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Books on the topic 'Chronic renal insufficiency'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

A, Nestlé Nutrition S. Chronic renal insufficiency. Nestlé Nutrition, 1989.

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2

G, Seyffart, ed. Drug dosage in renal insufficiency. Kluwer Academic Publishers, 1991.

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3

Rotellar, Carlos. Acute renal insufficiency made ridiculously simple. MedMaster, 1988.

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4

Morton, Gillian M. From captivity to liberation: Some theological and pastoral perspectives on chronic renal failure. University of Edinburgh, Department of Christian Ethics and Practical Theology, 1985.

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5

1941-, Mitch William E., ed. The Progressive natureof renal disease. Churchill Livingstone, 1986.

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6

Gromko, Linda. Complications: A doctor's love story : a memoir. Bainbridge Books, 2009.

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7

Nitta, Kosaku. Chronic kidney diseases: Recent advances in clinical and basic research. Karger, 2015.

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8

author, Senanayake M. S., Samarakoon, S. M. A., author, and Hector Kobbekaduwa Agrarian Research and Training Institute, eds. Socio economic impact of Chronic kidney disease of unknown etiology. Hector Kobbekaduwa Agrarian Research and Training Institute, 2015.

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9

1943-, Morris Peter J., and Knechtle Stuart J, eds. Kidney transplantation: Principles and practice. 6th ed. Saunders/Elsevier, 2008.

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10

Z, Kallenbach Judith, ed. Review of hemodialysis for nurses and dialysis personnel. 7th ed. Elsevier Mosby, 2005.

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11

Gabriel, Roger. A patient's guide to dialysis and transplantation. 3rd ed. MTP Press, 1987.

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12

Gabriel, Roger. A patient's guide to dialysis and transplantation. 3rd ed. MTP Press, 1987.

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13

Sakkas, Giorgos K., and Christoforos D. Giannaki. Sleep in chronic renal insufficiency. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0043.

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Chronic kidney disease is a significant and growing medical and public health problem, responsible for a substantial burden of illness and premature mortality. Renal disease has a dramatic impact on patients’ quality of life (QoL), with sleep disorders contributing significantly and 80% of the renal population reporting symptoms of disturbed sleep, including insomnia, sleep apnea, restless legs syndrome, daytime sleepiness, and fatigue. Many patients with sleep disorders remain underdiagnosed, since many of the signs and symptoms related to poor sleep are thought to be an unavoidable consequen

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14

Nutrition During Chronic Renal Insufficiency. Books on Demand GmbH, 2018.

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15

Bulla, Monika, and Ray A. Kunze. Renal Insufficiency in Children. Springer, 2011.

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16

Bulla, Monika. Renal Insufficiency in Children. Springer London, Limited, 2012.

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17

Seyffart, G. Drug Dosage in Renal Insufficiency. Springer London, Limited, 2012.

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18

Seyffart, G. Drug Dosage in Renal Insufficiency. Springer, 2012.

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19

Levin, Adeera, and Meguid El Nahas. Chronic Kidney Disease: A Practical Guide to Understanding and Management. Oxford University Press, Incorporated, 2009.

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20

Levin, Adeera, and Meguid El Nahas. Chronic Kidney Disease: A Practical Guide to Understanding and Management. Oxford University Press, 2014.

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21

Pugh-Clarke, Karen. Quality of life and physical function in chronic renal insufficiency. 2003.

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22

Noble, Helen, and Rachel Lewis. Kidney Disease Management: A Practical Approach for the Non-Specialist Healthcare Practitioner. Wiley & Sons, Incorporated, John, 2012.

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23

Noble, Helen, and Rachel Lewis. Kidney Disease Management: A Practical Approach for the Non-Specialist Healthcare Practitioner. Wiley & Sons, Incorporated, John, 2012.

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24

Noble, Helen, and Rachel Lewis. Kidney Disease Management: A Practical Approach for the Non-Specialist Healthcare Practitioner. Wiley & Sons, Incorporated, John, 2012.

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25

Rabin, Pauline L., and William J. Stone. End-Stage Renal Disease: An Integrated Approach. Elsevier Science & Technology Books, 2013.

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26

Thomas, Nicola. Advanced Renal Care. Wiley & Sons, Limited, John, 2008.

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27

Thomas, Nicola. Advanced Renal Care. Wiley & Sons, Incorporated, John, 2008.

