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Toxins
Special Issues
Renal Toxicity
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Renal Toxicity

A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: closed (30 June 2010) | Viewed by 84718

Special Issue Editor

Dr. Susan A. Elmore

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Guest Editor
NTP Pathologist and Staff Scientist, COTR, NTP Pathology Support Contracts, National Institute of Environmental Health Sciences, Cellular and Molecular Pathology Branch, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, USA

Special Issue Information

Dear Colleagues,

A wide variety of drugs and environmental chemicals are known to cause nephrotoxicity. The mammalian kidney is particularly susceptible to the toxic effects of noxious chemicals, in part, due to the unique physiologic and anatomic features of this organ. The excretory and metabolic functions of the kidneys place them at high risk following exposure to toxicants. Xenobiotics in the systemic circulation are delivered to the kidney in relatively high amounts because this organ receives about 25% of the resting cardiac output. Toxicants are also concentrated in the tubular fluid via the normal processes of urine concentration. For this reason, a nontoxic plasma concentration may achieve toxic concentrations within the kidney. Furthermore, the biotransformation of xenobiotics to toxic intermediates within the tubular epithelium also contributes to this increased renal susceptibility to toxic injury. Over the past decade, research into the pathophysiologic and molecular basis of renal disease has grown tremendously with the ultimate goal of assessing human health risk. This special journal issue provides a review of mechanisms of acute renal failure with examples of renal toxicity from a variety of agents including mycotoxins, herbicides, heavy metals, solvents, therapeutic agents and plants. Chemically induced α2u-globulin nephropathy is also reviewed.

Dr. Susan A. Elmore
Guest Editor

Keywords

  • nephrotoxicity
  • renal
  • xenobiotic
  • biotransformation
  • α2u-globulin

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Published Papers (4 papers)

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Research

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534 KiB  
Article
Contrasting Nephropathic Responses to Oral Administration of Extract of Cultured Penicillium polonicum in Rat and Primate
by Peter G. Mantle, Katharine M. McHugh and John E. Fincham
Toxins 2010, 2(8), 2083-2097; https://doi.org/10.3390/toxins2082083 - 9 Aug 2010
Cited by 11 | Viewed by 12518
Abstract
Liquid- or solid substrate-cultured Penicillium polonicum administered in feed to rats over several days evokes a histopathological response in kidney involving apoptosis and abnormal mitosis in proximal tubules. The amphoteric toxin is yet only partly characterized, but can be isolated from cultured sporulating [...] Read more.
Liquid- or solid substrate-cultured Penicillium polonicum administered in feed to rats over several days evokes a histopathological response in kidney involving apoptosis and abnormal mitosis in proximal tubules. The amphoteric toxin is yet only partly characterized, but can be isolated from cultured sporulating biomass in a fraction that is soluble in water and ethanol, and exchangeable on either anion- or cation-exchange resins. After several weeks of treatment renal proximal tubule distortion became striking on account of karyocytomegaly, but even treatment for nearly two years remained asymptomatic. Extract from a batch of solid substrate fermentation of P. polonicum on shredded wheat was incorporated into feed for rats during four consecutive days, and also given as an aqueous solution by oral gavage to a vervet monkey daily for 10 days. Treatment was asymptomatic for both types of animal. Rat response was evident as the typical renal apoptosis and karyomegaly. In contrast there was no such response in the primate; and neither creatinine clearance nor any haematological characteristic or serum component concentration deviated from a control or from historical data for this primate. The contrast is discussed concerning other negative findings for P. polonicum in pigs and hamsters. Renal karyomegaly, as a common rat response to persistent exposure to ochratoxin A, is not known in humans suspected as being exposed to more than the usual trace amounts of dietary ochratoxin A. Therefore the present findings question assumptions that human response to ochratoxin A conforms to that in the rat. Full article
(This article belongs to the Special Issue Renal Toxicity)
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Review

