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Books on the topic 'Renal toxicity'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

S, Goldstein Robin, ed. Mechanisms of injury in renal disease and toxicity. CRC Press, 1994.

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2

Redegeld, Franciscus Antonius Maria. Hepatic and renal toxicity of xenobiotics: The role of metabolism and transport. s.n.], 1989.

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3

P, Baetcke Karl, and United States. Environmental Protection Agency. Risk Assessment Forum., eds. Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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4

P, Baetcke Karl, and United States. Environmental Protection Agency. Risk Assessment Forum., eds. Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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5

P, Baetcke Karl, and United States. Environmental Protection Agency. Risk Assessment Forum, eds. Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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6

P, Baetcke Karl, and United States. Environmental Protection Agency. Risk Assessment Forum., eds. Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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7

P, Baetcke Karl, and United States. Environmental Protection Agency. Risk Assessment Forum., eds. Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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8

P, Boetche Karl, and United States. Environmental Protection Agency. Risk Assessment Forum, eds. Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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9

Handelsman, Harry. Hemoperfusion in conjunction with deferoxamine for the treatment of aluminum toxicity or iron overload in patients with end-stage renal disease. National Center for Health Services Research and Health Care Technology Assessment, U.S. Dept. of Health and Human Services, Public Health Service, 1987.

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10

Handelsman, Harry. Hemoperfusion in conjunction with deferoxamine for the treatment of aluminum toxicity or iron overload in patients with end-stage renal disease. National Center for Health Services Research and Health Care Technology Assessment, U.S. Dept. of Health and Human Services, Public Health Service, 1987.

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11

Inc, Eastern Research Group, and United States. Environmental Protection Agency. Risk Assessment Forum, eds. Report of the EPA peer review workshop on alpha 2u-globulin: Association with renal toxicity and neoplasia in the male rat. Risk Assessment Forum, U.S. Environmental Protection Agency, 1992.

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12

H, Bach P., Lock E. A, and Mudge Gilbert H, eds. Renal heterogeneity and target cell toxicity: Proceedings of the Second International Symposium on Nephrotoxicity, University of Surrey, UK, 6-9 August 1984. Wiley, 1985.

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13

1911-, Tanabe Tsuneyoshi, Hook Jerry B, Endou Hitoshi, Satellite Symposium on Nephrotoxicity of Antibiotics and Immunosuppressants (1986 : Sapporo-shi, Japan), and International Congress of Toxicology on Nephrotoxicity of Antibiotics and Immunosuppressants (4th : 1986 : Sapporo-shi, Japan), eds. Nephrotoxicity of antibiotics and immunosuppressants: Proceedings of the satellite symposium of the IVth International Congress of Toxicology on Nephrotoxicity of Antibotics and Immunosuppressants, held in Sapporo, Japan, July 26-28, 1986. Elsevier Science Publishers, 1986.

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14

Goldstein, Robin S., ed. Mechanisms of Injury in Renal Disease and Toxicity. CRC Press, 2020. http://dx.doi.org/10.1201/9781003069164.

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15

Goldstein, Robin S. Mechanisms of Injury in Renal Disease and Toxicity. Taylor & Francis Group, 2020.

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16

Goldstein, Robin S. Mechanisms of Injury in Renal Disease and Toxicity. Taylor & Francis Group, 2020.

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17

Goldstein, Robin S. Mechanisms of Injury in Renal Disease and Toxicity. Taylor & Francis Group, 2020.

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18

Goldstein, Robin S. Mechanisms of Injury in Renal Disease and Toxicity. Taylor & Francis Group, 2020.

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19

Bach, P. H. Renal Heterogeneity and Target Cell Toxicity (Monographs in Applied Toxicology, No 2). John Wiley & Sons Inc, 1985.

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20

Alpha[2u]-globulin: Association with chemically induced renal toxicity and neoplasia in the male rat. The Forum, 1992.

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21

D’Haese, Patrick C., Benjamin A. Vervaet, and Anja Verhulst. Heavy metal-induced tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0088.

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Environmental and occupational exposure to heavy metals should be considered an important health hazard, even more so since evidence has been provided in recent literature for toxic effects occurring even at low levels. The kidney is highly vulnerable to metal toxicity and the extent of renal damage depends on the nature, dose, route, and duration of exposure. Both acute and chronic intoxication have been demonstrated to cause kidney injury, with various levels of severity, ranging from tubular dysfunctions to severe chronic kidney disease. The epidemiology of heavy metals poisoning, their ren

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22

Harper, Lorraine, and David Jayne. The patient with vasculitis. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0160.

