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The Veterinary clinics of North America. Equine practice2022; 38(1); 1-12; doi: 10.1016/j.cveq.2021.11.001

Relevant Equine Renal Anatomy, Physiology, and Mechanisms of Acute Kidney Injury: A Review.

Abstract: Regulation of renal blood flow is by both extrinsic and intrinsic systems. Intrinsic regulation occurs via the afferent and efferent arterioles and tubuloglomerular feedback mechanisms with activation of the juxtaglomerular apparatus. Mechanisms of acute kidney injury are frequently associated with changes in renal blood flow. Acute tubular necrosis and apoptosis are common in horses following ischemic or toxic insults and in sepsis-associated acute kidney injury. Sepsis-associated renal injury often has a complex mechanism of disease involving both functional and obstructive changes in intrarenal circulation. Acute interstitial nephritis may occur following Leptospira sp infection or can be secondary to tubular necrosis.
Publication Date: 2022-03-10 PubMed ID: 35282956DOI: 10.1016/j.cveq.2021.11.001Google Scholar: Lookup
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Summary

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This article is a review of the anatomy and physiology of the horse’s kidney, with a focus on the causes and mechanisms of acute kidney injury.

Renal Blood Flow Regulation

The review highlights the dual system for the regulation of renal blood flow in horses. The two systems include:

  • Extrinsic Regulation: It does not provide details on how extrinsic regulation happens. However, typically, extrinsic regulation is led by nervous and hormonal controls that counters changes in blood pressure, generally from outside the kidneys.
  • Intrinsic Regulation: This type of regulation is within the kidneys. It brings about the myogenic and tubuloglomerular feedback mechanisms, activating the juxtaglomerular apparatus. This complex system involves various elements in the kidneys like the afferent and efferent arterioles, working to moderate the filtration rate.

Acute Kidney Injury Mechanisms

The paper associates changes in renal blood flow with the occurrence of acute kidney injuries. It describes several mechanisms leading to these injuries:

  • Acute Tubular Necrosis: This type of injury follows ischemic or toxic insults, which are damages caused by insufficient blood supply to the kidneys or exposure to poisonous substances. It leads to cell death (necrosis) of kidney tubules, causing serious functional damages.
  • Apoptosis: This is a programmed cell death, likely triggered by cell damage or disease. It’s common in horses following the same ischemic or toxic insults contributing to acute tubular necrosis.
  • Sepsis-associated Renal Injury: This acute kidney injury arises from a severe bodywide infection (sepsis). It presents a complex mechanism involving both functional and obstructive changes in intrarenal circulation, affecting kidney function.

Causes of Acute Interstitial Nephritis

In some cases, acute interstitial nephritis (inflammation of the kidneys) occurs. The review attributes this to two main causes:

  • Leptospira sp Infection: One cause might be an infection from Leptospira bacteria species, which are often transmitted to horses through contaminated water or soil.
  • Tubular Necrosis: A secondary cause could be the aforementioned tubular necrosis, which results in further inflammation of kidney tissues.

Cite This Article

APA
Divers TJ. (2022). Relevant Equine Renal Anatomy, Physiology, and Mechanisms of Acute Kidney Injury: A Review. Vet Clin North Am Equine Pract, 38(1), 1-12. https://doi.org/10.1016/j.cveq.2021.11.001

Publication

ISSN: 1558-4224
NlmUniqueID: 8511904
Country: United States
Language: English
Volume: 38
Issue: 1
Pages: 1-12
PII: S0749-0739(21)00072-9

Researcher Affiliations

Divers, Thomas J
  • College of Veterinary Medicine, Cornell University, 930 Campus Road, Ithaca, NY 14853-6401, USA. Electronic address: tjd8@cornell.edu.

MeSH Terms

  • Acute Kidney Injury / veterinary
  • Animals
  • Horse Diseases
  • Horses
  • Kidney
  • Nephritis, Interstitial / veterinary
  • Renal Circulation / physiology

Conflict of Interest Statement

Disclosure The author has nothing to disclose.

Citations

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