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657 KiB  
Review
Mechanisms of Cisplatin Nephrotoxicity
by Ronald P. Miller, Raghu K. Tadagavadi, Ganesan Ramesh and William Brian Reeves
Toxins 2010, 2(11), 2490-2518; https://doi.org/10.3390/toxins2112490 - 26 Oct 2010
Cited by 1308 | Viewed by 45051
Abstract
Cisplatin is a widely used and highly effective cancer chemotherapeutic agent. One of the limiting side effects of cisplatin use is nephrotoxicity. Research over the past 10 years has uncovered many of the cellular mechanisms which underlie cisplatin-induced renal cell death. It has [...] Read more.
Cisplatin is a widely used and highly effective cancer chemotherapeutic agent. One of the limiting side effects of cisplatin use is nephrotoxicity. Research over the past 10 years has uncovered many of the cellular mechanisms which underlie cisplatin-induced renal cell death. It has also become apparent that inflammation provoked by injury to renal epithelial cells serves to amplify kidney injury and dysfunction in vivo. This review summarizes recent advances in our understanding of cisplatin nephrotoxicity and discusses how these advances might lead to more effective prevention. Full article
(This article belongs to the Special Issue Renal Toxicity)
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136 KiB  
Review
Genomic Damage in Endstage Renal Disease—Contribution of Uremic Toxins
by Nicole Schupp, August Heidland and Helga Stopper
Toxins 2010, 2(10), 2340-2358; https://doi.org/10.3390/toxins2102340 - 11 Oct 2010
Cited by 28 | Viewed by 9186
Abstract
Patients with end-stage renal disease (ESRD), whether on conservative, peritoneal or hemodialysis therapy, have elevated genomic damage in peripheral blood lymphocytes and an increased cancer incidence, especially of the kidney. The damage is possibly due to accumulation of uremic toxins like advanced glycation [...] Read more.
Patients with end-stage renal disease (ESRD), whether on conservative, peritoneal or hemodialysis therapy, have elevated genomic damage in peripheral blood lymphocytes and an increased cancer incidence, especially of the kidney. The damage is possibly due to accumulation of uremic toxins like advanced glycation endproducts or homocysteine. However, other endogenous substances with genotoxic properties, which are increased in ESRD, could be involved, such as the blood pressure regulating hormones angiotensin II and aldosterone or the inflammatory cytokine TNF-a. This review provides an overview of genomic damage observed in ESRD patients, focuses on possible underlying causes and shows modulations of the damage by modern dialysis strategies and vitamin supplementation. Full article
(This article belongs to the Special Issue Renal Toxicity)
173 KiB  
Review
Assessment of the Role of Renal Organic Anion Transporters in Drug-Induced Nephrotoxicity
by Yohannes Hagos and Natascha A. Wolff
Toxins 2010, 2(8), 2055-2082; https://doi.org/10.3390/toxins2082055 - 9 Aug 2010
Cited by 78 | Viewed by 16214
Abstract
In the present review we have attempted to assess the involvement of the organic anion transporters OAT1, OAT2, OAT3, and OAT4, belonging to the SLC22 family of polyspecific carriers, in drug-induced renal damage in humans. We have focused on drugs with widely recognized [...] Read more.
In the present review we have attempted to assess the involvement of the organic anion transporters OAT1, OAT2, OAT3, and OAT4, belonging to the SLC22 family of polyspecific carriers, in drug-induced renal damage in humans. We have focused on drugs with widely recognized nephrotoxic potential, which have previously been reported to interact with OAT family members, and whose underlying pathogenic mechanism suggests the participation of tubular transport. Thus, only compounds generally believed to cause kidney injury either by means of direct tubular toxicity or crystal nephropathy have been considered. For each drug, or class of agents, the evidence for actual transport mediated by individual OATs under in vivo conditions is discussed. We have then examined their role in the context of other carriers present in the renal proximal tubule sharing certain substrates with OATs, as these are critical determinants of the overall contribution of OAT-dependent transport to intracellular accumulation and transepithelial drug secretion, and thus the impact it may have in drug-induced nephrotoxicity. Full article
(This article belongs to the Special Issue Renal Toxicity)
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