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The goals of treatment in renal vasculitis are to stop vasculitic activity and recover renal function. Subsequent strategies are required to prevent vasculitis returning and to address longer-term co-morbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk.Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as azathioprine, to prevent relapse. Plasma exchange improves renal recovery in severe presentations. Refractory disease resulting from a failure of induction or remission

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23

Freda, Benjamin J., and Gregory L. Braden. Other toxic acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0085.

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Chronic kidney disease (CKD) is often the result of incomplete recovery of renal function from a variety of causes of acute tubulointerstitial injury. Exposure to ethylene glycol, chlorinated hydrocarbons, paraquat, or toxic mushrooms often causes severe acute kidney injury (AKI), leading to chronic tubulointerstitial nephritis (TIN) and CKD, including end-stage renal disease. Ethylene glycol intoxication often leads to chronic TIN and CKD from direct renal tubular toxicity and from interstitial calcium oxalate deposition. Chlorinated hydrocarbon exposure can cause dialysis-dependent AKI, but

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24

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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25

Konrad, Martin, and Karl P. Schlingmann. Approach to the patient with hypomagnesaemia. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0040.

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The kidneys play a central role in the maintenance of a normal magnesium balance. The distal renal tubule, especially the thick ascending limb of the loop of Henle, and the distal convoluted tubule mediate the regulation of a normal magnesium balance. The clinical assessment of magnesium deficiency is described. Genetic causes are described in detail. Acquired causes are more common and often related to drug therapy or toxicity, or to metabolic acidosis or phosphate depletion.

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26

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by 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 no

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27

Jayne, David. Treatment of ANCA-associated vasculitis. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0132.

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The goals of treatment in anti-neutrophil cytoplasm antibody (ANCA) vasculitis are to stop vasculitic activity, to prevent vasculitis returning, and to address longer-term comorbidities caused by tissue damage, drug toxicity, and increased cardiovascular and malignancy risk. Cyclophosphamide and high-dose glucocorticoids remain the standard induction therapy with alternative immunosuppressives, such as methotrexate or azathioprine, to prevent relapse. Refractory disease resulting from a failure of induction or remission maintenance therapy requires alternative agents and rituximab has been par

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28

Kastritis, Efstathios, and Meletios A. Dimopoulos. The patient with myeloma. Edited by Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0153_update_001.

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Renal impairment is a common feature of multiple myeloma and often the presenting symptom of a patient with symptomatic myeloma. ‘Myeloma kidney’ results from the excess of immunoglobulin light chains which form aggregates and casts that result in tubular obstruction; however, light chains may cause renal damage with a variety of mechanisms, which often may coexist in the same patient. The presence of significant renal dysfunction in a patient with myeloma is associated with a risk for significant complications, including early death. Myeloma kidney is usually associated with high tumour burde

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29

Murtagh, Fliss E. M. End-stage kidney disease. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0156.

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End-stage kidney disease (ESKD) accounts for 1-2% of all deaths. Ageing populations means that this proportion will grow steadily over the coming years. Symptom burden in ESKD exceeds advanced cancer, with added renal-specific symptoms, such as itch and restless legs. Pain and depression are also more prevalent. Many renal symptoms go under-recognized and under-treated, especially as they arise from co-morbid conditions, rather than the renal disease itself. The most useful intervention to address symptoms is regular assessment of symptoms, using a valid and reliable global symptom score. Phar

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30

MacCallum, Niall S. Management of oncological complications in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0376.

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Important treatment complications relevant to critical care are discussed. Cancer-related pain is complex and requires multidisciplinary care, particularly in the peri-operative setting. Chemotherapeutic complications include pancytopenia, cardiac, pulmonary, renal, gastrointestinal, hepatic, and neurotoxicity. Radiotherapy complications include cardiac, pulmonary, and gastrointestinal toxicity. In general, management includes assessing the risk-benefit to cytotoxic therapy withdrawal and supportive care. There is a paucity of proven treatment options for most complications, althoughcertain th

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31

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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32

Ponticelli, Claudio, and Richard J. Glassock, eds. Treatment of Primary Glomerulonephritis. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784081.001.0001.

