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Książki na temat „Kidney Pathophysiology”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 1 lutego 2022

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1

Rose, Burton David. Pathophysiology of renal disease. Wyd. 2. New York: McGraw-Hill, 1987.

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2

Leaf, Alexander. Renal pathophysiology. Wyd. 3. New York: Oxford University Press, 1985.

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3

Rennke, Helmut G. Renal pathophysiology: The essentials. Wyd. 2. Philadelphia: Lippincott Williams & Wilkins, 2007.

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4

Rennke, Helmut G. Renal pathophysiology: The essentials. Wyd. 3. Baltimore, MD: Lippincott Williams & Wilkins, 2010.

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5

International, Forum "The Frontiers of Nephrology" (1989 Tokyo Japan). The frontiers of nephrology: Proceedings of the International Forum "The Frontiers of Nephrology", honoring Fuminori Sakai, held in Tokyo, Japan, 24-25 August 1989. Amsterdam: Excerpta Medica, 1990.

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6

Rose, Burton David. Renal pathophysiology: The essentials. Baltimore: Williams & Wilkins, 1994.

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7

Dixhoorn, Mieneke G. A. van. IgA in experimental kidney disease. [Leiden: University of Leiden, 1998.

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8

Höper, J. Influence of local oxygen deficiency on function and integrity of liver, kidney, and heart. Stuttgart: G. Fischer, 1991.

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9

Eleftheriadis, Theodoros. Vitamin D receptor agonists and kidney diseases. Hauppauge, N.Y: Nova Science Publishers, 2010.

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10

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. Redaktorzy Koide Hikaru i Hayashi T. Basel: Karger, 1994.

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11

Miyata, Toshio. Studies on Renal Disorders. Totowa, NJ: Springer Science+Business Media, LLC, 2011.

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12

Brewer, Jonathan Douglas. The coronary cure: A modified Mediterranean diet for the prevention of atherosclerosis, hypertension, obesity, diabetes, arthritis, and kidney stones : molecular mechanisms and practical guidelines : nutrition 101. [United States?]: J.D. Brewer, 2004.

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13

Koeppen, Bruce M. Renal physiology. Wyd. 3. St. Louis: Mosby, 2001.

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14

International Symposium of Nephrology (7th 1991 Montecatini Terme, Italy). Kidney, proteins, and drugs: An update : 7th International Symposium of Nephrology at Montecatini, Montecatini Terme, October 14-16, 1991. Redaktor Bianchi Claudio M. D. Basel: Karger, 1993.

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15

Gary, Abuelo J., red. Renal pathophysiology: The essentials. Baltimore: Williams & Wilkins, 1989.

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16

Rose, Burton David. Pathophysiology of Renal Disease. Wyd. 2. McGraw-Hill Health Professions Division, 1990.

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17

The Kidney: Physiology and pathophysiology. New York: Raven Press, 1985.

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18

The Kidney: Physiology and pathophysiology. Wyd. 2. New York: Raven Press, 1992.

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19

A, Shayman James, red. Renal pathophysiology. Philadelphia: J.B. Lippincott, 1995.

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20

Seldin, Donald W. The Kidney: Physiology and Pathophysiology. Wyd. 2. Raven Pr, 1992.

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21

W, Seldin Donald, i Giebisch Gerhard H, red. The Kidney: Physiology and pathophysiology. Wyd. 2. New York: Raven Press, 1991.

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22

W, Seldin Donald, i Giebisch Gerhard H, red. The kidney: Physiology and pathophysiology. New York: Raven Press, 1985.

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23

Goligorsky, Michael S., Julien Maizel, Radovan Vasko, May M. Rabadi i Brian B. Ratliff. Pathophysiology of acute kidney injury. Redaktor Norbert Lameire. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0221.

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In the intricate maze of proposed mechanisms, modifiers, modulators, and sensitizers for acute kidney injury (AKI) and diverse causes inducing it, this chapter focuses on several common and undisputable strands which do exist.Structurally, the loss of the brush border, desquamation of tubular epithelial cells, and obstruction of the tubular lumen are commonly observed, albeit to various degrees. These morphologic hallmarks of AKI are accompanied by functional defects, most consistently reflected in the decreased glomerular filtration rate and variable degree of reduction in renal blood flow, accompanied by changes in the microcirculation. Although all renal resident cells participate in AKI, the brunt falls on the epithelial and endothelial cells, the fact that underlies the development of tubular epithelial and vascular compromise.This chapter further summarizes the involvement of several cell organelles in AKI: mitochondrial involvement in perturbed energy metabolism, lysosomal involvement in degradation of misfolded proteins and damaged organelles, and peroxisomal involvement in the regulation of oxidative stress and metabolism, all of which become defective. Common molecular pathways are engaged in cellular stress response and their roles in cell death or survival. The diverse families of nephrotoxic medications and the respective mechanisms they induce AKI are discussed. The mechanisms of action of some nephrotoxins are analysed, and also of the preventive therapies of ischaemic or pharmacologic pre-conditioning.An emerging concept of the systemic inflammatory response triggered by AKI, which can potentially aggravate the local injury or tend to facilitate the repair of the kidney, is presented. Rational therapeutic strategies should be based on these well-established pathophysiological hallmarks of AKI.

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24

Leaf, Alexander. Renal pathophysiology. Wyd. 3. Oxford University Press, 1985.