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28

(Contributor), Cordelia Ashwanden, Jane Bentley (Contributor), Celia Eggeling (Contributor), and Nicola Thomas (Editor), eds. Advanced Renal Care. 2nd ed. Blackwell Publishing Limited, 2004.

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29

Thomas, Nicola. Advanced Renal Care. Wiley & Sons, Incorporated, John, 2008.

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30

Wild, Janet, and Richard Fluck. Kidney Failure Explained. Class Publishing, 2019.

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31

Phosphate and vitamin D in chronic kidney disease. Karger, 2013.

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32

Olyaei, Ali J., Ted A. Foster, and Edgar V. Lerma. Drug dosing in chronic kidney disease. Edited by William G. Bennett. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0363.

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This chapter is dedicated to the dosing of medications in patients with chronic kidney disease. It is important for clinicians to have a working understanding of basic pharmacokinetic and pharmacodynamic principles to ensure patients with chronic kidney disease achieve the therapeutic target without toxicity. This chapter will provide a systematic approach to medication dosing in patients with chronic kidney disease by obtaining a medical history and performing a thorough physical examination, calculating an accurate assessment of renal function, determining loading dose, determining a mainten

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33

Royal College of Physicians & Renal Association. The Treatment of Adult Patients with Renal Failure. Royal College of Physicians of London, 1995.

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34

Macdougall, Iain C. Iron management in renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0126.

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Although erythropoiesis-stimulating agent therapy is the mainstay of renal anaemia management, maintenance of an adequate iron supply to the bone marrow is also pivotal in the process of erythropoiesis. Thus, it is important to be able to detect iron insufficiency, and to treat this appropriately. Iron deficiency may be absolute (when the total body iron stores are exhausted) or functional (when the total body iron stores are normal or increased, but there is an inability to release iron from the stores rapidly enough to provide a ready supply of iron to the bone marrow). Several markers of ir

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35

Chronic Kidney Disease A Quiet Revolution In Nephrology Six Case Studies. RAND Corporation, 2010.

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36

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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37

Kidney Transplantation: Principles and Practice. Elsevier - Health Sciences Division, 2013.

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38

Gutch, Charles, Judith Z. Kallenbach, Martha Stoner, and Anna Corea. Review of Hemodialysis for Nurses and Dialysis Personnel (Review of Hemodialysis for Nurses & Dialysis Personnel). 7th ed. Mosby, 2005.

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39

Kallenbach, Judith Z. Review of Hemodialysis for Nurses and Dialysis Personnel. Elsevier - Health Sciences Division, 2015.

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40

Kallenbach, Judith Z. Review of Hemodialysis for Nurses and Dialysis Personnel. Mosby, 2020.

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41

Review of Hemodialysis for Nurses and Dialysis Personnel. Elsevier - Health Sciences Division, 2011.

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42

Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.

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The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate c

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43

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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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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44

Borrowed time: Artificial organs and the politics of extending lives. Temple University Press, 1986.

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45

Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghan. Disorders of plasma magnesium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0177.

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Normal serum magnesium levels are in the range of 0.7–1.0 mmol/l and, as for calcium, most of the total body magnesium is found in bone and soft tissues. Magnesium is essential for normal cell metabolism (as a cofactor for numerous enzymes) and for neuronal function, and regulates parathyroid hormone release. Alterations in serum magnesium levels are usually asymptomatic unless severe. As there are large tissue reserves of magnesium, hypomagnesaemia usually only develops with chronic gastrointestinal or renal losses, or prolonged dietary insufficiency. Hypermagnesaemia is almost always iatroge

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46

Sprague, Stuart M., and Menaka Sarav. Chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0115_update_001.

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The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyr

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47

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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48

Sunderkötter, Cord, and Luis Requena. Panniculitides. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0165.

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Panniculitis is an inflammation that originates primarily in the subcutaneous fatty tissue (panniculus adiposus). It is associated with rheumatological diseases and with adverse events to rheumatological therapies (e.g. poststeroid panniculitis, erythema nodosum, infective panniculitis). The panniculitides are classified histopathologically into mostly septal panniculitis and mostly lobular panniculitis, according to the major or denser localization of the infiltrate, and also into those with or without vasculitis. Additional criteria involve the composition of the inflammatory infiltrate, the

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