43

Barakat, Amin Y., and Russell W. Chesney, eds. Pediatric Nephrology for Primary Care. American Academy of Pediatrics, 2008. http://dx.doi.org/10.1542/9781581104356.

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Abstract (sommario):

This clinical resource is purpose-built to help primary caregivers take a lead role in diagnosis, evaluation, and treatment of diverse pediatric kidney diseases. Diagnose and manage renal diseases with confidence. The resource book has clear, concise overviews of the full range of renal conditions you're likely to encounter; evidence-based discussion of each condition's clinical course, pathogenesis, and etiology; expert management recommendations and valuable clinical pearls, tables, algorithms, and clinical calculators to help with differential diagnosis and patient workups; advice on when t

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44

Burdmann, Emmanuel A. Syphilis. Edited by Vivekanand Jha. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0192.

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Abstract (sommario):

Syphilis is an infectious disease caused by the bacterium Treponema pallidum. The transmission route is usually sexual, but prenatal contamination (congenital syphilis) and transmission by infected blood can also occur. The most frequent presentation of syphilis nephropathy is proteinuria, and the most common form of associated glomerular disease is membranous glomerulopathy. Kidney disease usually reverts with antibiotic therapy. Syphilis must always be considered in proteinuric HIV-infected patients. Renal biopsy is necessary to differentiate between HIV-associated nephropathy and syphilis-i

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45

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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Abstract (sommario):

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 t

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46

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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Abstract (sommario):

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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47

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Diabetic renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0164.

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Abstract (sommario):

Diabetic nephropathy is kidney damage occurring as a result of diabetes mellitus. Overt diabetic nephropathy is defined as proteinuria greater than 0.5 g/day. Diabetic nephropathy has a complicated pathogenesis including glomerular hypertension with hyperfiltration and advanced glycation end products. Poor glycaemic control is associated with progression to microalbuminuria and overt diabetic nephropathy. The lifetime risk is fairly equivalent for type 1 and type 2 diabetes mellitus. Early disease is usually asymptomatic. Hyperglycaemia causes an osmotic diuresis and, thus, diabetes can presen

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48

Ronco, Pierre M. Kidney involvement in plasma cell dyscrasias. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0150.

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Abstract (sommario):

Monoclonal proliferations of the B-cell lineage are characterized by abnormal and uncontrolled expansion of a single clone of B cells at different maturation stages, with a variable degree of differentiation to immunoglobulin-secreting plasma cells. Therefore, they are usually associated with the production and secretion in blood of a monoclonal immunoglobulin and/or a fragment thereof which may become deposited in tissues. These deposits can take the form of casts (in myeloma cast nephropathy), crystals (in myeloma-associated Fanconi syndrome), fibrils (in light-chain and exceptional heavy-ch

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49

Carrero, Juan Jesús, Hong Xu, and Bengt Lindholm. Diet and the progression of chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0101.

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Abstract (sommario):

The dietary management of non-dialysed CKD patients has focused on limiting the intake of substances which lead to accumulation of urea, potassium, phosphorus, and sodium. Recent advances in nutritional epidemiology have given us the opportunity to examine the relationships between diet and CKD. This chapter focuses on evidence relating to retarding progression of renal impairment in the early to mid stages of CKD. Limits may need to change if GFR falls. The hypothesis that a high dietary protein intake leads to progressive CKD through a mechanism of glomerular hyperfiltration has been taught

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50

Jardine, Alan G., and Rajan K. Patel. Lipid disorders of patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0102.

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Abstract (sommario):

The risk of developing cardiovascular (CV) disease is increased in patients with chronic kidney disease (CKD) and although dyslipidaemia is a major contributory factor to the development of premature CV disease, the relationship is complex. Changes in lipid fractions are related to glomerular filtration rate and the presence and severity of proteinuria, diabetes, and other confounding factors. The spectrum of CV disease changes from lipid-dependent, atheromatous coronary disease in early CKD to lipid-independent, non-coronary disease, manifesting as heart failure, and sudden cardiac death in a

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