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25

S, Goligorsky Michael, i Gross Steven S. 1951-, red. Nitric oxide and the kidney: Physiology and pathophysiology. New York: Chapman & Hall, 1997.

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26

Goligorsky, Michael S., i Steven S. Gross. Nitric Oxide and the Kidney: Physiology and Pathophysiology. Springer, 2012.

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27

Goligorsky, Michael S., i Steven S. Gross. Nitric Oxide And The Kidney: Physiology and Pathophysiology. Springer, 1997.

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28

Vishnu, Moorthy A., red. Pathophysiology of kidney disease and hypertension. Philadelphia, PA: Saunders/Elsevier, 2009.

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29

Pathophysiology of Kidney Disease and Hypertension. Elsevier, 2009. http://dx.doi.org/10.1016/c2009-0-36246-7.

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30

The Kidney today: Selected topics in renal science. Basel: Karger, 1992.

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31

Heptinstall's pathology of the kidney. Wyd. 5. Philadelphia: Lippincott-Raven, 1998.

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32

Howie, A. J. Handbook of Renal Biopsy Pathology. Springer, 2001.

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33

The Frontiers of Nephrology (International congress series). Elsevier, 1990.

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34

Howie, A. J. Handbook of Renal Biopsy Pathology. Springer, 2001.

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35

Leaf, Alexander, i Leaf. Renal Pathophysiology 2/E. Oxford University Press, 1992.

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36

Leaf, Alexander, i Leaf. Renal Pathophysiology 2/E. Oxford University Press, 1992.

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37

J, Alpern Robert, Herbert Steven C, Seldin Donald W. 1920- i Giebisch Gerhard H, red. Seldin and Giebisch's The kidney: Physiology & pathophysiology. Wyd. 4. Amsterdam: Academic, 2008.

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38

Seldin and Giebisch's the kidney: Physiology & pathophysiology. Wyd. 4. Amsterdam: Elsevier Inc., Academic Press, 2007.

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39

Bellomo, Rinaldo, i John R. Prowle. Pathophysiology of oliguria and acute kidney injury. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0211.

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Oliguria and acute kidney injury (AKI) are common in critically-ill patients with studies reporting AKI affecting more than 50% of critically-ill patients. AKI is independently associated with increased mortality and is a potentially modifiable aspect of critical illness. The pathogenesis of AKI is complex and varies according to aetiology. The most common trigger in ICU patients is sepsis—the pathophysiology of septic AKI is poorly understood and probably involves intrarenal haemodynamic and inflammatory processes. In the setting of septic AKI, the classic acute tubular necrosis described in experimental models does not occur and histological changes are only minor. Activation of neurohormonal mechanisms is also important, particularly in the hepatorenal syndrome, where activation of the remain-angiotensin system appears to play a major role. The treatment of oliguria and AKI in ICU patients has traditionally relied on the administration of intravenous fluids. While such therapy is warranted in patients with a clear history, and physical examination suggestive of intravascular and extravascular volume depletion, its usefulness in other patients (e.g. septic patients) remains controversial. Removal of nephrotoxins, rapid treatment of the triggering factors, and attention to cardiac output and mean arterial pressure remain the cornerstones of the prevention and treatment of AKI in ICU.

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40

Rennke, Helmut G., i Bradley M. Denker. The Renal Pathophysiology: The Essentials. Wyd. 2. Lippincott Williams & Wilkins, 2006.

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41

MD, J. Charles Jennette, Vivette D. D'Agati MD, Jean L. Olson MD i Fred G. Silva MD. Heptinstall's Pathology of the Kidney. LWW, 2014.

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42

Wolf, Gunter. Obesity And the Kidney. S. Karger AG (Switzerland), 2006.

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43

Heptinstall's Pathology of the Kidney 2 Volume Set. Wyd. 5. Lippincott Williams & Wilkins, 1998.

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44

Giebisch, Gerhard, Donald W. Seldin i Donald W. Seldin. The Kidney: Physiology and Pathophysiology (2-Volume Set). Wyd. 3. Lippincott Williams & Wilkins, 2000.

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45

Seldin And Giebischs The Kidney Physiology And Pathophysiology. Academic Press, 2012.

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46

Rath, Thomas, red. Chronic Kidney Disease - from Pathophysiology to Clinical Improvements. InTech, 2018. http://dx.doi.org/10.5772/66239.

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47

Tsai, Ching-Wei, Sanjeev Noel i 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 macrophages, dendritic cells, natural killer cells, and T and B lymphocytes. During the recovery phase, cell adhesion molecules as well as cytokines and chemokines may be instrumental by directing the migration, differentiation, and proliferation of renal epithelial cells; recent data also suggest a critical role of M2 macrophage and regulatory T cell in the recovery period. Other processes contributing to renal regeneration include renal stem cells and the expression of growth hormones and trophic factors. Subtle deviations in the normal repair process can lead to maladaptive fibrotic kidney disease. Further elucidation of these mechanisms will help discover new therapeutic interventions aimed at limiting the extent of AKI and halting its progression to CKD or ESRD.

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48

Renal tubular disorders: Pathophysiology, diagnosis, and management. New York: Dekker, 1985.

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49

F, Keane William, Hörl Walter H i Kasiske B. L, red. Lipids and the kidney. Basel: Karger, 1997.

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50

David, Humes H., red. Pathophysiology of electrolyte and renal disorders. New York: Churchill Livingstone, 1986.

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