Immunohistochemistry of Animal Renal Disease

A special issue of Veterinary Sciences (ISSN 2306-7381).

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 3226

Special Issue Editor


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Guest Editor
Laboratory of Veterinary Clinical Pathology, Joint Faculty of Veterinary Medicine, Kagoshima University, 1-21-24 Korimoto, Kagoshima 890-0065, Japan
Interests: chronic kidney disease; acute kidney injury; glomerular disease; renal biopsy; renal pathology; immuno-histochemistry; molecular pathology

Special Issue Information

Dear Colleagues, 

Kidney disease is a serious clinical problem in companion animals, with increasing incidence as these animals’ longevity improves. However, clinical courses of the disease vary significantly among animal species, and thus treatment strategies based on human medicine may not always be effective. To develop an adequate and effective method for combating kidney disease in companion animals, elucidating the species-specific mechanisms of the development and progression of the disease is necessary. For this purpose, pathophysiological events, including changes in the cytokines, growth factors, and other molecules, must be demonstrated for each nephron segment and renal structure. Immunohistochemistry would be a powerful tool in the study of kidney disease in companion animals.

This Special Issue is inviting the submission of papers providing scientific evidence regarding the species-specific pathophysiological mechanisms of kidney disease in companion animals, not only in dogs and cats but also horses, birds, and exotic animals. Research using in situ hybridization is also welcome. Reports are not limited to chronic kidney disease and acute kidney injury; those covering any type of kidney disease will be considered. Research about normal kidneys is also welcome if it has a clinical background.

Prof. Dr. Akira Yabuki
Guest Editor

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Keywords

  • immunohistochemistry
  • in situ hybridization
  • pathophysiology
  • kidney disease
  • chronic kidney disease
  • acute kidney injury
  • companion animal
  • dog
  • cat

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Published Papers (1 paper)

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Research

16 pages, 8532 KiB  
Article
Risperidone Administration Attenuates Renal Ischemia and Reperfusion Injury following Cardiac Arrest by Antiinflammatory Effects in Rats
by Yang Hee Kim, Tae-Kyeong Lee, Jae-Chul Lee, Dae Won Kim, Hyun-Jin Tae, Joon Ha Park, Ji Hyeon Ahn, Choong-Hyun Lee, Moo-Ho Won and Seongkweon Hong
Vet. Sci. 2023, 10(3), 184; https://doi.org/10.3390/vetsci10030184 - 28 Feb 2023
Cited by 2 | Viewed by 2386
Abstract
Multi-organ dysfunction following cardiac arrest is associated with poor outcome as well as high mortality. The kidney, one of major organs in the body, is susceptible to ischemia and reperfusion; however, there are few studies on renal ischemia and reperfusion injury (IRI) following [...] Read more.
Multi-organ dysfunction following cardiac arrest is associated with poor outcome as well as high mortality. The kidney, one of major organs in the body, is susceptible to ischemia and reperfusion; however, there are few studies on renal ischemia and reperfusion injury (IRI) following the return of spontaneous circulation (ROSC) after cardiac arrest. Risperidone, an atypical antipsychotic drug, has been discovered to have some beneficial effects beyond its original effectiveness. Therefore, the aim of the present study was to investigate possible therapeutic effects of risperidone on renal IRI following cardiac arrest. Rats were subjected to cardiac arrest induced by asphyxia for five minutes followed by ROSC. When serum biochemical analyses were examined, the levels of serum blood urea nitrogen, creatinine, and lactate dehydrogenase were dramatically increased after cardiac arrest, but they were significantly reduced by risperidone administration. Histopathology was examined using hematoxylin and eosin staining. Histopathological injury induced by cardiac arrest was apparently attenuated by risperidone administration. Furthermore, alterations in pro-inflammatory cytokines (interleukin-6 and tumor necrosis factor-α) and anti-inflammatory cytokines (interleukin-4 and interleukin-13) were examined by immunohistochemistry. Pro-inflammatory and anti-inflammatory cytokine immunoreactivities were gradually and markedly increased and decreased, respectively, in the kidneys following cardiac arrest; however, risperidone administration after cardiac arrest significantly attenuated the increased pro-inflammatory cytokine immunoreactivities and the decreased anti-inflammatory cytokine immunoreactivities. Collectively, our current results revealed that, in rats, risperidone administration after cardiac arrest protected kidneys from IRI induced by cardiac arrest and ROSC through anti-inflammatory effects. Full article
(This article belongs to the Special Issue Immunohistochemistry of Animal Renal Disease)
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