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Primary glomerulonephritis is one of the most common kidney diseases, and a main cause of end-stage renal disease (ESRD). Glomerulonephritis has multiple subtypes, each with different physiopathologies, clinical presentation, and management requirements, which makes treatment difficult. As a complex set of diseases, the choice of symptomatic and specific treatment is critical to ameliorating the relentless course of glomerulonephritis. Focusing on all subtypes of primary glomerulonephritis, from epidemiology and classification, to pathogenesis and treatment, this volume includes the latest res

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33

Majid, Adrian, and Bruce L. Gilliam. Future Antiretrovirals, Immune-Based Strategies, and Therapeutic Vaccines. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0023.

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Highly active antiretroviral therapy remains the mainstay of treatment for patients chronically infected with HIV. Novel drugs, both within existing classes and new ones, are in various stages of development and testing. New medications within existing classes of antiretroviral agents are in clinical trials and will likely offer activity against resistant HIV-1 strains and provide alternatives for combination pill therapy. Novel therapeutics including oral attachment inhibitors and monoclonal antibody treatments continue to show efficacy against HIV-1 and progress in clinical trials. Tenofovir

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34

Meyrier, Alain, and Patrick Niaudet. Primary focal segmental glomerulosclerosis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0057_update_001.

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Primary focal segmental glomerulosclerosis (FSGS) causes nephrotic syndrome and by definition is not caused by any of the known causes of podocyte toxicity or focal segmental sclerosis such as viral infections or toxins. A number of genetic causes of FSGS are commonly diagnosed in early childhood. Other causes of segmental scarring need to be distinguished. Genotypes in APOL1 of African origin are associated with higher incidence of FSGS and poorer responses to treatment. Cellular and collapsing FSGS are variants of FSGS in which there is overt acute podocytopathy and they have a relatively po

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35

Bach, Peter. Nephrotoxicity:In Vitro and in Vivo, Animals to Man. Springer, 1989.

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36

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0062_update_001.

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A common rule of thumb in primary membranous glomerulonephritis (MGN) is that one-third of patients improve spontaneously, one-third progress, and one-third continue to have substantial proteinuria. The rate of spontaneous recovery may be near the truth, but MGN is usually an indolent condition and few studies have run long enough to give accurate outcomes for the remainder. However MGN is an important cause of end-stage renal failure. Treatment regimens that include cyclophosphamide or chlorambucil can improve the outcome of patients at greatest risk of deterioration, but their toxicity has l

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37

Cui, Zhao, Neil Turner, and Ming-hui Zhao. Antiglomerular basement membrane disease. Edited by 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 b

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38

Kuypers, Dirk R. J., and Maarten Naesens. Immunosuppression. Edited by Jeremy R. Chapman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0281_update_001.

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Combination immunosuppressive therapy produces excellent short-term results after kidney transplantation. Long-term graft survival has improved, but less dramatically. Death with a functioning graft remains the primary cause of graft loss. Dosing of current immunosuppressive therapy balances between careful clinical interpretation of time-driven immunological risk assessments and drug-related toxicity on the one hand, and the use of simple surrogate drug exposure indicators like blood/plasma concentrations on the other. The combined use of calcineurin-inhibitors (CNIs) with mycophenolic acids

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39

Maysinger, Dusica, P. Kujawa, and Jasmina Lovrić. Nanoparticles in medicine. Edited by A. V. Narlikar and Y. Y. Fu. Oxford University Press, 2017. http://dx.doi.org/10.1093/oxfordhb/9780199533060.013.14.

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This article examines the applications of nanoparticles in medicine. Nanomedicine is a promising field that can make available different nanosystems whose novel, usually size-dependent, physical, chemical and/or biological properties are exploited to combat the disease of interest. One kind of particulate systems represents a vast array of either metallic,semiconductor, polymeric, protein or lipid nanoparticles that can be exploited for diagnosis and treatment of various diseases. This article first provides an overview of general issues related to physicochemical and biological properties of

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40

Berrill, Andrew, and Pawan Gupta. General principles of regional anaesthesia. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0052.

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Regional anaesthesia is now extremely safe in experienced hands. The vast majority of upper and lower limb procedures can now be performed with either a peripheral regional block alone or in combination with a general anaesthetic. Neuraxial blocks can provide reliable postoperative pain relief for operations on the trunk and lower limbs. There is no consensus on the maximum safe dose of local anaesthetics. It is important therefore to use a minimum optimal dose of a local anaesthetic for any nerve block to reduce the risk of toxicity and to improve the success rate. Adjuncts, such as clonidine

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